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Overexpression of Lymphocyte Antigen 6 Complex, Locus E in Gastric Cancer Promotes Cancer Cell Growth and Metastasis

Authors :
Yun Zuo
Qin Jiang
Xiaojing Shi
Cong Cao
Yu Song
Chen Ni
Zhi-Peng Chen
Yan Lv
Shao-Kai Wang
Source :
Cellular Physiology and Biochemistry, Vol 45, Iss 3, Pp 1219-1229 (2018)
Publication Year :
2018
Publisher :
Cell Physiol Biochem Press GmbH & Co KG, 2018.

Abstract

Background/Aims: Lymphocyte antigen 6 complex, locus E (LY6E) is a member of the lymphostromal cell membrane Ly6 superfamily protein. The present study investigated the clinical significance and potential biological function of LY6E in gastric cancer (GC). Methods: LY6E mRNA and protein expressions in human GC tissues and GC cells were tested. Relationship between LY6E expression and the GC patients’ clinicopathologic characteristics was analyzed. LY6E was silenced by siRNA in the cultured GC cells. Results: The RNA expression microarray profiling assay results demonstrated that LY6E mRNA was significantly increased in multiple human GC tumor tissues. Immunohistochemistry (IHC) staining analysis revealed that 59 of 75 (78.7%) GC specimens were LY6E positive. LY6E over-expression in human GC was correlated with the histology grade, AJCC stage, N classification, lymphatic invasion, and tumor location. Notably, functional LY6E expression was also detected in AGS and other established GC cell lines. LY6E knockdown by targeted-siRNA inhibited AGS cell survival and proliferation. Meanwhile, the LY6E siRNA induced G1-S cell cycle arrest and apoptosis in AGC cells. Additionally, AGC cell migration was also inhibited by LY6E knockdown. Expressions of tumor-suppressing proteins, including PTEN (phosphatase and tensin homolog) and E-Cadherin, were increased in LY6E-silenced AGS cells. Conclusion: LY6E over-expression in GC is potentially required for cancer cell survival, proliferation and migration.

Details

Language :
English
ISSN :
14219778 and 10158987
Volume :
45
Issue :
3
Database :
OpenAIRE
Journal :
Cellular Physiology and Biochemistry
Accession number :
edsair.doi.dedup.....60a982b416202f26e5e8f8541e4b5e1d