Oncology Research 26(5) Abstracts

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Oncology Research, Vol. 26, pp. 665-673, 2018
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
14908298412505
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

Knockdown of Long Noncoding RNA TUG1 Inhibits the Proliferation and Cellular Invasion of Osteosarcoma Cells by Sponging miR-153

Heping Wang,* Yanzhang Yu,Shuxin Fan,* and Leifeng Luo*

*Department of Orthopedics, Zhoukou Central Hospital, Zhoukou, P.R. China
†Department of Surgery, Zhoukou Central Hospital, Zhoukou, P.R. China

Long noncoding RNA (lncRNA) taurine-upregulated gene 1 (TUG1) has been confirmed to be involved in the progression of various cancers; however, its mechanism of action in osteosarcoma has not been well addressed. In our study, TUG1 was overexpressed and miR-153 was downregulated in osteosarcoma tissues and cell lines. A loss-of-function assay showed that TUG1 knockdown suppressed the viability, colony formation, and invasion of osteosarcoma cells in vitro. Moreover, TUG1 was confirmed to be an miR-153 sponge. Ectopic expression of TUG1 reversed the inhibitory effect of miR-153 on the proliferation and invasion of osteosarcoma cells. Further transplantation experiments proved the carcinogenesis of TUG1 in osteosarcoma in vivo. Collectively, our study elucidated that TUG1 contributes to the development of osteosarcoma by sponging miR-153. These findings may provide a novel lncRNA-targeted therapy for patients with osteosarcoma.

Key words: Taurine-upregulated gene 1 (TUG1); miR-153; Proliferation; Invasion; Osteosarcoma

Address correspondence to Heping Wang, Department of Orthopedics, Zhoukou Central Hospital, East Section of Renmin Road, Zhoukou 466000, P.R. China. Tel: +86-0394-8222893; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 675-681, 2018
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DOI: https://doi.org/10.3727/096504017X
14920318811730
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Long Noncoding RNA PVT1 Promotes Melanoma Progression via Endogenous Sponging miR-26b

Bao-Juan Wang,* Hong-Wei Ding,† and Guo-An Ma†

*Department of Traditional Chinese Medicine, The Second Hospital of Hengshui City, Hengshui City, Hebei Province, P.R. China
†Department of Dermatology, Harrison International Heping Hospital, Hengshui City, Hengshui City, Hebei Province, P.R. China

Melanoma is an extremely aggressive malignant skin tumor with a high mortality. Various long noncoding RNAs (lncRNAs) have been reported to be associated with the oncogenesis of melanoma. The purposes of this study were to investigate the potential role of lncRNA PVT1 in melanoma progression and to explore its possible mechanisms. A total of 35 patients who were diagnosed with malignant melanoma were enrolled in this study. Expression of PVT1 was significantly upregulated in melanoma tissue and was associated with a poor prognosis. Loss-of-function experiments showed that PVT1 knockdown markedly suppressed the proliferation activity, induced cell cycle arrest at the G0/G1
phase, and enhanced the apoptosis of melanoma cell lines. Bioinformatics analysis and dual-luciferase reporter assay revealed that PVT1 directly bound to miR-26b, which had been verified to be a tumor suppressor in melanoma. Moreover, further functional rescue experiments revealed that PVT1 knockdown could observably reverse the tumor-promoting role of the miR-26b inhibitor. Overall, our study demonstrates the oncogenic role of PVT1 as a miR-26b sponge, possibly providing a novel therapeutic target for melanoma.

Key words: Melanoma; Long noncoding RNAs (lncRNAs); PVT1; miR-26b; Sponge

Address correspondence to Guo-An Ma, Department of Dermatology, Harrison International Heping Hospital, No. 180 People Middle Road, Taocheng District, Hengshui City, Hebei Province 053000, P.R. China. Tel: +86-0318-212383; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 683-690, 2018
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DOI: https://doi.org/10.3727/096504017X
14982585511252
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

miR-144-3p Targets FosB Proto-oncogene, AP-1 Transcription Factor Subunit (FOSB) to Suppress Proliferation, Migration, and Invasion of PANC-1 Pancreatic Cancer Cells

Shidan Liu,1 Jiaxi Luan,1 and Yan Ding

The First Department of General Surgery, Daqing Oilfield General Hospital, Daqing, Heilongjiang, P.R. China

