Impact of Nischarin on EMT regulators in breast cancer cell lines

• Published in: Oncology letters 2020-09, Vol.20 (6), p.1-1
• Main Authors: Cai, Yuan-Jie, Ma, Bo, Wang, Mei-Li, Chen, Jie, Zhao, Fu-Guang, Zhou, Juan-Di, Guo, Xu, Zheng, Lei, Xu, Chun-Jing, Wang, Yi, He, Yi-Bo, Liu, Jian, Xie, Shang-Nao
• Format: Article
• Language: English
• Subjects: Antibodies; Apoptosis; Breast cancer; Cell adhesion & migration; Cell culture; Cell growth; Efficiency; Gene expression; Kinases; Medical equipment; Oncology; Ovarian cancer; Plasmids; Proteins; Signal transduction
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2020.12154

Nischarin is an integrin-binding protein, which is well known as a novel tumor suppressor. In breast cancer, Nischarin serves a critical role in breast cancer cell migration and invasion. However, the molecular mechanism underlying the role of Nischarin remains unclear. Recent findings have demonstrated that epithelial-mesenchymal transition (EMT) increases the capacity of cell migration and invasion. As a member of the integrin family, it was hypothesized that Nischarin may regulate cellular processes via various signaling pathways associated with the EMT process. The present study detected the mRNA levels of EMT regulators via reverse transcription-quantitative PCR and related protein levels via western blotting in breast cancer cells, following NISCH-overexpression and -knockdown. The results demonstrated that Nischarin inhibits cell proliferation, migration and invasion in breast cancer cells. Furthermore, when the NISCH gene was overexpressed, the relative mRNA level of E-cadherin was increased, while the relative mRNA levels of several transcription factors, such as Snail, ZEB1, N-cadherin, Slug, Twist1 and vimentin, decreased. When NISCH was silenced, these results were reversed. The present results demonstrated that Nischarin suppresses cell migration and invasion via inhibiting the EMT process.