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Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells.

Mol Med Rep. 2019 Feb;19(2):1159-1167. doi:10.3892/mmr.2018.9722. Epub 2018 Dec 04
Shuang Liu 1 , Huan Hou 1 , Panpan Zhang 1 , Yifan Wu 1 , Xuanhong He 1 , Hua Li 2 , Nianlong Yan 1
Shuang Liu 1 , Huan Hou 1 , Panpan Zhang 1 , Yifan Wu 1 , Xuanhong He 1 , Hua Li 2 , Nianlong Yan 1
+ et al

[No authors listed]

Author information
  • 1 Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
  • 2 Department of Biochemistry and Molecular Biology, Centre of Experimental Medicine, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

摘要


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 β1 (TGF‑β1) have been investigated for promoting EMT. However, in the present study, the role of the sphingomyelin synthase 1 (SMS1) in TGF‑β1‑induced EMT development was investigated. Firstly, bioinformatics analysis demonstrated that the overexpression of SMS1 negatively regulated the TGFβ receptor I (TβRI) 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‑β1 for 72 h. Furthermore, the present study constructed an overexpression cells model of SMS1 and these cells were treated by TGF‑β1. These results demonstrated that overexpression of SMS1 inhibited TGF‑β1‑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 TβRI 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‑β/Smad signaling pathway.