Open AccessAspirin inhibits colon cancer cell line migration through regulating epithelial‑mesenchymal transition via Wnt signaling
Author(s) -
Shenghang Jin,
Xiaoyang Wu
Publication year - 2019
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2019.10089
Subject(s) - epithelial–mesenchymal transition , wnt signaling pathway , microbiology and biotechnology , cancer research , oncogene , biology , carcinogenesis , signal transduction , cell migration , chemistry , metastasis , cell cycle , cancer , cell , genetics
The mechanism responsible for the initiation of tumor metastasis and epithelial-mesenchymal transition (EMT) is not well understood. During EMT, epithelial cells lose their polarity and adhesion to surrounding cells and migrate, resulting in transition into mesenchymal cells. Canonical Wnt signaling has been implicated in controlling gene transcription and body axis pattern formation during development. However, canonical Wnt signaling has also been indicated to serve a role in carcinogenesis by regulating EMT. In the present study, it was demonstrated that the expression of several positive regulators of EMT and Wnt signaling was repressed by aspirin treatment in SW480 tumor cells, and that this reduction was due to alterations in the localization of zinc finger E-box binding homeobox 1 and Snail family transcriptional repressor 2. It was also demonstrated that aspirin may be an effective inhibitor of EMT, reducing the viability and migration ability of SW480 tumor cells, including cells induced by TGF-β1.