Oncology Research 27(1) Abstracts

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Oncology Research, Vol. 27, pp. 1-8, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15172738893959
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

Propofol Inhibits Lung Cancer A549 Cell Growth and Epithelial–Mesenchymal Transition Process by Upregulation of MicroRNA-1284

Wei-Zhen Liu and Nian Liu

Department of Anesthesia, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, P.R. China

Propofol has been widely used in lung cancer resections. Some studies have demonstrated that the effects of propofol might be mediated by microRNAs (miRNAs). This study aimed to investigate the effects and mechanisms of propofol on lung cancer cells by regulation of miR-1284. A549 cells were treated with different concentrations of propofol, while transfected with miR-1284 inhibitor, si-FOXM1, and their negative controls. Cell viability, migration, and invasion, and the expression of miR-1284, FOXM1, and epithelial–mesenchymal transition (EMT) factors were detected by CCK-8, TranswellqRT-PCR, and Western blot assays, respectively. In addition, the regulatory and binding relationships among propofol, miR-1284, and FOXM1 were assessed, respectively. Results showed that propofol suppressed A549 cell viability, migration, and invasion, upregulated E-cadherin, and downregulated N-cadherin, vimentin, and Snail expressions. Moreover, propofol significantly promoted the expression of miR-1284. miR-1284 suppression abolished propofol-induced decreases of cell viability, migration, and invasion, and increased FOXM1 expression and the luciferase activity of FOXM1-wt. Further, miR-1284 negatively regulated FOXM1 expression. FOXM1 knockdown reduced cell viability, migration, and invasion by propofol treatment plus miR-1284 suppression. In conclusion, our study indicated that propofol could inhibit cell viability, migration, invasion, and the EMT process in lung cancer cells by regulation of miR-1284.

Key words: Propofol; MicroRNA-1284; Cell viability; Epithelial–mesenchymal transition (EMT); Migration; Invasion

Address correspondence to Nian Liu, Department of Anesthesia, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, No. 283 Tongzipo Road, Yuelu District, Changsha 410013, Hunan Province, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 9-17, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15178732625479
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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miR-630 Inhibits Epithelial-to-Mesenchymal Transition (EMT) by Regulating the Wnt/β-Catenin Pathway in Gastric Cancer Cells

Dong Li,*1 Bo Tian,†1 and Xiaosheng Jin

*Medical Care Branch of Panjin Vocational and Technical College, Panjin, P.R. China
†Department of Surgical Oncology, Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, P.R. China
‡Department of Gastroenterology, Ruian People’s Hospital, Ruian, P.R. China

Despite availability of different treatments, gastric cancer remains the second highest cause of cancer-related deaths worldwide. This study was aimed to explore the role of miR-630 in gastric cancer by investigating the underlying mechanism of inhibiting epithelial-to-mesenchymal transition (EMT) of SGC-7901 and BGC-823 cells through the Wnt/
b-catenin pathway. Results showed that miR-630 was downregulated in several gastric cancer cell lines, including SGC-7901 and BGC-823. Transfection of miR-630 mimic showed a significant decrease in wound healing in a scratch assay in both cell lines compared to a scramble group. Also, transfection of miR-630 mimic inhibited cell viability, migration, and invasion of gastric cancer cells. miR-630 mimic transfection suppressed EMT by activating the Wnt/b-catenin pathway. This was supported by the fact that miR-630-mediated suppression of the EMT phenotype was reversed in the presence of the Wnt/b-catenin inhibitor ICG001. miR-630 plays a protective role against gastric cancer by suppressing EMT through activating the Wnt/b-catenin pathway.