This study aimed to investigate the role of miR-144-3p in pancreatic cancer (PC) carcinogenesis and to explore the mechanism of its function in PC. miR-144-3p was downregulated in PC tissues and cells. miR-144-3p overexpression significantly inhibited PC cell proliferation, migration, and invasion. FosB proto-oncogene, AP-1 transcription factor subunit (FOSB) was a target gene of miR-144-3p. miR-144-3p could repress PC cell proliferation, migration, and invasion by inhibiting the expression of FOSB. In conclusion, miR-144-3p plays an important role in PC cell proliferation, migration, and invasion by targeting FOSB. miR-144-3p may provide a new target for the development of therapeutic agents against PC.

Key words: Pancreatic cancer (PC); miR-144-3p; FosB proto-oncogene, AP-1 transcription factor subunit (FOSB); Cell proliferation; Cell migration; Cell invasion

1These authors provided equal contribution to this work.
Address correspondence to Yan Ding, The First Department of General Surgery, Daqing Oilfield General Hospital, No. 9 Zhongkang Street, Saertu District, Daqing, Heilongjiang 163000, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 691-701, 2018
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DOI: https://doi.org/10.3727/096504017X
15101398724809
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Downregulated Trophinin-Associated Protein Plays a Critical Role in Human Hepatocellular Carcinoma Through Upregulation of Tumor Cell Growth and Migration

Yifan Lian,*1 Weiming Fan,†1 Yanlin Huang,‡ Hongbo Wang,* Jialiang Wang,* Liang Zhou,‡ Xiaojuan Wu,‡ Meihai Deng,† and Yuehua Huang*‡

*Guangdong Province Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, P.R. China
†Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, P.R. China
‡Department of Infectious Diseases, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, P.R. China

Trophinin-associated protein (TROAP) was a protein first identified to mediate the process of embryo transplantation and later found to be involved in microtubule regulation. However, little is known about the role of TROAP in hepatocellular carcinoma (HCC). In the present study, we reported that both TROAP mRNA and protein expressions were downregulated in human HCC samples as well as cell lines. A high level of TROAP was associated with small tumor size (p < 0.05), minor tumor nodules (p < 0.01), and mild vein invasion (p < 0.05). We further constructed in vitro TROAP depletion and overexpression HCC cell models. TROAP depletion significantly enhanced the proliferation and colony formation abilities, whereas TROAP overexpression had an inhibitory effect on the growth of HCC cells. The G1/S phase arrest by TROAP overexpression correlated with increased cell cycle inhibitors p21 and p27, and declined cell cycle promoting kinase complex CDK6/cyclin D1. Depressed TROAP expression enhanced the migration ability, while the opposite influence was observed in TROAP-overexpressed HCC cells. Taken together, these results indicate that TROAP suppresses cellular growth and migration in HCC. This discovery will further our understanding of the pathogenic mechanisms of human HCC.

Key words: Trophinin-associated protein (TROAP); Hepatocellular carcinoma (HCC); Cell cycle; Tumor growth; Migration

1These authors provided equal contribution to this work.
Address correspondence to Yuehua Huang, M.D., Ph.D., Department of Infectious Diseases and Guangdong Provincial Key Laboratory of Liver Disease Research, The Third Affiliated Hospital of Sun Yat-Sen University, 600 Tian He Road, Guangzhou 510630, P.R. China. Tel: 8620-85252702; Fax: 8620-85253305; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Meihai Deng, M.D., Department of Hepatobiliary Surgery, The Third Affiliated Hospital of Sun Yat-Sen University, 600 Tian He Road, Guangzhou 510630, P.R. China. Tel: 8620-85252700; Fax: 8620-85253305; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 703-712, 2018
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DOI: https://doi.org/10.3727/096504017X
14982569377511
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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miR-181a-5p Promotes Proliferation and Invasion and Inhibits Apoptosis of Cervical Cancer Cells via Regulating Inositol Polyphosphate-5-Phosphatase A (INPP5A)

Meng Yang,* Xu Zhai,† Tingting Ge,* Chang Yang,* and Ge Lou*

*Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, P.R. China
†Department of Anesthesia, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, P.R. China

