MicroRNA-340 promotes the tumor growth of human gastric cancer by inhibiting cyclin G2

Yin,Guozhi; Zhou,Huayou; Xue,Yumo; Yao,Bowen; Zhao,Wei

doi:10.3892/or.2016.4876

MicroRNA-340 promotes the tumor growth of human gastric cancer by inhibiting cyclin G2

Authors:
- Guozhi Yin
- Huayou Zhou
- Yumo Xue
- Bowen Yao
- Wei Zhao
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Affiliations: Department of Hepatobiliary Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, P.R. China, Department of General Surgery, Hanzhong Central Hospital, Hanzhong 723000, P.R. China, Department of General Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, P.R. China
Published online on: June 15, 2016 https://doi.org/10.3892/or.2016.4876
Pages: 1111-1118

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Abstract

Aberrant expression and function of microRNAs (miRNAs) play a critical role in the development and progression of various human cancers including gastric cancer. However, the clinical significance and underlying mechanisms of miR-340 remain largely unknown in gastric cancer. In the present study, we demonstrated that the expression of miR-340 was aberrantly elevated in both gastric cancer tissues and cells. Moreover clinical association analyses disclosed that the elevated level of miR-340 was significantly associated with unfavorable clinicopathological characteristics of the gastric cancer patients, such as poor differentiation, large tumor size and advanced tumor-node-metastasis (TNM) stage. Gastric cancer patients with high expression of miR-340 had prominently shorter overall survival and disease-free survival. Functionally, forced expression of miR-340 promoted cell viability, proliferation, colony formation and cell cycle progression in the SGC-7901 cells, while miR-340 silencing reduced cell viability, proliferation, colony formation and cell cycle progression in MGC-803 cells. Furthermore, in vivo experiments indicated that miR-340 knockdown suppressed the tumor growth of MGC-803 cells. Notably, alteration of miR-340 expression affected the luciferase activity of wild-type 3'-UTR of cyclin G2 (CCNG2) and regulated CCNG2 abundance in gastric cancer cells, indicating that CCNG2 is a direct target of miR-340. Moreover, CCNG2 knockdown eradicated the effects of miR-340 silencing on gastric cancer cells. In conclusion, our data suggest that miR-340 may potentially serve as a novel prognostic biomarker and therapeutic target for gastric cancer.

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