Key words: MicroRNA 630 (miR-630); Epithelial–mesenchymal transition (EMT); Wnt/β-catenin pathway; Gastric cancer

1These authors provided equal contribution to this work.
Address correspondence to Xiaosheng Jin, Department of Gastroenterology, Ruian People’s Hospital, No. 108 Wansong Road, Ruian 325200, Zhejiang Province, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 19-27, 2019
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DOI: https://doi.org/10.3727/096504018X
15193469240508
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

MicroRNA-623 Targets Cyclin D1 to Inhibit Cell Proliferation and Enhance the Chemosensitivity of Cells to 5-Fluorouracil in Gastric Cancer

Lihua Jiang,*1 Wenchuan Yang,*1 Weishi Bian,† Hailin Yang,* Xia Wu,* Yuhua Li,* Wen Feng,* and Xuejian Liu*

*Department of Oncology, Linyi Third People’s Hospital, Shandong, P.R. China
†Department of Cardiology, Linyi Third People’s Hospital, Shandong, P.R. China

The dysregulation of microRNAs (miRNAs) plays an important function in the onset and progression of gastric cancer (GC). In addition, aberrantly expressed miRNAs affect the chemosensitivity of GC cells to chemotherapeutic drugs. Hence, miRNA-based targeted therapy might be applied to treat patients with GC exhibiting chemotherapeutic resistance. In this study, miRNA-623 (miR-623) expression was downregulated in GC tissues and cell lines. Functional analysis showed that the restored miR-623 expression could inhibit the proliferation of GC cells and enhance their chemosensitivity to 5-FU via the cell apoptosis pathway. Cyclin D1 (CCND1) was identified as a direct target gene of miR-623 in GC. The overexpressed CCND1 in GC tissues was negatively correlated with miR-623 level. The recovered CCND1 expression counteracted the effects of miR-623 on GC cell proliferation, chemosensitivity, and 5-FU-induced apoptosis. Thus, our results suggest that miR-623 might function as a tumor suppressor in GC and could be a promising therapeutic target for patients with GC, especially those with chemotherapeutic resistance.

Key words: MicroRNA-623; Gastric cancer (GC); Chemosensitivity; 5-Fluorouracil (5-FU); Cyclin D1 (CCND1)

1These authors provided equal contribution to this work.
Address correspondence to Xuejian Liu, Department of Oncology, Linyi Third People’s Hospital, 117 Huaxia Road, Linyi, Shandong 276023, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 29-38, 2019
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DOI: https://doi.org/10.3727/096504018X
15179694020751
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Silencing Artemis Enhances Colorectal Cancer Cell Sensitivity to DNA-Damaging Agents

Hai Liu,* Xuanxuan Wang,* Aihua Huang,† Huaping Gao,‡ Yikan Sun,§ Tingting Jiang,* Liming Shi,* Xianjie Wu,¶ Qinghua Dong,# and Xiaonan Sun*

*Department of Radiation Oncology, Sir Run Run Shaw Hospital, Sir Run Run Shaw Institute of Clinical Medicine of Zhejiang University, Hangzhou, P.R. China
†Department of Pathology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, P.R. China
‡Department of Pharmacy, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, P.R. China
§Faculty of Medicine, University of New South Wales, Sydney, Australia
¶Department of Dermatology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, P.R. China
#Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, P.R. China

Artemis is a key protein of NHEJ (nonhomologous end joining), which is the major pathway for the repair of IR-induced DSBs in mammalian cells. However, the expression of Artemis in tumors and the influence of silencing Artemis on tumor sensitivity to radiation have not been investigated fully. In this study, we investigated how the expression levels of Artemis may affect the treatment outcome of radiotherapy and chemotherapy in colorectal cancer cells. First, we found that the expression of Artemis is strong in some human rectal cancer samples, being higher than in adjacent normal tissues using immunohistochemical staining. We then knocked down Artemis gene in a human colorectal cancer cell line (RKO) using lentivirus-mediated siRNAs. Compared to the control RKO cells, the Artemis knockdown cells showed significantly increased sensitivity to bleomycin, etoposide, camptothecin, and IR. Induced by DNA-damaging agents, delayed DNA repair kinetics was found by the
g-H2AX foci assay, and a significantly increased cell apoptosis occurred in the Artemis knockdown RKO cells through apoptosis detection methods and Western blot. We also found that the p53/p21 signaling pathway may be involved in the apoptosis process. Taken together, our study indicates that manipulating Artemis can enhance colorectal cancer cell sensitivity to DNA-damaging agents. Therefore, Artemis can serve as a therapeutic target in rectal cancer therapy.