Expression of miR-181a-5p associates with the proliferation and progression of cancer cells via its targets. This study was designed to investigate the effect of miR-181a-5p and its target inositol polyphosphate-5-phosphatase A (INPP5A) on the progression of cervical cancers. Upregulation of miR-181a-5p was revealed in the cervical cancer cell lines HeLa and SiHa in comparison with a normal cervical epithelium cell line End1/E6E7 (p < 0.001). The inhibition and upregulation of miR-181a-5p in cervical cancer cell lines significantly reduced or increased cell proliferation and invasion capacity, accompanied with enhanced or reduced apoptosis (p < 0.05). Moreover, INPP5A overexpression significantly inhibited cell proliferation and invasion capacity and enhanced cell apoptosis. The target relationship of miR-181a-5p to INPP5A was demonstrated by both the results of the Dual-Luciferase Reporter Assay and the fact that the miR-181a-5p mimic attenuated INPP5A’s effect on cell proliferation, invasion, and apoptosis. To sum up, the overexpression of miR-181a-5p enhanced cell proliferation and invasion and inhibited apoptosis of cervical cancer cells by negatively targeting INPP5A. Therefore, inhibition of miR-181a-5p might benefit the inhibition of cervical cancer cell invasion.

Key words: Cervical cancer; miR-181a-5p; Proliferation; Inositol polyphosphate-5-phosphatase A (INPP5A)

Address correspondence to Ge Lou, Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin Medical University, No. 6 Baojian Road, Nangang District, Harbin, Heilongjiang 150081, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 713-723, 2018
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DOI: https://doi.org/10.3727/096504017X
15016337254641
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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miR-204 Regulates Cell Proliferation and Invasion by Targeting EphB2 in Human Cervical Cancer

Shanhong Duan,* Ali Wu,† Zhengyu Chen,‡ Yarong Yang,* Liying Liu,* and Qi Shu*

*Department of Gynecology, Shaanxi Nuclear Industry 215 Hospital, Xianyang, Shaanxi, P.R. China
†Department of Endoscopy, Shaanxi Nuclear Industry 215 Hospital, Xianyang, Shaanxi, P.R. China
‡Department of Spine Surgery, The First People’s Hospital of Xianyang City, Xianyang, Shaanxi, P.R. China

MicroRNAs (miRNAs) are small noncoding RNAs that are involved in human carcinogenesis and progression. miR-204 has been reported to be a tumor suppressor in several cancer types. However, the function and underlying molecular mechanism of miR-204 in cervical cancer (CC) are still unclear. In the present study, the expression level of miR-204 was measured using the qRT-PCR method in 30 paired CC clinical samples and in 6 CC cell lines. We found that the expression of miR-204 was significantly downregulated in CC tissues and cell lines compared to normal cervical tissues and cell line. miR-204 was overexpressed by transfection with the miR-204 mimic in HeLa and C33A cell lines in the following experiments. The results showed that overexpression of miR-204 dramatically suppressed cell proliferation, migration, and invasion, caused cell cycle arrest at the G0/G1
phase, promoted cell apoptosis in vitro, and inhibited tumor growth in vivo. Western blot results indicated that overexpressing miR-204 decreased the expressions of CDK2, cyclin E, MMP2, MMP9, Bcl2, whereas it enhanced Bax expression and suppressed the activation of the PI3K/AKT signaling pathways in CC cells. Ephrin type B receptor 2 (EphB2) was identified as a direct target of miR-204 in CC cells according to bioinformatics analysis and luciferase reporter assay. Furthermore, knockdown of EphB2 mimicked the inhibitory effect of miR-204 on the proliferation, invasion, and migration of CC cells. These findings suggested that miR-204 might serve as a tumor suppressor in the development of CC by directly targeting EphB2.

