| Literature DB >> 28731185 |
Sun Young Ma1, Jin-Hee Park2, Hana Jung2, Sung-Min Ha2, Yeonye Kim2, Dong Hyen Park3, Deuk Hee Lee3, Sooyong Lee1, In-Ho Chu4, So Young Jung5, Il-Hwan Kim6, Il-Whan Choi2, Chang Soo Choi4, Saegwang Park2.
Abstract
Snail, a zinc-finger transcriptional repressor of E-cadherin expression, is one of the key inducers of epithelial-mesenchymal transition (EMT) in epithelial cancer. In breast cancer, EMT has been associated with malignancies, including metastasis, cancer stem-like properties, and resistance to chemotherapy and radiotherapy. In this study, we analysed the role of Snail in the highly metastatic mesenchymal TUBO‑P2J mouse breast cancer cells, by loss of function using short hairpin RNA. Though silencing Snail did not restore the E-cadherin expression or induce morphological changes, Snail silencing significantly ablated in vitro and in vivo metastatic potentials. In addition, Snail silencing also reduced resistance to chemotherapy drugs and cancer stem-like properties, such as CD44 expression, aldehyde dehydrogenase (ALDH) activity, colony formation, and in vivo tumour formation and growth. However, radioresistance was not decreased by silencing Snail. Collectively, this study suggested that Snail is a main regulator of the maintenance of malignancy potentials and is a good target to prevent cancer metastasis and to increase chemotherapy susceptibility.Entities:
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Year: 2017 PMID: 28731185 DOI: 10.3892/or.2017.5834
Source DB: PubMed Journal: Oncol Rep ISSN: 1021-335X Impact factor: 3.906