Key words: Colorectal cancer; Artemis; Small interfering RNA (siRNA); DNA repair; Ionizing radiation

Address correspondence to Xiaonan Sun, Ph.D., Department of Radiation Oncology, Sir Run Run Shaw Hospital, Sir Run Run Shaw Institute of Clinical Medicine of Zhejiang University, 3 Qinchun Road, Hangzhou, Zhejiang 310016, P.R. China. Tel: 86-571-86096916; Fax: 86-571-86044817; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 39-45, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15199482824130
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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lncRNA FEZF1-AS1 Is Associated With Prognosis in Lung Adenocarcinoma and Promotes Cell Proliferation, Migration, and Invasion

Zhenjun Liu,* Pei Zhao,* Yuping Han,† and Song Lu*

*ICU of Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, P.R. China
†Department of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, P.R. China

Long noncoding RNAs (lncRNAs) have been reported to play important roles in tumorigenesis. In the present study, we demonstrated that lncRNA forebrain embryonic zinc finger protein 1 (FEZF1) antisense RNA1 (FEZF1-AS1) is markedly upregulated in human lung adenocarcinoma (LAD) tissues and cell lines and is associated with poor prognosis. Loss of function revealed that deletion of FEZF1-AS1 expression significantly inhibited the LAD cell proliferation, invasion, and migration. Further studies revealed that downregulation of FEZF1-AS1 reduced mRNA and protein expression of its sense-cognate gene FEZF1 in LAD cells, and vice versa. Correlation analysis indicated that there was a positive correlation between FEZF1-AS1 and FEZF1 expression in LAD tissues. Additionally, rescue assay confirmed that the function of FEZF1-AS1 in LAD was mediated by FEZF1. Our findings suggested that dysregulation of FEZF1-AS1 contributed to the progression of LAD, which might be a potential target for LAD therapy.

Key words: Lung adenocarcinoma (LAD); FEZF1-AS1; FEZF1; Poor prognosis; Proliferation; Migration; Invasion

Address correspondence to Song Lu, ICU of Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, No. 55, the Fourth Section of Renmin South Road, Chengdu 610041, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 47-53, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15193843443255
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Knockdown of Long Noncoding RNA ENST457720 Inhibits Proliferation of Non-Small Cell Lung Cancer Cells In Vitro and In Vivo

Jia Yu, Qiyu Fang, and Shuyan Meng

Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, P.R. China

Non-small cell lung cancer (NSCLC) represents the leading cause of cancer-related mortality worldwide. More and more reports have identified important roles for long noncoding RNAs (lncRNAs) in cancer development. ENST457720 expression was upregulated in lung adenocarcinoma in a microarray-based lncRNA screen. We determined the expression levels of ENST457720 in NSCLC tissues with quantitative real-time PCR and then studied their clinical significance. We explored the biological significance of ENST457720 with gain- and loss-of-function analyses in vitro and in vivo. In this study, ENST457720 was expressed at higher levels in NSCLC tissues than in paired normal tissues. Higher ENST457720 expression was associated with larger tumor sizes, lymph node metastasis, and advanced TNM stage. ENST457720 silencing suppressed NSCLC cell proliferation in vitro and in vivo. Moreover, ENST457720 knockdown inhibited NSCLC invasion and reversed the epithelial-to-mesenchymal transition. ENST457720 promoted NSCLC proliferation and invasion, which may be a novel potential therapeutic target for NSCLC.

