Oncology Research 23(5) Abstracts

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Oncology Research, Vol. 23, pp. 205-217, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14549667334007
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Review

Regulation of lncRNA and Its Role in Cancer Metastasis

Juan Li, Hui Meng, Yun Bai, and Kai Wang

Department of Medical Genetics, College of Basic Medical Sciences, Third Military Medical University, Chongqing, China

Metastasis is the primary cause of cancer-related death all over the world. Metastasis is a process by which cancer spreads from the place at which it first arose to distant locations in the body. It is well known that several steps are necessary for this process, including cancer cell epithelial-mesenchymal transition (EMT), cell migration, resistance to anoikis, and angiogenesis. Therefore, investigating the molecular mechanism of regulating cancer metastasis progress may provide helpful insights in the development of efficient diagnosis and therapeutic strategy. Recent studies have indicated that long noncoding RNAs (lncRNAs) play important roles in cancer metastasis. lncRNAs are the nonprotein coding RNAs that have a size longer than 200 nucleotides. More and more studies have indicated that lncRNAs are involved in a broad range of biological processes and are associated with many diseases, such as cancer. The role of lncRNAs in cancer metastasis has been widely studied; however, lncRNAs are mainly involved in the EMT process on the current literature. This review focuses on the mechanisms underlying the role of lncRNAs in cancer metastasis.

Key words: Noncoding RNAs; Long noncoding RNAs (lncRNAs); Cancer metastasis; Gene regulation

Address correspondence to Dr. Kai Wang, Department of Medical Genetics, Third Military Medical University, Chongqing 400038, China. Tel: +86 23 68752250; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it or Dr. Yun Bai, Department of Medical Genetics, Third Military Medical University, Chongqing 400038, China. E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 219-228, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14567549091260
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Thermal Radiofrequency Ablation as an Adjuvant Therapy for Patients With Colorectal Liver Metastasis

Yaohua Fan,*†1 Xiyan Zhu,*1 Qiuping Lan,* Fang Lou,* Yu Zheng,* Haizhou Lou,* Yong Fang,* Wei Jin,* Hongming Pan,* and Kaifeng Wang*‡

*Department of Oncology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China
†Department of Oncology, Jiaxing the First Hospital, Jiaxing, China
‡Cancer Center, the Affiliated Hospital of Hangzhou Normal University, Hangzhou, China

Radiofrequency ablation (RFA) is a minimally invasive technology for the treatment of liver malignancies and is used as an adjuvant therapy in patients with colorectal liver metastasis (CLM). This study enrolled a total of 49 CLM patients who underwent RFA treatment. Univariate and multivariate analyses were performed using the log-rank test and Cox proportional hazard model, respectively. Univariate analysis showed that OS was closely correlated with tumor size, frequency of RFA treatment, resection of the liver lesion, and CEA levels before RFA (p < 0.05). Multivariate analysis revealed that resection of CLM lesions after RFA, frequency of RFA treatment, and serum CEA levels before RFA were independent risk factors for the survival of CLM patients (p < 0.05). Tumor lesion size, resection of the liver lesion after RFA, frequency of RFA treatment, and serum CEA levels before RFA may be important prognostic factors of CLM patients treated with RFA therapy.

Key words: Liver metastasis; Radiofrequency ablation (RFA); Influence factor

1These authors provided equal contribution to this work.
Address correspondence to Kaifeng Wang, Cancer Center, the Affiliated Hospital of Hangzhou Normal University, Hangzhou 310000, China. Tel: +86-0571-86006926; Fax: +86-0571-86436673; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 229-236, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14550280421449
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Plasmid-Based Stat3 siRNA Delivered by Functional Graphene Oxide Suppresses Mouse Malignant Melanoma Cell Growth

Di Yin,*†1 Yang Li,*1 Baofeng Guo,‡ Zhewen Liu,* Yang Xu,§ Xiaoqin Wang,* Yanwei Du,* Libo Xu,* Yan Meng,* Xuejian Zhao,* and Ling Zhang*

*Prostate Diseases Prevention and Treatment Research Centre and Department of Pathophysiology, Norman Bethune Medical School, Jilin University, Changchun, China
†Department of Pathology, Basic School of Guangzhou Medical University, Guangzhou, China
‡Department of Surgery, China-Japan Union Hospital, Norman Bethune Medical School, Jilin University, Changchun, China
§Department of Pediatric Surgery, The First Hospital, Jilin University, Changchun, Jilin, China

RNA interference (RNAi) has been used for cancer gene therapy in recent years. However, the application of RNAi is hindered in the absence of safe and efficient gene delivery. In this article, a novel vehicle of graphene oxide functionalized with polyethylenimine and polyethylene glycol (GO-PEI-PEG) was successfully synthetized and then used to deliver plasmid-based Stat3 siRNA. The carrier can readily bind plasmid with high transfection efficiency. Moreover, molecular biology studies reveal that Stat3-related gene and protein expressions were significantly inhibited, suggesting that the formation of GO-PEI-PEG complexes could be utilized as a promising gene delivery in cancer therapy.

