Sphingomyelin synthase 1 regulates the epithelial-to-mesenchymal transition mediated by the TGF-[beta]/Smad pathway in MDA-MB-231 cells

Breast cancer is the most common cancer in women and a leading cause of cancer-associated mortalities in the world. Epithelial-to-mesenchymal transition (EMT) serves an important role in the process of metastasis and invasive ability in cancer cells, and transforming growth factor [beta]1 (TGF-[beta...

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Published inMolecular medicine reports Vol. 19; no. 2; p. 1159
Main Authors Liu, Shuang, Hou, Huan, Zhang, Panpan, Wu, Yifan, He, Xuanhong, Li, Hua, Yan, Nianlong
Format Journal Article
LanguageEnglish
Published Spandidos Publications 01.02.2019
Subjects
Bone morphogenetic proteins
Breast cancer
Cancer
Cancer cells
Cancer metastasis
Care and treatment
Cellular signal transduction
Computational biology
Development and progression
Gene expression
Genetic aspects
Health aspects
Mortality
Phospholipids
Stem cells
Transforming growth factors
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Summary:Breast cancer is the most common cancer in women and a leading cause of cancer-associated mortalities in the world. Epithelial-to-mesenchymal transition (EMT) serves an important role in the process of metastasis and invasive ability in cancer cells, and transforming growth factor [beta]1 (TGF-[beta]1) have been investigated for promoting EMT. However, in the present study, the role of the sphingomyelin synthase 1 (SMS1) in TGF-[beta]1-induced EMT development was investigated. Firstly, bioinformatics analysis demonstrated that the overexpression of SMS1 negatively regulated the TGF[beta] receptor I (T[beta]RI) level of expression. Subsequently, the expression of SMS1 was decreased, whereas, SMS2 had no significant difference when MDA-MB-231 cells were treated by TGF-[beta]1 for 72 h. Furthermore, the present study constructed an overexpression cells model of SMS1 and these cells were treated by TGF-[beta]1. These results demonstrated that overexpression of SMS1 inhibited TGF-[beta]1-induced EMT and the migration and invasion of MDA-MB-231 cells, increasing the expression of E-cadherin while decreasing the expression of vimentin. Furthermore, the present study further confirmed that SMS1 overexpression could decrease T[beta]RI expression levels and blocked smad family member 2 phosphorylation. Overall, the present results suggested that SMS1 could inhibit EMT and the migration and invasion of MDA-MB-231 cells via TGF-[beta]/Smad signaling pathway.Key words: sphingomyelin synthase 1, transforming growth factor [beta]1, epithelial-to-mesenchymal transition, MDA-MB-231 cells
ISSN:1791-2997
1791-3004
DOI:10.3892/mmr.2018.9722