Oncology Research 25(2) Abstracts

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Oncology Research, Vol. 25, pp. 157-166, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14719078133203
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of Long Noncoding RNA FTX Inhibits Proliferation, Migration, and Invasion in Renal Cell Carcinoma Cells

Xiangfei He, Fuguang Sun, Fengfu Guo, Kai Wang, Yisheng Gao, Yanfei Feng, Bin Song, Wenzhi Li, and Yang Li

Department of Urology, Linyi People’s Hospital, Linyi City, Shandong Province, P.R. China

Renal cell carcinoma (RCC) is one of the most common kidney cancers worldwide. Although great progressions have been made in the past decades, its morbidity and lethality remain increasing. Long noncoding RNAs (lncRNAs) are demonstrated to play significant roles in the tumorigenesis. This study aimed to investigate the detailed roles of lncRNA FTX in RCC cell proliferation and metastasis. Our results showed that the transcript levels of FTX in both clinical RCC tissues and the cultured RCC cells were significantly upregulated and associated with multiple clinical parameters of RCC patients, including familial status, tumor sizes, lymphatic metastasis, and TNM stages. With cell proliferation assays, colony formation assays, and cell cycle assays, we testified that knockdown of FTX in A498 and ACHIN cells with specific shRNAs inhibited cell proliferation rate, colony formation ability, and arrested cell cycle in the G0/G1 phase. FTX depletion also suppressed cell migration and invasion with Transwell assays and wound-healing assays. These data indicated the prooncogenic potential of FTX in RCC, which makes it a latent therapeutic target of RCC diagnosis and treatment in the clinic.

Key words: Long noncoding RNAs (lncRNAs); FTX; Proliferation; Metastasis; Renal cell carcinoma (RCC)

Address correspondence to Yang Li, M.D., Department of Urology, Linyi People’s Hospital, No. 27 Jiefang Road, Lanshan District, Linyi City, Shandong Province, P.R. China. Tel: +86-0539-8078000; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 167-176, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150307
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of SOX9 Inhibits the Proliferation, Invasion, and EMT in Thyroid Cancer Cells

Jie Huang* and Li Guo†

*Department of General Surgery, Weifang People’s Hospital, Weifang, P.R. China
†Department of Pharmacy, The Affiliated Hospital of Weifang Medical College, Weifang, P.R. China

Sex-determining region Y (SRY)-box 9 (SOX9) is a member of the SOX transcription factor family. Increasing evidence has reported that SOX9 plays different roles in various types of malignancies. However, the role of SOX9 in papillary thyroid cancer (PTC) is still unclear. The aim of this study was to investigate the role of SOX9 in PTC. Our results showed that SOX9 was upregulated in PTC tissues and cell lines. In addition, knockdown of SOX9 significantly inhibited PTC proliferation, colony formation, migration, and invasion, as well as epithelial–mesenchymal transition (EMT) phenotype in TPC-1 and BCPAP cells. Moreover, knockdown of SOX9 significantly inhibited the expression levels of β-catenin, cyclin D1, and c-Myc in PTC cells. In conclusion, this is the first report demonstrating that knockdown of SOX9 inhibited PTC cell proliferation, invasion, and the EMT process via suppressing Wnt/β-catenin signaling pathway. Thus, SOX9 may act as a novel molecular target for the prevention and treatment of PTC.

Key words: SOX9; Papillary thyroid cancer (PTC); Invasion; Epithelial–mesenchymal transition (EMT)

Address correspondence to Jie Huang, Department of General Surgery, Weifang People’s Hospital, No. 151 of Guangwen Road, Weifang 261041, P.R. China. Tel: +86-0536-819213; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 177-186, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150343
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

CXCL5 Plays a Promoting Role in Osteosarcoma Cell Migration and Invasion in Autocrine- and Paracrine-Dependent Manners

Hongsheng Dang, Wuzhou Wu, Bo Wang, Cao Cui, Juwei NiuJie Chen, Ziqiu Chen, and Yi Liu

Department of OrthopaedicsTaihe Hospital, Hubei University of Medicine, Shiyan, Hubei, P.R. China

