MiR-638 acts as a tumor suppressor gene in gastric cancer
Metrics: PDF 696 views | HTML 1918 views | ?
Yu Shen1,*, Haiqun Chen2,*, Ling Gao1, Weigang Zhang1, Jun He1, Xiaohua Yang1, Lei Qin1, Xiaofeng Xue1 and Zhaoji Guo1
1Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou 215006, P.R. China
2Department of General Surgery, Xinhua Hospital Affiliated to Jiaotong University Chongming Branch, Shanghai 200000, P.R. China
*These authors have contributed equally to this work
Lei Qin, email: firstname.lastname@example.org
Xiaofeng Xue, email: email@example.com
Zhaoji Guo, email: firstname.lastname@example.org
Keywords: miR-638; SOX2; gastric cancer; cell proliferation; invasion
Received: January 25, 2017 Accepted: September 05, 2017 Published: November 20, 2017
Gastric cancer is one of the major causes of cancer mortality. Several microRNAs play a role in the tumor growth and invasion. However, the underlying molecular mechanism remains poorly understood. We detected the miR-638 expression levels in tumor samples and adjacent noncancerous tissues from 68 patients with gastric cancer as well as in the gastric cancer cell line SGC-7901 and SC-M1. The cell cycle was analyzed by flow cytometry, cell proliferation was observed by CCK-8 assay and cell invasion was detected using Transwell assay. MiR-638 was down-regulated in human GC tissues and its expression level was negatively correlated to TNM stage and lymph metastasis. In the cell lines, aberrant expression of miR-638 was related to the cell proliferation, cell cycle and invasion. We also found that SOX2 had a negative correlation with miR-638 in GC tissues, and miR-638 overexpression could decrease SOX2 expression level by directly binding the 3’-UTR of SOX2. in vitro, down-regulating SOX2 by siRNA could counteract the effect of miR-638 inhibitor on GC cells proliferation and invasion. Our results demonstrate that miR-638 may play a pivotal role in the growth and invasion of GC.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.