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Epigenetically downregulated Semaphorin 3E contributes to gastric cancer.

Abstract
Axon guidance protein Semaphorin 3E (Sema3E) promotes tumor metastasis and suppresses tumor cell death. Here, we demonstrated that Sema3E was decreased in gastric cancer. Its levels were inversely associated with tumor progression. Levels of Sema3E were associated with low p300 and high class I histone deacetylase (class I HDAC). Ectopic expression of Sema3E inhibited proliferation and colony formation of gastric cancer cell lines in vitro and xenografts in vivo. Sema3E overexpression inhibited migration and invasion of gastric cancer cells, which was associated with induction of E-cadherin and reduction of Akt and ERK1/2 phosphorylation. We suggest that silencing of Sema3E contributes to the pathogenesis of gastric cancer.
AuthorsHui Chen, Guo-Hua Xie, Wei-Wei Wang, Xiang-Liang Yuan, Wen-Ming Xing, Hong-Jing Liu, Jin Chen, Min Dou, Li-Song Shen
JournalOncotarget (Oncotarget) Vol. 6 Issue 24 Pg. 20449-65 (Aug 21 2015) ISSN: 1949-2553 [Electronic] United States
PMID26036259 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • SEMA3E protein, human
  • Semaphorins
Topics
  • Animals
  • Cell Line, Tumor
  • Down-Regulation
  • Epigenomics
  • Female
  • HEK293 Cells
  • Heterografts
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Middle Aged
  • Semaphorins (biosynthesis, genetics, metabolism)
  • Stomach Neoplasms (genetics, metabolism, pathology)

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