Key words: MicroRNA; Cervical cancer (CC); Cell proliferation; Metastasis; Ephrin type-B receptor 2 (EphB2)

Address correspondence to Shanhong Duan, Department of Gynecology, Shaanxi Nuclear Industry 215 Hospital, No 35 Weiyang West Road, Xianyang, 712000 Shaanxi, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 725-734, 2018
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DOI: https://doi.org/10.3727/096504017X
15119467381615
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Long Noncoding RNA (lncRNA) HOTAIR Affects Tumorigenesis and Metastasis of Non-Small Cell Lung Cancer by Upregulating miR-613

Caiyu Jiang, Yan Yang, Yang Yang, Lu Guo, Jiang Huang, Xingren Liu, Chi Wu, and Jun Zou

Department of Respiratory and Critical Care Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital, Sichuan, P.R. China

Non-small cell lung cancer (NSCLC) is one of the most deadly cancers with poor prognosis. Recent findings suggested that the lncRNA HOTAIR played an important role in tumorigenesis and metastasis. In the present study, HOTAIR was highly expressed in NSCLC tumor tissues and cell lines (H1299, H23, H292, and A549). Downregulation of HOTAIR suppressed cell proliferation and invasion, while it promoted apoptosis of NSCLC cells. The targeting relationship between HOTAIR and miR-613 was first revealed by bioinformatics prediction. miR-613 was found to be lowly expressed in NSCLC tumor tissues and cell lines. Knockdown of HOTAIR increased the expression of miR-613 significantly, and cotransfection with miR-613 inhibitor reversed this increase, indicating that the expression of miR-613 was negatively regulated by HOTAIR. The targeting relationship between HOTAIR and miR-613 was further confirmed through the luciferase report assay. Moreover, the cotransfection of HOTAIR shRNA and miR-613 inhibitor counteracted the tumor inhibition effects of HOTAIR shRNA through promoting cell proliferation and invasion while suppressing apoptosis in NSCLC cells, suggesting that the HOTAIR/miR-613 axis was involved in tumorigenesis and metastasis of NSCLC. In vivo experiments revealed that knockdown of HOTAIR decreased tumor growth and invasion and increased apoptosis and miR-613 expression. In conclusion, our study indicated that downregulation of HOTAIR suppressed tumorigenesis and metastasis of NSCLC via upregulating the expression of miR-613. The HOTAIR/miR-613 axis might provide a new potential therapeutic strategy for NSCLC treatment.

Key words: Hox transcript antisense intergenic RNA (HOTAIR); Drug resistance; Non-small cell lung cancer (NSCLC); Autophagy

Address correspondence to Yan Yang, Department of Respiratory and Critical Care Medicine, Sichuan Academy of Medical Sciences and Sichuan Provincial People’s Hospital, No. 32 West Second Section First Ring Road, Chengdu, 610072 Sichuan, P.R. China. Tel: 028-87394148; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 735-741, 2018
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DOI: https://doi.org/10.3727/096504017X
15021536183490
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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miR-641 Functions as a Tumor Suppressor by Targeting MDM2 in Human Lung Cancer

Qinglong Kong, Nan Shu, Jun Li, and Ning Xu

Department of Thoracic Surgery, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, P.R. China

Lung cancer is the leading cause of deaths due to cancer. Studies suggest an important role of microRNAs (miRNAs) in a variety of cancers, including lung cancer. In the present study, we evaluated the role of miR-641 in human lung cancer A549 cells. Quantitative RT-PCR and Western blot were used to measure mRNA and protein expression, respectively. Cell viability and cell apoptosis were respectively measured by MTT assay and flow cytometry. In addition, luciferase activity assay was used to identify the target of miR-641. The expression of miR-641 was downregulated in lung cancer tissues and lung cancer cell lines (p < 0.05 or p < 0.01). Overexpression of miR-641 significantly inhibited proliferation and induced apoptosis of lung cancer cells (p < 0.05, p < 0.01, or p < 0.001). MDM2 was identified as a direct target of miR-641. Overexpression of miR-641 decreased the expression of MDM2 and increased the expression of p53 in lung cancer cells.

Key words: miR-641; Cell proliferation; Murine double minute 2 (MDM2); Lung cancer; p53; Apoptosis

Address correspondence to Qinglong Kong, Department of Thoracic Surgery, Dalian Municipal Central Hospital Affiliated of Dalian Medical University, No. 42 Xuegong Street, Dalian 116033, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 743-751, 2018
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DOI: https://doi.org/10.3727/096504017X
15120379906339
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Knockdown of NF-κB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo

Amanda Ikegami,* Luiz Felipe S. Teixeira,* Marina S. Braga,† Matheus Henrique Dos S. Dias,‡ Eduardo C. Lopes,‡ and Maria Helena Bellini*