CXCL5, a CXC-type chemokine, is an important attractant for granulocytic immune cells by binding to its receptor CXCR2. Recently, CXCL5/CXCR2 has been found to play an oncogenic role in many human cancers. However, the exact role of CXCL5 in osteosarcoma cell migration and invasion has not been revealed. Here we found that the protein expression of CXCL5 was significantly increased in osteosarcoma tissues compared with that in matched adjacent nontumor tissues. Moreover, the expression of CXCL5 was significantly associated with advanced clinical stage and metastasis. Further investigation showed that the CXCL5 expression levels were also significantly increased in osteosarcoma cell lines, including Saos-2, MG63, U2OS, and SW1353, when compared with those in normal osteoblast hFoB1.19 cells. U2OS cells were further transfected with CXCL5-specific siRNA or overexpression plasmid. Knockdown of CXCL5 significantly suppressed U2OS cell migration and invasion. On the contrary, overexpression of CXLC5 remarkably promoted the migration and invasion of U2OS cells. Interestingly, both exogenous CXCL5 treatment and the conditioned medium of CXCL5-overexpressing hFoB1.19 cells could also enhance the migration and invasion of U2OS cells, suggesting that the promoting role of CXCL5 in U2OS cell migration and invasion is also in a paracrine-dependent manner. According to these data, our study demonstrates that CXCL5 is upregulated in osteosarcoma and may play an oncogenic role in osteosarcoma metastasis. Therefore, CXCL5 may become a potential therapeutic target for osteosarcoma treatment.

Key words: Osteosarcoma; CXCL5; Migration; Invasion; Metastasis

Address correspondence to Hongsheng Dang, Ph.D., M.D., Chief Physician, Department of OrthopaedicsTaihe Hospital, Hubei University of Medicine, 32 Renmin South Road, Shiyan, Hubei 442000, P.R. China. Tel: +86-719-8801785; Fax: +86-719-8801785; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 187-194, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150389
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
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miR-422a Inhibits Glioma Proliferation and Invasion by Targeting IGF1 and IGF1R

Haiyang Wang,* Chongyang Tang,* Meng Na,* Wei Ma,* Zhenfeng Jiang,* Yifei Gu,* Guizhen Ma,† Haitao Ge,* Hong Shen,* and Zhiguo Lin*

*Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, P.R. China
†Department of Operating Room, The First Affiliated Hospital of Harbin Medical University, Harbin, P.R. China

Glioma is a common type of malignant brain tumor characterized by aggressive metastasis capability. Recent evidence has suggested that noncoding RNAs, including microRNAs, have important functions in the pathophysiology of glioma development. In this study, we investigated the biological function of miR-422a in human glioma. We found that miR-422a was downregulated in glioma tissues. We also demonstrated that expression of miR-422a in glioma cells markedly suppressed cell proliferation, migration, and invasion. In addition, we identified insulin-like growth factor 1 (IGF1) and IGF1 receptor (IGF1R) as inhibitory targets of miR-422a in glioma cells. We established that the expression levels of miR-422a were negatively correlated with the expression levels of IGF1/IGF1R and the clinical parameters in glioma patients. An IGFR inhibitor, AG1024, completely blocked the activity of miR-442a on glioma cell proliferation and invasion, which further confirmed that miR-422a functions through IGF1 and IGF1R.

Key words: miR-422a; Insulin-like growth factor 1 (IGF1); Insulin-like growth factor 1 receptor (IGF1R); Glioma

Address correspondence to Zhiguo Lin, M.D., Ph.D., Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Harbin, Heilongjiang Province 150001, P.R. China. Tel: +86-451-85555803; Fax: +86-451-53670428; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 195-205, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150424
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Ror2, a Developmentally Regulated Kinase, Is Associated With Tumor Growth, Apoptosis, Migration, and Invasion in Renal Cell Carcinoma

