Journal
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES
Volume 53, Issue 2, Pages 213-222Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10863-021-09872-w
Keywords
Esophageal squamous cell carcinoma (ESCC); TRIM15; Epithelial-mesenchymal transition (EMT); Metastasis; Wnt/beta-catenin pathway
Categories
Funding
- standardized endoscopic diagnosis and treatment of early upper gastrointestinal cancer and related proteins [2018ZDXM-SF-055]
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Knockdown of TRIM15 significantly inhibits proliferation, migration, and invasion of ESCC cells, partly through blocking the Wnt/β-catenin signaling pathway, suggesting TRIM15 as a potential therapeutic target for ESCC.
TRIM15 is a member of tripartite motif-containing protein (TRIM) protein family, which plays important roles in several cancers. The aim of the present study was to evaluate the role of TRIM15 in esophageal squamous cell carcinoma (ESCC). Our results showed that TRIM15 was upregulated in human ESCC tissues and cell lines. In vitro studies showed that knockdown of TRIM15 significantly inhibited the proliferation, migration, and invasion of ESCC cells. Knockdown of TRIM15 caused a significant increase in E-cadherin expression, as well as decreases in expression of N-cadherin and Vimentin proteins. Moreover, in vivo assay proved that tumor growth was suppressed by knockdown of TRIM15. Furthermore, the protein expression levels of beta-catenin, C-myc, and CyclinD1 were markedly decreased in sh-TRIM15-infected ESCC cells. Additionally, treatment with LiCl reversed the inhibitory effects of TRIM15 knockdown on ESCC cells. In conclusion, these findings indicated that knockdown of TRIM15 blocked the growth and metastasis of ESCC in part through inhibiting the Wnt/beta-catenin signaling pathway. Thus, TRIM15 might serve as a promising therapeutic target for ESCC.
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