Key words: Non-small cell lung cancer (NSCLC); Long noncoding RNAs (lncRNAs); ENST457720; Proliferation; Apoptosis

Address correspondence to Shuyan Meng, Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 507 Minzhen Road, Yangpu District, Shanghai 200433, P.R. China. Tel: +86-02165115006-3068; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 55-64, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15201143705855
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

Genglong Zhu,* Xialei Liu,* Yonghui Su,† Fangen Kong,‡ Xiaopeng Hong,* and Zhidong Lin†

*Department of Hepatobiliary Surgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, P.R. China
†Department of General Surgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, P.R. China
‡Department of Neurosurgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, P.R. China

Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and CXCR4 in MHCC97 cells was altered by transient transfection. The effects of UCA1 and miR-301 on cell viability, migration, invasion, and apoptosis were assessed. The results revealed that UCA1 expression was relatively higher in MHCC97 cells than in MG63, hFOB1.19, and OS-732 cells. Knockdown of UCA1 reduced cell viability, inhibited migration and invasion, and promoted cell apoptosis. However, the effect of UCA1 knockdown on cell growth and migration was blocked by miR-301a overexpression, whose expression was regulated by UCA1. We also found that miR-301a positively regulated CXCR4 expression. CXCR4 inhibition reversed the effect of miR-301a overexpression on cell growth and migration. Moreover, miR-301a activated the Wnt/
b-catenin and NF-kB pathways via regulating CXCR4. The present study demonstrated that UCA1 inhibition exerted an antigrowth and antimigration role in MHCC97 cells through regulating miR-301a and CXCR4 expression.

Key words: Urothelial carcinoma-associated 1 (UCA1); MicroRNA-301a; CXCR4; Cell apoptosis; Migration and invasion; Liver cancer

Address correspondence to Zhidong Lin, Department of General Surgery, The Fifth Affiliated Hospital of Sun Yat-Sen University, No. 52 Meihua Dong Road, Zhuhai 519000, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 65-71, 2019
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DOI: https://doi.org/10.3727/096504018X
15191223015016
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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miR-188-5p Suppresses Gastric Cancer Cell Proliferation and Invasion via Targeting ZFP91

Yuping Peng, Xuning Shen, Honggang Jiang, Zhiheng Chen, Jiaming Wu, Yi Zhu, Yuan Zhou, and Jin Li

Department of Gastrointestinal Surgery, Jiaxing First Hospital, Jiaxing, Zhejiang Province, P.R. China

MicroRNAs (miRNAs) have been demonstrated to be essential regulators in the development and progression of various cancers. The role of miR-188-5p in gastric cancer (GC) has not been determined. In this study, we found that the expression of miR-188-5p was downregulated in GC tissues compared with adjacent normal tissues. The lowly expressed miR-188-5p was significantly associated with lymph node metastasis and advanced TNM stage. Moreover, overexpression of miR-188-5p significantly inhibited GC cell proliferation, migration, and invasion but promoted cellular apoptosis. Mechanistically, we identified transcription factor ZFP91 as a target gene of miR-188-5p in GC. We found that miR-188-5p overexpression significantly inhibited the expression of ZFP91 in GC cell lines. There was an inverse correlation between the expression of miR-188-5p and ZFP91 in GC tissues. We found that restoration of ZFP91 in miR-188-5p-overexpressed MGC-803 and SGC-7901 cells promoted cell proliferation, migration, and invasion. Finally, we also showed that overexpressionof miR-188-5p inhibited tumor growth in vivo. Taken together, our findings indicated that miR-188-5p serves as a tumor suppressor in human GC by targeting ZFP91, suggesting that miR-188-5p might be a promising therapeutic target for GC treatment.

Key words: miR-188-5p; Gastric cancer; Proliferation; Metastasis; ZFP91

Address correspondence to Yuping Peng, Department of Gastrointestinal Surgery, Jiaxing First Hospital, 1882 Zhonghuan South Road, Nanhu District, Jiaxing 314000, Zhejiang Province, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 73-80, 2019
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DOI: https://doi.org/10.3727/096504018X
15201099883047
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

TIMP-3 Increases the Chemosensitivity of Laryngeal Carcinoma to Cisplatin via Facilitating Mitochondria-Dependent Apoptosis

Xiaohui Shen, Xia Gao, Hui Li, Yajun Gu, and Junguo Wang

Department of Otolaryngology Head and Neck, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, Nanjing, P.R. China