Chun-ming Yang,* Shan Ji,† Yan Li,‡ Li-ye Fu,‡ Tao Jiang,‡ and Fan-dong Meng‡

*Department of Urology, The First Affiliated Hospital, China Medical University, Shenyang, P.R. China
†Department of Endocrinology, The Fifth People’s Hospital of Shenyang, Shenyang, P.R. China
‡Department of Biotherapy, Cancer Research Institute, The First Affiliated Hospital, China Medical University, Shenyang, P.R. China

Renal cell carcinoma (RCC) represents one of the most resistant tumors to radiation and chemotherapy. Current therapies for RCC patients are inefficient due to the lack of diagnostic and therapeutic markers. The expression of novel tumor-associated kinases has the potential to dramatically shape tumor cell behavior. Identifying tumor-associated kinases can lend insight into patterns of tumor growth and characteristics. In the present study, we investigated the receptor tyrosine kinase-like orphan receptor 2 (Ror2), a new tumor-associated kinase, in RCC primary tumors and cell lines. Knockdown of Ror2 expression in RCC cells with specific shRNA significantly reduced cell proliferation and induced apoptosis. Using in vitro migration and Matrigel invasion assays, we found that cell migration and invasive ability were also significantly inhibited. In RCC, Ror2 expression correlated with expression of genes involved at the cell cycle and migration, including PCNA, CDK1, TWIST, and MMP-2. Furthermore, in vivo xenograft studies in nude mice revealed that administration of a Ror2 shRNA plasmid significantly inhibited tumor growth. These findings suggest a novel pathway of tumor-promoting activity by Ror2 within renal carcinomas, with significant implications for unraveling the tumorigenesis of RCC.

Key words: Renal cell carcinoma (RCC); Receptor tyrosine kinase-like orphan receptor 2 (Ror2); Apoptosis; Migration; Invasion

Address correspondence to Fan-dong Meng, Department of Biotherapy, Cancer Research Institute, The First Affiliated Hospital, China Medical University, No. 92 Beier Street, Heping District, Shenyang 110001, Liaoning 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. 25, pp. 207-214, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150460
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Downregulation of miR-222 Induces Apoptosis and Cellular Migration in Adenoid Cystic Carcinoma Cells

Ziliang Zhou,*†1 Lijie Zhou,*‡1 Fangfang Jiang,* Binghui Zeng,* Changbo Wei,* Wei Zhao,* and Dongsheng Yu*

*Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou, P.R. China
†Department of Stomatology, Xiangyang Hospital of Chancheng District, Foshan, Guangdong, P.R. China
‡Department of Stomatology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, P.R. China

Previous studies have shown that miR-222 targets the p53 upregulated modulator of apoptosis (PUMA) to regulate cell biological behavior in some human malignancies. We hypothesized that there was a negative regulation, which might induce apoptosis, between miR-222 and PUMA in adenoid cystic carcinoma (ACC). In this study, the expression levels of miR-222 and the PUMA gene after transfection with antisense miR-222 (As-miR-222) were evaluated by RT-PCR and Western blot assays. Cell proliferation and migratory abilities were detected by CCK-8 and Transwell assays. Cell cycle and apoptosis were analyzed by flow cytometry. Our results showed that, when compared with the control and scramble-transfected groups, the expression of miR- 222 in the As-miR-222 group was downregulated, while the expression of PUMA at both mRNA and protein levels was upregulated, cell proliferation and migratory abilities were inhibited, and apoptosis was increased. Our results suggested that As-miR-222 transfection could upregulate the expression of PUMA to induce apoptosis in ACC, providing a new concept for the treatment of ACC.

Key words: Adenoid cystic carcinoma (ACC); miR-222; p53 upregulated modulator of apoptosis (PUMA); Apoptosis; Migration

1These authors provided equal contribution to this work.
Address correspondence to Wei Zhao, Department of Oral and Maxillofacial Surgery, Guanghua School of Stomatology, Sun Yat-sen University, 56 Lingyuan West Road, Guangzhou 510055, P.R. China. Tel: +86-20-8386-2543; Fax: +86-20-8382-2803; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or Dongsheng Yu, Department of Oral and Maxillofacial Surgery, Guanghua School of Stomatology, Sun Yat-sen University, 56 Lingyuan West Road, Guangzhou 510055, P.R. China. Tel: +86-20-8386-2543; Fax: +86-20-8382-2803; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 215-223, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150541
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

miR-202 Promotes Cell Apoptosis in Esophageal Squamous Cell Carcinoma by Targeting HSF2