*Department of Biotechnology, IPEN-CNEN/SP, Sao Paulo, Brazil
†Department of Pharmacy, Faculty of Pharmaceutical Sciences, University of Sao Paulo, Sao Paulo, Brazil
Laboratorio Especial de Toxinologia Aplicada (LETA), Center of Toxins, Immune-Response and Cell Signaling (CeTICS), Instituto Butantan, Sao Paulo, Brazil

Renal cell carcinoma (RCC) accounts for approximately 2%–3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the biggest obstacles to the effective treatment of RCC. The NF-κB transcription factor is one of several molecules identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have demonstrated the activation of NF-κB in RCC, and many have implicated NF-κB1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to deliver shRNA targeting NF-κB1 into mouse RCC (Renca) cells. It was determined that the knockdown of the NF-κB1 gene led to a reduction in cell proliferation and late apoptosis/necrosis in vitro. Flow cytometry analysis demonstrated G2/M arrest in the cells. In addition, immunoblotting analysis revealed a significant increase in cyclin B1 and Bax. In vivo experiments showed that Renca-shRNA-NF-κB1 cells have significantly diminished tumorigenicity. Moreover, immunohistochemical analysis revealed an increase in necrotic areas of Renca-shRNA-NF-κB1 tumors. Thus, this study indicates that downregulation of NF-κB1 can suppress RCC tumorigenesis by inducing late apoptosis/necrosis. Therefore, NF-κB1 may be a potential therapeutic target for RCC.

Key words: Renal cell carcinoma (RCC); Proliferation; Short hairpin RNA (shRNA); Nuclear factor κ-light-chain-enhancer of activated B cells 1 (NF-κB1)

Address correspondence to Maria Helena Bellini, Department of Biotechnology, IPEN-CNEN/SP, 2242 Av. Lineu PrestesCidade UniversitariaButanta 05508-000, Sao Paulo, Brazil. Tel: +55-011-31339706; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 753-764, 2018
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DOI: https://doi.org/10.3727/096504017X
15024946480113
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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lncRNA C2dat1 Promotes Cell Proliferation, Migration, and Invasion by Targeting miR-34a-5p in Osteosarcoma Cells

Daofu Jia,* Yanping Niu,† Dongling Li,‡ and Zhaorui Liu§

*Department of Emergency Medicine, Jinan Central Hospital, Jinan, Shandong, P.R. China
†Department of Outpatient Service Center, Qianfoshan Hospital of Shandong University, Jinan, Shandong, P.R. China
‡Department of Operation Room, Qilu Children’s Hospital of Shandong University, Jinan, Shandong, P.R. China
§Department of Orthopedic Surgery, Jinan Central Hospital, Jinan, Shandong, P.R. China

Osteosarcoma is a highly aggressive malignant bone tumor with poor prognosis. Evidence has suggested that lncRNAs are deregulated in multiple cancers. In this study, we investigated the role of the lncRNA C2dat1 on the biological functions of osteosarcoma cells. The expressions of C2dat1, miR-34a-5p, and Sirt1 in human osteosarcoma cells were altered by transfection with their specific vectors/shRNA or mimic/inhibitor. Cell viability, migration, invasion, and apoptosis were assessed posttransfection. The mRNA and protein levels of C2dat1, miR-34a-5p, and Sirt1 were detected by qRT-PCR and Western blot. The results showed that C2dat1 suppression reduced cell viability, invasion, and migration, whereas it increased cell apoptosis in OS-732 cells. The expression of miR-34a-5p was downregulated when C2dat1 was overexpressed, whereas it negatively regulated Sirt1 expression. miR-34a-5p overexpression inhibited cell viability, migration, and invasion and promoted cell apoptosis in osteosarcoma cells by downregulation of Sirt1. Furthermore, miR-34a-5p overexpression deactivated the p38/ERK/AKT and Wnt/b-catenin signaling pathways by inhibition of Sirt1.

