Open AccessC1QTNF6 is overexpressed in gastric carcinoma and contributes to the proliferation and migration of gastric carcinoma cells
Author(s) -
Haixia Qu,
Lin Chen,
Xiangchuan Meng,
Zhijie Wang,
Yanxin Cui,
YunPeng Yu,
Dong Wang,
Xiangjun Jiang
Publication year - 2018
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2018.3978
Subject(s) - cell cycle , gene knockdown , apoptosis , cancer research , oncogene , cell growth , biology , cancer , small hairpin rna , cell culture , cell , cell migration , flow cytometry , cancer cell , microbiology and biotechnology , biochemistry , genetics
In the present study, proteins differentially expressed between gastric cancer tissue and para‑tumoral normal gastric tissues were screened, and the function of the highly expressed protein C1QTNF6 in gastric carcinoma was investigated. The differential expression of mRNAs extracted from the tumor and adjacent tissues was analyzed using GeneChip assay. An AGS si‑C1QTNF6 cell line was constructed using shRNA‑C1QTNF6 lentivirus. The cell invasion and migration ability of C1QTNF6‑knockdown cells were determined by Transwell chamber migration and wound healing assays, respectively. The effects of C1QTNF6 on AGS cell cycle distribution and apoptosis were detected using a FACScan flow cytometer. The results demonstrated that the expression of 109 genes was increased and the expression of 129 was decreased in tumor tissues. Among these genes, the C1QTNF6 gene was highly expressed in tumor tissues and the AGS7901 cell line. C1QTNF6‑knockdown decreased the cell growth, and the proliferative and migration ability, as well as increasing the apoptosis of gastric carcinoma cells. In addition, the number of AGS cells in the G2/M phase was significantly increased after 5 days of C1QTNF6‑shRNA lentivirus infection. The results of the present study indicated that C1QTNF6 serves an important role in the development of gastric carcinoma. C1QTNF6 is involved in promoting the proliferation and migration, and in reducing the apoptosis of gastric carcinoma cells. These results provided a potential therapeutic target for the treatment of gastric carcinoma.