Laryngeal carcinoma is a type of head and neck carcinoma with a high incidence and mortality. Chemotherapy treatments of human laryngeal carcinoma may fail due to the development of chemoresistance. Tissue inhibitor of metalloproteinase 3 (TIMP-3) has been shown to be implicated in a number of pathological processes typical for cancer. The present study aims to investigate the involvement of TIMP-3 in the chemoresistance of laryngeal carcinoma. We showed that TIMP-3 expression was significantly decreased in chemoresistant laryngeal carcinoma tissues compared with chemosensitivity tissues. Patients with low TIMP-3 expression exhibited poorer overall survival than those with high TIMP-3 expression. Moreover, cisplatin-resistant Hep-2 cells (Hep-2/R) were associated with the inhibition of mitochondrial membrane potential (MtMP) depolarization after cisplatin challenge. In addition, cisplatin resulted in a more pronounced mitochondrial cytochrome c release into the cytoplasm in Hep-2 cells than in their resistant variants. Overexpression of TIMP-3 by an adenovirus encoding TIMP-3 cDNA remarkably enhanced cisplatin-induced apoptosis, cytochrome c release, and caspase activation in Hep-2/R cells, thereby sensitizing cancer cells to cisplatin. On the other hand, downregulation of TIMP-3 markedly inhibited cisplatin-induced apoptosis in Hep-2 cells through attenuating mitochondria-dependent pathway activation. Taken together, these results demonstrate that decreased TIMP-3 expression may contribute to cisplatin resistance via inhibition of mitochondria-dependent apoptosis, indicating that forced TIMP-3 expression may be a useful strategy to improve the efficacy of cisplatin to treat laryngeal carcinoma.

Key words: Cisplatin; Chemoresistance; Laryngeal carcinoma; Mitochondria; Apoptosis; Tissue inhibitor of metalloproteinase 3 (TIMP-3)

Address correspondence to Xiaohui Shen, Department of Otolaryngology Head and Neck, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, 321 Zhongshan Road, Nanjing 210008, P.R. China. Tel: 86-025-83105888; Fax: 86-025-83105888; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it or Xia Gao, Department of Otolaryngology Head and Neck, Nanjing Drum Tower Hospital Affiliated to Nanjing University Medical School, 321 Zhongshan Road, Nanjing 210008, P.R. China. Tel: 86- 025-83105888; Fax: 86- 025-83105888; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 81-88, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15202988139874
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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miR-148b Functions as a Tumor Suppressor by Targeting Endoplasmic Reticulum Metallo Protease 1 in Human Endometrial Cancer Cells

Jinfeng Qu,* Lei Zhang,† Lanyu Li,* and Yujie Su*

*Department of Obstetrics and Gynecology, Jinan Central Hospital, Jinan, P.R. China
†Department of Obstetrics and Gynecology, Dongying People’s Hospital, Dongying, P.R. China

This study investigated the tumor-suppressive role of miR-148b in regulating endoplasmic reticulum metalloprotease 1 (ERMP1) expression and the oxidative stress response in endometrial cancer cells. Human endometrial cancer RL95-2 cells were used and transfected with miR-148b mimic, miR-148b inhibitor, or their scrambled negative control. Thereafter, the transfection efficiency was determined by RT-qPCR, and cell proliferation was assessed by MTT assay. The dual-luciferase reporter assay, Western blot, and RT-qPCR were conducted to determine the target gene of miR-148b. ERMP1 is a putative target of miR-148b, and thereby the overexpression and downregulation of ERMP1 on the proliferation of RL95-2 cells were assessed. Next, the expressions of hypoxia-inducible factor 1 (HIF-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) were analyzed by Western blot. Intracellular reactive oxygen species (ROS) was determined using dichlorofluorescin diacetate (DCFDA). Results showed that differential expression of miR-148b or ERMP1 was observed in normal endometrial tissues and endometrial cancerous tissues. Enhanced expression of miR-148b effectively inhibited proliferation of RL95-2 cells. ERMP1 was the target of miR-148b. ERMP1 silencing obviously suppressed proliferation of RL95-2 cells. Thus, miR-148b repressed cell proliferation, likely through downregulating ERMP1. Furthermore, it was observed that miR-148b significantly decreased expression of HIF-1 and Nrf2 by downregulating ERMP1. The intracellular ROS level was enhanced by miR-148b via downregulating ERMP1. To conclude, our results suggested that miR-148b suppressed cell proliferation and regulated the oxidative stress response in human endometrial cancer RL95-2 cells by inhibiting ERMP1.