Key words: Osteosarcoma; C2dat1; miR-34a-5p; Sirt1

Address correspondence to Zhaorui Liu, Department of Orthopedic Surgery, Jinan Central Hospital, No. 105 Jiefang Road, Lixia District, Jinan 250013, Shandong, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 765-773, 2018
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
15021536183535
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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MicroRNA-152 Suppresses Human Osteosarcoma Cell Proliferation and Invasion by Targeting E2F Transcription Factor 3

Chao Ma, Jinfeng Han, Dong Dong, and Nanya Wang

The First Hospital of Jilin University, Changchun, P.R. China

MicroRNA-152 (miR-152) expression has been reported to be downregulated in osteosarcoma (OS). However, the role of miR-152 in OS is not well documented. In the present study, we aimed to explore the function and underlying mechanism of miR-152 in OS. We found that miR-152 was underexpressed in OS tissues and cell lines. Decreased miR-152 was inversely correlated with lymph node metastasis and advanced clinical stage. Overexpression of miR-152 significantly inhibited cell proliferation, colony formation, migration, and invasion of OS cells. Bioinformatics analyses showed that miR-152 directly targeted E2F transcription factor 3 (E2F3), as further confirmed by a dual-luciferase reporter assay. E2F3 expression was upregulated and inversely correlated with miR-152 expression level in human OS tissues. Moreover, the inhibitory effects of miR-152 on OS growth and invasion were attenuated by E2F3 overexpression. Taken together, our findings indicated that miR-152 reduced OS growth and invasion by targeting E2F3 and provided new evidence of miR-152 as a potential therapeutic target for OS.

Key words: Osteosarcoma (OS); miR-152; E2F transcription factor 3 (E2F3); Proliferation; Invasion

Address correspondence to Nanya Wang, The First Hospital of Jilin University, #71 Xinmin Street, Changchun 130021, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 775-783, 2018
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DOI: https://doi.org/10.3727/096504017X
15132494420120
E-ISSN 1555-3906
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MicroRNA-296 Targets Specificity Protein 1 to Suppress Cell Proliferation and Invasion in Cervical Cancer

Lili Lv* and Xiaodong Wang†

*Department of Oncology and Hematology, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China
†Department of Digestive Endoscopy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China

Cervical cancer is the third most commonly diagnosed malignancy and the fourth leading cause of cancer-related deaths in women worldwide. MicroRNA-296 (miR-296) is aberrantly expressed in a variety of human cancer types. However, the expression levels, biological roles, and underlying molecular mechanisms of miR-296 in cervical cancer remain unclear. This study aimed to detect miR-296 expression in cervical cancer and evaluate its roles and underlying mechanisms in cervical cancer. This study demonstrated that miR-296 was significantly downregulated in cervical cancer tissues and cell lines. Restoring the expression of miR-296 inhibited the proliferation and invasion of cervical cancer cells. Moreover, miR-296 directly targeted the 3¢-untranslated regions of specificity protein 1 (SP1) and decreased its endogenous expression at both the mRNA and protein levels. Similar to induced miR-296 expression, SP1 knockdown suppressed the proliferation and invasion of cervical cancer cells. Besides, resumption expression of SP1 rescued the tumor-suppressing roles of miR-296 in cervical cancer. These results indicated that miR-296 may act as a tumor suppressor in cervical cancer by directly targeting SP1. Therefore, SP1 may be developed as a therapeutic target for the treatment of patients with this malignancy.

Key words: MicroRNA-296; Cervical cancer; Proliferation; Invasion; Specificity protein 1 (SP1)

Address correspondence to Xiaodong Wang, Department of Digestive Endoscopy, The Second Hospital of Jilin University, 218 Ziqiang Street, Changchun 130000, Jilin, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 785-794, 2018
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DOI: https://doi.org/10.3727/096504017X
15127309628257
E-ISSN 1555-3906
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miR-188 Inhibits Glioma Cell Proliferation and Cell Cycle Progression Through Targeting β-Catenin

Nan Li,*† Hangyu Shi,† Lu Zhang,‡ Xu Li,§ Lu Gao,† Gang Zhang,† Yongqiang Shi,† and Shiwen Guo*

*Department of Neurosurgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, P.R. China
†Department of Neurosurgery, Xi’an Children’s Hospital, Xi’an, Shaanxi, P.R. China
‡Department of Foreign Languages, Ming De College of Northwestern Polytechnical University, Xi’an, Shaanxi, P.R. China
§Department of First Internal Medicine, Shaanxi Province Tumor Hospital, Xi’an, Shaanxi, P.R. China