Xiangrui Meng,*1 Xiaoqi Chen,†1 Peng Lu,‡ Wang Ma,* Dongli Yue,* Lijie Song,* and Qingxia Fan*

*Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, P.R. China
†Department of Digestive Oncology, The First Affiliated Hospital of Henan University of TCM, Zhengzhou, P.R. China
‡Department of Gastrointestinal Surgery, People’s Hospital of Zhengzhou, Zhengzhou, P.R. China

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant cancers with high mortality around the world. However, the regulatory mechanism of ESCC carcinogenesis is not completely known. Here we demonstrate the novel role of miR-202 in regulating ESCC cell apoptosis. The analysis of data obtained from the GEO database showed that the expression of miR-202 is aberrantly decreased in tumor tissue from ESCC patients and cultured ESCC cell lines. After transfection with miR-202 mimic or inhibitor, the apoptotic capacity of ESCC cells was significantly increased by miR-202 overexpression but reduced by miR-202 repression. We then identified HSF2 as a direct target of miR-202 with the binding site on the 3ʹ-UTR of HSF2 mRNA in ESCC cells. The apoptosis of ESCC cells induced by the miR-202 mimic could be repressed by HSF2 overexpression. Further studies indicated that HSF2 overexpression strongly upregulated the expression of Hsp70 at both the mRNA and protein levels. In addition, HSF2/Hsp70 suppressed ESCC cell apoptosis by preventing caspase 3 activation. In conclusion, miR-202 is a potential tumor suppressor in human ESCC and acts by regulating the apoptosis of ESCC cells by targeting HSF2, in which caspase 3 activation is involved. This might provide a novel therapeutic target for human ESCC.

Key words: miR-202; Esophageal squamous cell carcinoma (ESCC); Apoptosis; HSF2; Hsp70

1These authors provided equal contribution to this work.
Address correspondence to Xiangrui Meng, Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Jianshe East Road No. 1, Zhengzhou 450000, P.R. China. Tel: +86-0371-66913095; Fax: +86-0371-66913095; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 225-232, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732772150587
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of Collagen Triple Helix Repeat Containing 1 (CTHRC1) Inhibits Epithelial–Mesenchymal Transition and Cellular Migration in Glioblastoma Cells

Jianpeng Liu,* Wei Li,† Shunshun Liu,* Xu Zheng,* Lin Shi,* Weitao Zhang,* and Hongfa Yang*

*Department of Neurotrauma, The First Hospital of Jilin University, Changchun, Jilin Province, P.R. China
†The Key Laboratory of Pathobiology, Ministry of Education, Basic Medical College, Jilin University, Changchun, Jilin Province, P.R. China

Collagen triple helix repeat containing 1 (CTHRC1), an extracellular matrix-related protein, has been found to be upregulated in many solid tumors and contributes to tumorigenesis. We found that CTHRC1 is overexpressed in glioblastoma tissues and cells. By using the technique of RNA interference, the expression of CTHRC1 in the human glioblastoma U-87MG cell line was downregulated, and the proliferation and migration of U-87MG cells were examined. The results showed that the knockdown of CTHRC1 exerts inhibitory effects on the proliferation and migration ability of U-87MG cells. Knockdown of CTHRC1 expression in U-87MG cells resulted in upregulation in the expression of E-cadherin and downregulation in the expression of N-cadherin, SNAIL, and Slug, suggesting that CTHRC1 inhibits glioblastoma cell migration by suppressing epithelial–mesenchymal transition (EMT). Knockdown of CTHRC1 led to remarkably decreased b-catenin protein levels in the nucleus. These results indicate that CTHRC1 might play an important role in the development of glioblastoma and offer a candidate molecular target for glioblastoma prevention and therapy.

