期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 293, 期 11, 页码 3949-3964出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.RA117.001103
关键词
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资金
- National Nature Science Foundation of China [81472493, 81500373, 81502282, 81672609, 81502975]
- Program for Excellent Talents and Scientific Research Program of Anhui Medical University Grant [2013xkj006]
- Anhui Provincial Academic and Technical Leader Reserve Candidate Grant [2016H074]
- Key Program of Outstanding Young Talents in Higher Education Institutions of Anhui Grant [gxyqZD2016046]
- Natural Science Foundation of Anhui Province Grant [1608085MH193]
- Scientific Research Foundation of Anhui Medical University Grant [2015xkj043]
- China Postdoctoral Science Foundation Grants [2016T90413, 2015M581693]
Gastric cancer remains a malignancy with poor survival outcome. We herein report that GSE1, a proline-rich protein, possesses a role in the progression of human gastric cancer. The expression of GSE1 was observed to be much higher in human gastric cancer tissues compared with normal gastric tissues, and GSE1 expression correlated positively with lymph node metastasis, histological grade, depth of invasion, and clinical stage in gastric cancer patients. Moreover, GSE1 expression was also associated with decreased post-operative relapse-free survival and overall survival in the cohort. The forced expression of GSE1 in gastric cancer cell lines resulted in increased cell proliferation, increased colony formation, enhanced cell migration, and invasion. Furthermore, forced expression of GSE1 also increased tumor size and enhanced lung metastasis in xenograft models. The depletion of endogenous GSE1 with shRNAs decreased the oncogenicity and invasiveness of gastric cancer cells both in vitro and in vivo. In addition, GSE1 was determined to be a direct target of miR-200b and miR-200c. Furthermore, GSE1 positively regulated the downstream gene SLC7A5 (also known as LAT-1), which was scanned and verified from mRNA sequencing. GSE1 therefore possesses an oncogenic role in human gastric cancer, and targeted therapeutic approaches to inhibit GSE1 function in gastric cancer warrant further consideration.
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