MicroRNAs (miRNAs) play important roles in several human cancers. Although miR-188 has been suggested to function as a tumor repressor in cancers, its precise role in glioma and the molecular mechanism remain unknown. In the present study, we investigated the effect of miR-188 on glioma and explored its relevant mechanisms. We found that the expression of miR-188 is dramatically downregulated in glioma tissues and cell lines. Subsequent investigation revealed that miR-188 expression was inversely correlated with β-catenin expression in glioma tissue samples. Using a luciferase reporter assay, β-catenin was determined to be a direct target of miR-188. Overexpression of miR-188 reduced β-catenin expression at both the mRNA and protein levels, and inhibition of miR-188 increased β-catenin expression. Moreover, we found that overexpression of miR-188 suppressed glioma cell proliferation and cell cycle G1–S transition, whereas inhibition of miR-188 promoted glioma cell proliferation. Importantly, silencing β-catenin recapitulated the cellular and molecular effects seen upon miR-188 overexpression, which included inhibiting glioma cell proliferation and G1–S transition. Taken together, our results demonstrated that miR-188 inhibits glioma cell proliferation by targeting β-catenin, representing an effective therapeutic strategy for glioma.

Key words: Glioma; MicroRNA-188 (miR-188); β-Catenin; Proliferation; Cell cycle

Address correspondence to Shiwen Guo, Department of Neurosurgery, The First Affiliated Hospital of Xi’an Jiaotong University, No. 277 West Yanta Road, Xi’an 710054, Shaanxi, P.R. China. Tel: +86-0373-63587789; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 795-800, 2018
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
15004613574679
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

miR-133a-3p Targets SUMO-Specific Protease 1 to Inhibit Cell Proliferation and Cell Cycle Progress in Colorectal Cancer

Guo-Qiang Zhou,* Fu Han,* Zhi-Liang Shi,* Liang Yu,* Xue-Feng Li,* Cheng Yu,* Cheng-Long Shen,* Dai-Wei Wan,† Xin-Guo Zhu,† Rui Li,‡ and Song-Bing He†

*Department of Gastrointestinal Surgery, Changshu No. 2 Hospital, Suzhou, P.R. China
†Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China
‡Department of Gastroenterology, The First Affiliated Hospital of Soochow University, Suzhou, P.R. China

Dysregulation of SUMO-specific protease 1 (SENP1) expression has been reported in several kinds of cancer, including human colorectal and prostate cancers, proposing SENP1 as an oncogene with a critical role in cancer progression. miR-133a-3p has been reported as a tumor suppressor in several malignant neoplasias. However, the precise molecular mechanisms underlying its role in colorectal cancer remain largely unknown. The aim of this work was to investigate the relationship between miR-133a-3p and SENP1 in colorectal cancer cells. We found that miR-133a-3p expression was downregulated in colorectal cancer tissues. In silico analyses indicated that SENP1 is one of the target genes of miR-133a-3p. Overexpression of miR-133a-3p mimics was able to inhibit cell growth with G1
arrest of colorectal cancer cells. Overexpression of miR-133a-3p antisense promoted cell growth of colorectal cancer cells. The luciferase reporter experiments showed that miR-133a-3p regulated the expression of SENP1 by combining with its 3′-UTR and resulted in downregulation of SENP1 and upregulation of CDK inhibitors such as p16, p19, p21, and p27. These results suggest that the miR-133a-3p–SENP1 axis might play a role in cell proliferation and cell cycle regulation of colorectal cancer cells.

Key words: Colorectal cancer; miR-133a-3p; SUMO-specific protease 1 (SENP1); CDK inhibitors

Address correspondence to Song-Bing He, M.D., Ph.D., Department of General Surgery, The First Affiliated Hospital of Soochow University, No. 188 Shizi Street, Suzhou, Jiangsu Province 215006, P.R. China. Tel: +86-512-67780107; Fax: +86-512-67780107; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 801-807, 2018
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
15139039328978
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

Clinical Analysis of Hypersensitivity Reactions to Oxaliplatin Among Colorectal Cancer Patients

Yuping Shen, Chunyan Li, Weixing Liu, Wei Mao, Hong Qian, Hui Wang, and Qing Xu

Department of Oncology, The Tenth People’s Hospital of Shanghai, Tongji University, Shanghai, P.R. China