Key words: Endometrial cancer cells; miR-148b; ERMP1; HIF; Nrf2; Oxidative stress

Address correspondence to Jinfeng Qu, Department of Obstetrics and Gynecology, Jinan Central Hospital, No. 105 Jiefang Road, Jinan 250013, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 89-98, 2019
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DOI: https://doi.org/10.3727/096504018X
15199511344806
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Knockdown of Long Noncoding RNA CAT104 Inhibits the Proliferation, Migration, and Invasion of Human Osteosarcoma Cells by Regulating MicroRNA-381

Bo Xia,* Lei Wang,† Li Feng,* Baofang Tian,* Yuanjie Tan,‡ and Baoyin Du*

*Department of Emergency Trauma Surgery, Jining No. 1 People’s Hospital, Jining, Shandong, P.R. China
†Second Department of Orthopedics, The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, Shandong, P.R. China
‡Department of Cardiology, Weihai Hospital of Traditional Chinese Medicine, Weihai, Shandong, P.R. China

Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. This study aimed to explore the effects of long noncoding RNA CAT104 and microRNA-381 (miR-381) on osteosarcoma cell proliferation, migration, invasion, and apoptosis, as well as the underlying potential mechanism. We found that CAT104 was highly expressed in osteosarcoma MG63 and OS-732 cells. Knockdown of CAT104 significantly inhibited OS-732 cell proliferation, migration, and invasion, but promoted cell apoptosis. CAT104 regulated the expression of miR-381, and miR-381 participated in the effects of CAT104 on OS-732 cells. Zinc finger E-box-binding homeobox 1 (ZEB1) was a direct target gene of miR-381, which was involved in the regulatory roles of miR-381 in OS-732 cell proliferation, migration, invasion, and apoptosis, as well as c-Jun N-terminal kinase (JNK) and Wnt/
b-catenin pathways. In conclusion, our research verified that suppression of CAT104 exerted significant inhibitory effects on osteosarcoma cell proliferation, migration, and invasion by regulating the expression of miR-381 and downstream ZEB1, as well as JNK and Wnt/b-catenin pathways.

Key words: Osteosarcoma; Long noncoding RNA CAT104; MicroRNA-381; JNK pathway; Zinc-finger E-box-binding homeobox 1 (ZEB1); Wnt/β-catenin pathway

Address correspondence to Baoyin Du, Department of Emergency Trauma Surgery, Jining No. 1 People’s Hospital, No. 6 Jiankang Road, Jining 272011, 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. 27, pp. 99-106, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15195193936573
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Long Noncoding RNA XIST Regulates miR-137–EZH2 Axis to Promote Tumor Metastasis in Colorectal Cancer

Xingxiang Liu,*† Lin Cui,† and Dong Hua*‡

*Department of Oncology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu, P.R. China
†Department of Oncology, The Second People’s Hospital of Taizhou, Taizhou, Jiangsu Province, P.R. China
‡Department of Oncology, Affiliated Hospital of Jiangnan University, The Fourth People’s Hospital of Wuxi, Wuxi, Jiangsu, P.R. China