Key words: Collagen triple helix repeat containing 1 (CTHRC1); Glioblastoma; RNA interference; Epithelial–mesenchymal transition (EMT)

Address correspondence to Hongfa Yang, Department of Neurotrauma, The First Hospital of Jilin University, No. 71 of Xinmin Road, Changchun 130021, Jilin Province, P.R. China. Tel: 86-0431-88785891; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 233-239, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14742891049073
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Induction of Apoptosis by Berberine in Hepatocellular Carcinoma HepG2 Cells via Downregulation of NF-κB

Min Li,*† Mao Zhang,* Zhi-lang Zhang,* Ning Liu,* Xiao-yu Han,* Qin-cheng Liu,* Wei-jun Deng,† and Cai-xian Liao*

*Department of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China
†Department of General Surgery, ShiLong People’s Hospital, Southern Medical University, Dongguan, Guangdong, P.R. China

Hepatocellular carcinoma (HCC) is highly resistant to traditional chemotherapeutic approaches, which causes difficulty in the development of effective drugs for the treatment of HCC. Berberine, a major ingredient of Rhizoma coptidis, is a natural alkaloid used in traditional Chinese medicine. Berberine exhibits potent antitumor activity against HCC due to its high efficiency and low toxicity. In the present study, we found that berberine sensitized HepG cells to NF-κB-mediated apoptosis. Berberine exhibited a significant antiproliferation effect on the HepG2 cells and promoted apoptosis. Both qRT-PCR and immunofluorescence staining revealed that berberine reduced the NF-κB p65 levels in HepG2 cells. Moreover, p65 overexpression rescued berberineinduced cell proliferation and prevented HepG2 cells from undergoing apoptosis. These results suggest that berberine inhibits the growth of HepG2 cells by promoting apoptosis through the NF-κB p65 pathway.

Key words: Hepatocellular carcinoma (HCC); Berberine; NF-κB; p65; Apoptosis

Address correspondence to Caixian Liao, Department of Hepatobiliary Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China. Tel: +86-13688969169; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it  or This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 241-248, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14742891049118
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Downregulation of Rab23 in Prostate Cancer Inhibits Tumor Growth In Vitro and In Vivo

Junkai Chang,*1 Weibo Xu,*1 Guangchao Liu,† Xinyi Du,* and Xiaodong Li*

*Department of Urology, Huaihe Hospital of Henan University, Kaifeng, Henan Province, P.R. China
†Antibody Drug Engineering Laboratory of Henan Province, Kaifeng, Henan Province, P.R. China

Rab23, a novel member of the Rab GTPase family, was found to be implicated in the progression of some human cancers. However, what role Rab23 plays in prostate cancer (PCa) remains to be illustrated. In the present study, we investigated the expression pattern and roles of Rab23 in PCa. The study results showed that Rab23 was upregulated in PCa tissues and cell lines. Moreover, downregulation of Rab23 remarkably suppressed the proliferation, migration, and invasion of PCa cells. In addition, downregulation of Rab23 significantly downregulated the protein expression levels of Shh and Gli1. Furthermore, we found that the Gli1 inhibitor GANT-61 greatly enhanced the suppressive effect of Rab23 downregulation on PCa cells. In conclusion, we suggested Rab23 as a potential therapeutic target for PCa treatment.

Key words: Rab23; Proliferation; Migration; Invasion; Prostate cancer (PCa)

1These authors provided equal contribution to this work.
Address correspondence to Xinyi Du, Department of Urology, Huaihe Hospital of Henan University, No. 8 Baobei Road, Kaifeng 475000, Henan Province, P.R. China. Tel: +86-0378-3906000; Fax: +86-0378-3906000; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 249-257, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
693164
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Knockdown of Ubiquitin-Specific Protease 14 (USP14) Inhibits the Proliferation and Tumorigenesis in Esophageal Squamous Cell Carcinoma Cells

Jin Zhang, Danjie Zhang, and Liangzhang Sun

Department of Thoracic Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, P.R. China