This study investigated the characteristics of oxaliplatin-induced hypersensitivity reactions (HSRs) and evaluated the efficacy of premedication for controlling HSRs among colorectal cancer patients. A retrospective study was performed on the clinical records of 291 patients with colorectal cancer in The Tenth People’s Hospital of Shanghai from January 2008 to January 2016. Patients who experienced HSRs to oxaliplatin were compared with those who did not. A total of 291 colorectal cancer patients received oxaliplatin, with 39 (13.40%) experiencing HSRs. Oxaliplatin-free interval and premedication with dexamethasone and antihistamine were independent variables for oxaliplatin-related HSRs. Rechallengingpatients with premedication was successful in 72.2% of the patients who successfully completed their treatment. Attention should be paid to patients with any prior exposure to oxaliplatin. Patients with grades 1 and 2 HSRs can successfully rechallenge with oxaliplatin and complete their treatment by premedication with dexamethasone and antihistamine.

Key words: Oxaliplatin; Hypersensitivity reaction (HSR); Colorectal cancer; Premedication

Address correspondence to Qing Xu, Ph.D., Department of Oncology, The Tenth People’s Hospital of Shanghai, Tongji University, No. 301 Yanchang Middle Road, 200072 Shanghai, P.R. China. Tel: +86 02166313384; Fax: +86 02166313384; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 809-816, 2018
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
15123872205507
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

Review

Aberrant lncRNA Expression in Multiple Myeloma

Hui Meng,*1 Lei Han,†1 Chun Hong,* Jinya Ding,* and Qianchuan Huang*

*Department of Medical Laboratory, Wuhan General Hospital of PLA, Wuhan, P.R. China
†Discipline Section of Medical Department, Wuhan General Hospital of PLA, Wuhan, P.R. China

Multiple myeloma (MM), a type of malignant tumor, is characterized by dysplasia of clonal plasma cells in the bone marrow. People with MM will have damaged organs or tissues due to secretion of large amounts of monoclonal immunoglobulin or fragments (M protein). Despite improved survivability by novel treatment strategies over the last decade, MM is still incurable by current therapies. Long noncoding RNAs (lncRNAs), with length of more than 200 nucleotides, have been reported to act as important regulators in many diseases, including MM. Recent studies have reported aberrant lncRNA expression in MM; these dysregulated lncRNAs can play oncogenic and/or tumor-suppressive roles in the development and progression of MM. In this article, we present a general overview on the role of lncRNAs in MM pathogenesis and discuss their potential as prognostic biomarkers and targets for treatment.

Key words: Long noncoding RNAs (lncRNAs); Multiple myeloma (MM); Expression

1These authors provided equal contribution to this work.
Address correspondence to Qianchuan Huang, Wuhan General Hospital of PLA, No. 627 Wuluo Road, Wuchang District, Wuhan, Hubei 430070, P.R. China. Tel: +86-027-50772652; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 26, pp. 817-826, 2018
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504017X
15130753659625
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

Review

The Peritoneal Macrophages in Inflammatory Diseases and Abdominal Cancers

Ting Liu,1 Fang Liu,1 Lei-Wen Peng, Li Chang, and Yong-Mei Jiang

Department of Laboratory Medicine, West China Second University Hospital, and Key Laboratory of Birth Defects and Related Diseases of Women and Children of MOE, Sichuan University, Chengdu, P.R. China

Peritoneal macrophages (PMs) are the major cell type of peritoneal cells that participate in multiple aspects of innate and acquired immunity in the peritoneal cavity. PMs have an ability to release a large amount of proinflammatory and anti-inflammatory cytokines and therefore play a critical role in regulating the differentiation of innate immune cells and inflammatory T cells. Accumulating studies demonstrate that the immunological reactions and inflammatory responses of PMs are strongly related to the pathogenic processes of various inflammatory diseases and abdominal cancers. Consequently, the regulation of PM activation has gradually emerged as a promising target for immunotherapy, and better understanding of the distinctly biological function of PMs in individual diseases is crucial for designing specific and effective therapeutic agents. This review covers the characterization and immunological function of PMs in hosts with inflammatory diseases and abdominal cancers.

Key words: Peritoneal macrophages (PMs); Inflammatory diseases; Abdominal cancers

1These authors provided equal contribution to this work.
Address correspondence to Yong-Mei Jiang, Department of Laboratory Medicine, West China Second University Hospital, Sichuan University, No. 20, Section 3, Renmin South Road, Chengdu, Sichuan 610041, P. R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it