We aimed to investigate the significant role of long noncoding RNA X inactive specific transcript (XIST) in regulating tumor metastasis in colorectal cancer (CRC), as well as its possible mechanism. Expression of lncRNA XIST in CRC tissues and CRC cells was detected. CRC cells were transfected with pc-XIST, blank control si-XIST, or si-control, and then the effects of lncRNA XIST on CRC cell migration and invasion were investigated, along with the interaction between lncRNA XIST and miR-137. lncRNA XIST was upregulated in CRC tissues. Compared with HT29 cells that had low metastatic potential, XIST was markedly more highly expressed in LoVo cells that had a higher metastatic potential. Overexpression of XIST promoted the migratory and invasive potential of HT29 cells, while knockdown of XIST inhibited the migratory and invasive potential of LoVo cells. Moreover, epithelial–mesenchymal transition (EMT) markers, including E-cadherin, N-cadherin, and vimentin, exhibited corresponding expression changes. In addition, miR-137 was inhibited by XIST, and inhibition of miR-137 could reverse the effects of knockdown of XIST on the migratory and invasive potential of LoVo cells. Furthermore, enhancer of zestehomolog 2 (EZH2) was confirmed as a target of miR- 137. Our data reveal that lncRNA XIST may promote tumor metastasis in CRC possibly through regulating the miR-137–EZH2 axis. lncRNA XIST may serve as a prognostic indicator for CRC progression.

Key words: Colorectal cancer (CRC); miR-137; Enhancer of zeste homolog 2 (EZH2); Metastasis; Long noncoding RNA (lncRNA) X inactive specific transcript (XIST); Epithelial–mesenchymal transition (EMT)

Address correspondence to Dong Hua, Department of Oncology, The Second Affiliated Hospital of Soochow University, NO 1055 Sanxiang Road, Suzhou, Jiangsu 215004, P.R. China. Email: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 107-115, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15205622257163
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
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Long Noncoding RNA TUNAR Represses Growth, Migration, and Invasion of Human Glioma Cells Through Regulating miR-200a and Rac1

Jinhua Dai,* Jianbo Ma,* Bixia Yu,† Zhankun Zhu,* and Yanqin Hu†

*Department of Clinical Laboratory, Ningbo No. 2 Hospital, Ningbo, P.R. China
†Department of Clinical Laboratory, Zhenhai Longsai Hospital, Ningbo, P.R. China

Glioma is the most common primary adult brain tumor. Mounting research has illustrated the function of long noncoding RNAs (lncRNAs) in glioma progress, but almost no studies have reported the role of TCL1 upstream neural differentiation-associated RNA (TUNAR) in glioma cells. This study aimed to investigate the function of TUNAR in glioma. The GL15 cell line was used in this study. The interactions between TUNAR and miR-200a, or miR-200a and Rac1 were determined by cotransfection experiments. TUNAR overexpression significantly inhibited glioma malignancy by decreasing cell viability, migration, and invasion and promoting cell apoptosis. TUNAR was confirmed to positively regulate miR-200a, and knockdown of miR-200a reversed the TUNAR-induced inhibitory effects on glioma cells. Further, Rac1 was negatively regulated by miR-200a. Rac1 overexpression abolished miR-200a overexpression-induced inhibition of viability, migration, and invasion, as well as the increase in apoptosis. Rac1 knockdown inhibited glioma by inactivating the Wnt/
b-catenin and NF-kB signaling pathways. Our findings suggested that TUNAR played an anticancer role in glioma cells by upregulating miR-200a and inhibiting Rac1, and so might represent a potential therapeutic target for the treatment of human glioma.

Key words: Glioma; TUNAR; miR-200a; Rac1; Wnt/β-catenin pathway; NF-kB pathway

Address correspondence to Yanqin Hu, Department of Clinical Laboratory, Zhenhai Longsai Hospital, No. 356 Shengli Road, Zhaobaoshan Street, Zhenhai District, Ningbo 315200, P.R. China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 27, pp. 117-124, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15213031799835
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

MicroRNA-338-3p Inhibits Proliferation and Promotes Apoptosis of Multiple Myeloma Cells Through Targeting Cyclin-Dependent Kinase 4