Ubiquitin-specific protease 14 (USP14), one of three proteasome-associated deubiquitinating enzymes (DUBs), plays an essential role in the development of human carcinoma. However, to the best of our knowledge, the role of USP14 in esophageal squamous cell carcinoma (ESCC) is unknown. In the current study, we investigated the expression and role of USP14 in ESCC. Our results showed that the level of USP14 was significantly increased in ESCC tissues and cell lines. Downregulation of USP14 significantly inhibited ESCC cell proliferation and ESCC tumor growth in nude mice. Downregulation of USP14 also suppressed the migration/invasion in ESCC cells. Mechanically, downregulation of USP14 decreased the protein expression levels of β-catenin, cyclin D1, and c-Myc in ESCC cells. In conclusion, our study shows that USP14 plays an important role in the progression and metastasis of ESCC. Therefore, these data suggest that USP14 may be a potentially useful therapeutic strategy for the treatment of ESCC.

Key words: Ubiquitin-specific protease 14 (USP14); Esophageal squamous cell carcinoma (ESCC); Proliferation; Invasion

Address correspondence to Jin Zhang, Department of Thoracic Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, No. 157 West Wu Road, Xi’an, Shaanxi 710004, P.R. China. Tel: +86-029-87679309; Fax: +86-029-87679309; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 259-265, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732503870766
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
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Knockdown of Long Noncoding RNA NR_026689 Inhibits Proliferation and Invasion and Increases Apoptosis in Ovarian Carcinoma HO-8910PM Cells

Xin Zhang,* Shaowen Li,† Chunli Dong,‡ Xiuying Xie,* and Yunping Zhang*

*Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P.R. China
†Department of Pediatrics, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P.R. China
‡Department of Anesthesiology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P.R. China

Ovarian cancer is one of the leading causes of gynecological cancer-related deaths worldwide. We investigated the role of a newly discovered long noncoding RNA, NR_026689, in cell proliferation, metastasis, and apoptosis in ovarian cancer cells. Our results showed that NR_026689 was overexpressed in both clinical ovarian cancer patients and cultured ovarian cancer cells. Knockdown of NR_026689 in HO-8910PM cells significantly decreased the cell proliferative rate and the ability to form colonies. Transwell assays revealed that depletion of NR_026689 suppressed cell migration ability by 68% and cell invasive capacity by 71% in HO-8910PM cells. Moreover, specific shRNAs against NR_026689 notably promoted cell apoptosis in HO-8910PM cells by upregulating the expression of proapoptotic proteins, including caspase 3, caspase 9, cytochrome C, and PARP. Our study suggests an oncogenic potential of NR_026689 in ovarian cancer and might provide novel clues for the diagnosis and treatment of ovarian cancer in the clinic. 

Key words: NR_026689; Ovarian cancer; Proliferation; Metastasis; Apoptosis

Address correspondence to Xin Zhang, M.D., Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Xi’an Jiaotong University, No. 157 Neixi Road, Xi’an City, Shanxi Province 710004, P.R. China. Tel: +86-029-87679000; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 267-275, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732510786564
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
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Overexpression of miR-140 Inhibits Proliferation of Osteosarcoma Cells via Suppression of Histone Deacetylase 4

Qianren Xiao,*1 Lu Huang,†1 Zhongzu Zhang,‡1 Xiang Chen,* Jiaquan Luo,* Zhanmin Zhang,§ Shaoqing Chen,§ Yong Shu,* Zhimin Han,* and Kai Cao*

*Department of Orthopedics, The First Affiliated Hospital of Nanchang University, Nanchang, P.R. China
†Department of Children Health and Care, Jiangxi Maternal and Child Health Hospital, Nanchang, Jiangxi, P.R. China
‡Department of Orthopedics, The Yongchuan Hospital of Chongqing Medical University, Chongqing, P.R. China
§Department of Oncology, The First Affiliated Hospital of Nanchang University, Nanchang, P.R. China

miRNAs play a pivotal role in the development and progression of osteosarcoma (OS). Previous studies indicated that miR-140 acts as a tumor suppressor in many cancers. However, its accurate expression and exact function in OS cells remain unknown. Herein, we demonstrated the lower expression of miR-140 in 40 paired OS tissues. Restoring miR-140 expression in OS cells had a marked effect on inhibiting cell proliferation andinvasion, inducing cell apoptosis in vitro, and suppressing tumor growth in vivo. Moreover, a bioinformatics prediction indicated that the histone deacetylase 4 (HDAC4) is a target gene of miR-140 and is involved in miR-140-mediated suppressive effects. In conclusion, our findings show that miR-140 acts as a tumor suppressor in OS by targeting HDAC4.

