J Cancer 2022; 13(8):2694-2704. doi:10.7150/jca.65822 This issue

Research Paper

TMEM158 Regulates the Canonical and Non-Canonical Pathways of TGF-β to Mediate EMT in Triple-Negative Breast Cancer

Jiaci Tong, Haoran Li, Ye Hu, ZuoWei Zhao, Man Li

Department of Oncology & Department of Breast Surgery, The Second Hospital of Dalian Medical University, Dalian, 116023 China

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Citation:
Tong J, Li H, Hu Y, Zhao Z, Li M. TMEM158 Regulates the Canonical and Non-Canonical Pathways of TGF-β to Mediate EMT in Triple-Negative Breast Cancer. J Cancer 2022; 13(8):2694-2704. doi:10.7150/jca.65822. Available from https://www.jcancer.org/v13p2694.htm

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Abstract

Graphic abstract

Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer with high metastatic potential. To date, no directed treatment options have been developed for the treatment of metastatic or advanced TNBC. The oncogene TMEM158, also known as RIS1, is upregulated by Ras-induced cellular senescence. Although TMEM158 has been shown to be involved in tumor progression, little is known about the molecular function and expression of TMEM158 in breast cancer. The present study evaluated the expression and prognostic relevance of TMEM158 in breast cancer patients from several databases. Gene set enrichment analysis (GSEA) showed that TMEM158 was closely associated with epithelial-mesenchymal transition (EMT) and TGF-β pathways. Gain- and loss-of-function assays indicated that overexpressed TMEM158 might participate in EMT by activating the TGF-β pathway, which in turn promotes tumor migration, invasion, and metastasis. These findings suggest that TMEM158 has the potential to become a new therapeutic target for TNBC.

Keywords: Carcinogenesis, Triple-negative breast cancer, EMT, TGF-β signal pathway, TMEM158