Key words: Graphene oxide (GO); Stat3; Cancer

1These authors provided equal contribution to this work.
Address correspondence to Ling Zhang, Department of Pathophysiology, Basic Medical College, Jilin University, No.126 Xinmin Street, Changchun, Jilin 130021, China. Tel: +13944827950; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 237-248, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14562725373671
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

Raltitrexed Inhibits HepG2 Cell Proliferation via G0/G1 Cell Cycle Arrest

Hongwei Zhao, Yubao Zhang, Jianmin Sun, Chao Zhan, and Liang Zhao

Department of Hepatopancreatobiliary Surgery, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, China

Raltitrexed
(RTX) is an antimetabolite drug used as a chemotherapeutic agent for treating colorectal cancer, malignant mesothelioma, and gastric cancer. The antitumor capacity of RTX is attributed to its inhibitory activity on thymidylate synthase (TS), a key enzyme in the synthesis of DNA precursors. The current study is aimed at investigating the potential antitumor effects of RTX in liver cancer. Using the HepG2 cell line as an in vitro model of liver cancer, we evaluated the effects of RTX on cell proliferation employing both a WST-8 assay and a clone formation efficiency assay. In addition, we monitored the ultrastructure changes of HepG2 cells in response to RTX with transmission electric microscopy. To investigate the mechanism underlying the regulation of cell proliferation by RTX, we analyzed cell cycle using cell flow cytometry. Moreover, real-time PCR and Western blot analyses were conducted to examine expression levels of cell cycle regulatory proteins cyclin A and cyclin-dependent kinase 2 (CDK2), as well as their mediators tumor suppressor genes p53 and p16. Our results demonstrate that RTX inhibits HepG2 proliferation by arresting the cell cycle at G0/G1. This cell cycle arrest function was mediated via downregulation of cyclin A and CDK2. The observed elevated expression of p53 and p16 by RTX may contribute to the reduction of cyclin A/CDK2. Our study indicates that RTX could serve as a potential chemotherapeutic agent in the treatment of hepatocellular carcinoma.

Key words: Raltitrexed (RTX); Hepatocellular carcinoma (HCC); Cell cycle arrest; Cyclin A; Cyclin-dependent kinase 2 (CDK2); p16; p53

Address correspondence to Yubao Zhang, M.D., Department of Hepatopancreatobiliary Surgery, Harbin Medical University Cancer Hospital, 150 Haping Road, Nangang District, Harbin, Heilongjiang 150081, China. Tel: +86-13936588077; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 249-256, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14562725373716
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

IL-17A Promotes the Migration and Invasiveness of Colorectal Cancer Cells Through NF-κB-Mediated MMP Expression

Hongtao Ren,* Zhongwei Wang,* Shuqun Zhang,* Hongbing Ma,* Yali Wang,* Lijun Jia,* and Yiming Li†

*Department of Oncology, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China
†Department of General Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, China

Interleukin-17A (IL-17A) plays a significant role in many inflammatory diseases and cancers. The aim of this study is to investigate the effect of IL-17A on the invasiveness of colorectal cancer. In the study, we found that IL-17A could promote the migration and invasion of colorectal cancer cells. Furthermore, after being treated with IL-17A, the expression and activity of matrix metalloproteinase 2 (MMP-2) and MMP-9 were upregulated. Moreover, the nuclear/overall fractions and DNA-binding activity of p65 and p50 were dramatically elevated by IL-17A. Pretreatment with a nuclear factor-κB (NF-κB) inhibitor (PDTC) or PI3K/AKT inhibitor (LY294002) was proven to abolish the promoting effect of IL-17A on the invasion ability of colorectal cancer cells and upregulation of MMP-2/9. In conclusion, our findings demonstrated that IL-17A could promote the invasion of colorectal cancer cells by activating the PI3K/AKT/NF-κBsignaling pathway and subsequently upregulating the expression of MMP-2/9. Our results suggest that IL-17A could serve as a promising therapeutic target for colorectal cancer.

Key words: Interleukin-17A (IL-17A); Colorectal cancer; Migration; Invasion; Nuclear factor-κB (NF-κB)

Address correspondence to Dr. Yiming Li, Department of General Surgery, The Second Affiliated Hospital of Xi’an Jiaotong University, No. 157 Xiwu Road, Xi’an 710004, China. Tel/Fax: +86-29-87679851; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it


Oncology Research, Vol. 23, pp. 257-266, 2016
0965-0407/16 $90.00 +.00
DOI: http://dx.doi.org/10.3727/096504016X14562725373752
E-ISSN 1555-3906
Copyright ©2016 Cognizant, LLC. 
Printed in the USA. All rights reserved

MicroRNA-20b Downregulates HIF-1α and Inhibits the Proliferation and Invasion of Osteosarcoma Cells

Ming Liu, Dan Wang, and Ning Li

Department of Orthopaedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China

Osteosarcoma (OS) is the most common malignant primary bone tumor disease. HIF-1α was predicted to be the target gene of microRNA-20b (miR-20b). The present study was designed to illustrate the effect of miR-20b in regulating osteosarcoma via targeting HIF-1α. In this study, we found that the expression of HIF-1α was significantly increased, while miR-20b obviously decreased in OS patients and OS cell lines compared with healthy controls. Moreover, the luciferase report confirmed the targeting reaction between miR-20b and HIF-1α. Additionally, the overexpression of miR-20b suppressed the invasion and growth of both MG63 and U2OS cells, and inhibited the expressions of HIF-1α and VEGF pathway proteins, while the inhibition of miR-20b led to the reverse results. Furthermore, the overexpression of HIF-1α affected the suppression effect of miR-20b in MG63 cells, indicating that miR-20b suppresses the tumor cell process via inhibiting the expression of HIF-1α. Taken together, our results suggest that the upregulation of miR-20b affects the expression of HIF-1α, downregulates the VEGF pathway proteins, and suppresses cell invasion and proliferation rate. These results provide a potential therapeutic strategy for osteosarcoma.

Key words: Osteosarcoma (OS); Hypoxia-inducible transcription factor-1α (HIF-1α); MicroRNA-20b (miR-20b); Vascular endothelial growth factor (VEGF) pathway

Address correspondence to Dan Wang, Department of Orthopaedics, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou 450052, Henan, China. Tel: +86-15038369371; E-mail: This e-mail address is being protected from spambots. You need JavaScript enabled to view it