Key words: miR-140; Osteosarcoma; Histone deacetylase 4 (HDAC4); Hypoxia-inducible factor 1α (HIF-1α)

1These authors provided equal contribution to this work.
Address correspondence to Dr. Kai Cao, Department of Orthopedic Surgery, The First Affiliated Hospital of Nanchang University, No. 17 Yongwai Street, Nanchang 330006, P.R. China. Tel: 86-791-88694553; Fax: 86-791-88693153; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 277-283, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732514133203
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

miR-4262 Promotes Proliferation and Invasion of Human Breast Cancer Cells Through Directly Targeting KLF6 and KLF15

Ke Wang, Yu Ren, Yang Liu, Jian Zhang, and Jian-jun He

Department of Breast Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, P.R. China

miRNAs have been shown to be involved in breast cancer growth and progression. miR-4262 is a potential tumor promoter in human cancers. In this study, we first investigated the role of miR-4262 in the proliferation and invasion of human breast cancer cells. Our results showed that, compared with the adjacent tissues and MCF-10A normal breast epithelial cells, miR-4262 was markedly increased in the breast cancer tissues and five cell lines, including MDA-MB-231, MDA-MB-468, MDA-MB-435, SKBR3, and MCF-7. Then the miR-4262 mimic or oligo anta-miR-4262 was transfected into MDA-MB-231 and MCF-7 breast cancer cell lines. The results showed that the miR-4262 mimic greatly increased the miR-4262 level and the proliferation and invasion of MDA-MB-231 and MCF-7 cells. In contrast, the anta-miR-4262 had a completely opposite effect on miR-4262 expression, cell proliferation, and cell invasion in MDA-MB-231 and MCF-7 cells. Moreover, bioinformatics and luciferase reporter gene assays confirmed that miR-4262 targeted the mRNA 3ʹ-UTR region of KLF6 and KLF15, two characterized tumor suppressor genes. miR-4262 suppressed protein levels of KLF6 and KLF15 in MDA-MB-231 cells, and the suppression could be rescued by the transfection of pcDNA-KLF6and -KLF15. In conclusion, miR-4262 positively regulates proliferation and invasion of human breast cancer cells via suppression of KLF6 and KLF15.

Key words: miR-4262; Breast cancer; Cell proliferation and invasion; KLF6; KLF15

Address correspondence to Jian-jun He, Department of Breast Surgery, The First Affiliated Hospital of Xi’an Jiaotong University, 277 Yanta West Road, Xi’an 710061, P.R. China. Tel: +86-029-85324605; Fax: +86-029-85324605; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 285-293, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732523471442
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

CKLF-Like MARVEL Transmembrane Domain-Containing Member 3 (CMTM3) Inhibits the Proliferation and Tumorigenisis in Hepatocellular Carcinoma Cells

Wujun Li* and Shaobo Zhang†

*Department of General Surgery, The First Affiliated Hospital of Xi’an Medical University, Xi’an, P.R. China
†Department of Surgery, Xi’an Red Cross Hospital, Affiliated to School of Medicine, Xi’an Jiaotong University, Xi’an, P.R. China

The CKLF-like MARVEL transmembrane domain-containing 3 (CMTM3), a member of the CMTM family, was found in several human tumors and plays an important role in the development and progression of tumors. However, the role of CMTM3 in hepatocellular carcinoma (HCC) remains largely unknown. Thus, in the present study, we explored its expression pattern in human HCC cell lines, as well as its functions in HCC cells. Our results demonstrated that the expression of CMTM3 is lowly expressed in HCC cell lines. In vitro, we found that overexpression of CMTM3 obviously inhibited the proliferation, invasion, and EMT process in HCC cells. Furthermore, overexpression of CMTM3 significantly downregulated the expression levels of phosphorylation of JAK2 and STAT3 in HepG2 cells. In vivo, overexpression of CMTM3 attenuated the tumor growth in Balb/c nude mice. In conclusion, we demonstrated that CMTM3 could play an important role in HCC metastasis by EMT induction via, at least partially, suppressing the JAK2/STAT3 signaling pathway. Therefore, CMTM3 may serve as a potential molecular target in the prevention and/or treatment of HCC invasion and metastasis. 