Yang Cao,* Xu Shi,† Yingmin Liu,‡ Ren Xu,§ and Qing Ai*

*Clinical Laboratory, the First Affiliated Hospital, Jilin University, Chaoyang District, Changchun, P.R. China
†Central Laboratory, the First Affiliated Hospital, Jilin University, Chaoyang District, Changchun, P.R. China
‡Department of Hematology Cancer Center, the First Affiliated Hospital, Jilin University, Chaoyang District, Changchun, P.R. China
§Department of Respiratory, the First Affiliated Hospital, Jilin University, Chaoyang District, Changchun, P.R. China

MicroRNA-338-3p (miR-338-3p) has been reported to be a tumor suppressor in multiple cancer types. However, the biological role of miR-338-3p and its underlying mechanism in multiple myeloma (MM) remain unclear. In the present study, we investigated the biological role and potential of miR-338-3p in MM. We found that miR-338-3p was significantly decreased in newly diagnosed and relapsed MM tissues and cell lines. Overexpression of miR-338-3p in MM cells significantly inhibited proliferation and promoted apoptosis, caspase 3, and caspase 8 activity. Bioinformatics algorithm analysis predicted that cyclin-dependent kinase 4 (CDK4) was a direct target of miR-338-3p, and this was experimentally verified by a dual-luciferase reporter assay. Furthermore, overexpression of miR-338-3p inhibited CDK4 expression on mRNA and protein levels. Of note, the restoration of CDK4 expression markedly abolished the effect of miR-338-3p overexpression on cell proliferation, apoptosis, caspase 3, and caspase 8 activities in MM cells. Taken together, the present study is the first to demonstrate that miR-338-3p functions as a tumor suppressor in MM through inhibiting CDK4. This finding implies that miR-338-3p is a potential therapeutic target for the treatment of MM.

Key words: Multiple myeloma (MM); MicroRNAs; miR-338-3p; CDK4

Address correspondence to Qing Ai, Clinical Laboratory, the First Affiliated Hospital, Jilin University, 71# Xinmin Street, Chaoyang District, 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. 27, pp. 125-137, 2019
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504018X
15213115046567
E-ISSN 1555-3906
Copyright ©2018 Cognizant, LLC.
Printed in the USA. All rights reserved.

Kinesin Motor Protein KIFC1 Is a Target Protein of miR-338-3p and Is Associated With Poor Prognosis and Progression of Renal Cell Carcinoma

Gang Li,* Tie Chong,* Jie Yang,† Hongliang Li,* and Haiwen Chen*

*Department of Urology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, P.R. China
†Department of Nursing, Xi’an Beifang Chinese Medicine Skin Disease Hospital, Xi’an, Shaanxi Province, P.R. China

KIFC1 (kinesin family member C1) plays a critical role in clustering of extra centrosomes in various cancer cells and thus could be considered as a promising therapeutic target. However, whether KIFC1 is involved in the procession of renal cell carcinoma (RCC) still remains unclear. In this study, we found that KIFC1 was upregulated in RCC tissues and is responsible for RCC tumorigenesis (
p < 0.001). The high expression of KIFC1 correlates with aggressive clinicopathologic parameters. Kaplan–Meier analysis suggested that KIFC1 was associated with poor survival prognosis in RCC. Silencing KIFC1 dramatically resulted in inhibition of proliferation, delayed the cell cycle at G2/M phase, and suppressed cell invasion and migration in vitro. The antiproliferative effect of KIFC1 silencing was also observed in xenografted tumors in vivo. miR-338-3p could directly bind to the 3¢-untranslated region (3¢-UTR) of KIFC1, and ectopic miR-338-3p expression mimicked the inhibitory functions of KIFC1 silencing on RCC cells through inactivation of the PI3K/AKT signaling pathway. Therefore, these results revealed that KIFC1 may be a novel biomarker and an effective therapeutic target for the treatment of RCC.

Key words: KIFC1; miR-338-3p; Renal cell carcinoma (RCC); Proliferation; Poor prognosis

Address correspondence to Tie Chong, Department of Urology, The Second Affiliated Hospital of Xi’an Jiaotong University, No. 157 Xiwu Road, 710004, Xi’an, Shaanxi Province, P.R. China. Tel: 029-87679442; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it