Key words: The CKLF-like MARVEL transmembrane domain-containing 3 (CMTM3); Hepatocellular carcinoma (HCC); Metastasis; JAK2/STAT3 pathway

Address correspondence to Shaobo Zhang, Department of Surgery, Xi’an Red Cross Hospital, Affiliated to School of Medicine, Xi’an Jiaotong University, No. 76 Nanguo Road, Xi’an 710054, P.R. China. Tel: +86-029-87800002; Fax: +86-029-87800002; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 25, pp. 295-304, 2017
0965-0407/17 $90.00 +.00
DOI: https://doi.org/10.3727/096504016X
14732527645922
E-ISSN 1555-3906
Copyright ©2017 Cognizant, LLC.
Printed in the USA. All rights reserved

Intratumoral Photodynamic Therapy With Newly Synthesized Pheophorbide a in Murine Oral Cancer

Mee-Young Ahn,*1 Hyo-Eun Yoon,†1 Seong-Yong Moon,‡ Yong-Chul Kim,§ and Jung-Hoon Yoon†

*College of Medical and Life Sciences, Division of Bio-industry, Major in Pharmaceutical Engineering, Silla University, Busan, South Korea
†Department of Oral and Maxillofacial Pathology, College of Dentistry, Wonkwang Bone Regeneration Research Institute, Daejeon Dental Hospital, Wonkwang University, Daejeon, South Korea
‡Department of Oral and Maxillofacial Surgery, School of Dentistry, Chosun University, Gwangju, South Korea
§Department of Life Sciences, Gwangju Institute of Science and Technology, Gwangju, South Korea

Photodynamic therapy (PDT) is a therapeutic alternative for malignant tumors that uses a photosensitizer. Our group recently synthesized photosensitizer pheophorbide a (Pa) from chlorophyll-a. The present study investigated the therapeutic effect of PDT using intratumoral administration of the synthetic photosensitizer Pa in an in vivo murine oral squamous cell carcinoma (OSCC) animal model. Pa accumulation was measured using the fluorescence spectrum and imaging in living C3H mice. Intratumoral treatment of Pa-PDT (IT Pa-PDT) significantly inhibited the growth of transplanted OSCC cells. Histopathological examination of tumor tissues showed that PCNA expression was significantly decreased, while TUNEL-stained cells were markedly increased in the IT Pa-PDT group compared to controls. IT Pa-PDT-induced apoptosis was confirmed by immunoblot. Reduction of Bcl-2 and cleavage of caspase 3 and PARP were observed in IT Pa-PDT. These data demonstrate that IT Pa-PDT inhibited tumor cell proliferation and induced apoptosis, which is correlated with the anticancer activity of IT Pa-PDT. These potent antitumor activities of IT Pa-PDT were observed in both the immunohistochemistry and Western blot experiments. Our findings suggest the intratumoral therapeutic potential of Pa-PDT on OSCC. Additionally, demonstrated detection of Pa using a fluorescence spectroscopy system or molecular imaging system provides a means for simultaneous diagnosis and treatment of OSCC.

Key words: Pheophorbide a (Pa); Photodynamic therapy (PDT); Intratumoral administration; Oral squamous cell carcinoma (OSCC)

1These authors provided equal contribution to this work.
Address correspondence to Jung-Hoon Yoon, D.D.S., Ph.D., Department of Oral and Maxillofacial Pathology, College of Dentistry, Daejeon Dental Hospital, Wonkwang University, Daejeon 302-120, South Korea. Tel: 82-42-366-1146; Fax: 82-42-366-1115; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it