Transmembrane protein 106C accelerates the progression of breast cancer through the activation of PI3K/AKT/mTOR signaling

• Published in: Molecular & cellular toxicology Vol. 19; no. 1; pp. 99 - 108
• Main Authors: Shang, Jian, Liu, Xiu, Bi, Yanqing, Yan, LiXia, Tian, Cuiping, Guan, Yu
• Format: Journal Article
• Language: English
• Published: Singapore Springer Nature Singapore 2023; Springer Nature B.V; 대한독성 유전단백체 학회
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Biomedical and Life Sciences; Breast cancer; Cell Biology; Gene expression; Life Sciences; Original Article; Overexpression; Pharmacology/Toxicology; Phenotypes; Solid tumors; TOR protein; Transmembrane proteins; Western blotting; Wortmannin; 생물학; TMEM106C; Breast cancer; PI3K/AKT/mTOR pathway; Proliferation; Migration; Apoptosis
• ISSN: 1738-642X; 2092-8467
• DOI: 10.1007/s13273-022-00248-8

Background Breast cancer is one of the solid tumors investigated for gene expression. Objective Our research aimed to investigate the roles of transmembrane protein 106C (TMEM106C) on breast cancer and the underlying mechanisms. Results The results from GEPIA website indicated that TMEM106C was up-regulated in breast cancer and the TMEM106C over-expression was concerned with poor outcomes in breast cancer patients. Moreover, western blotting and qRT-PCR assay also showed that TMEM106C level was up-regulated in breast cancer cells. Our results showed that over-expression of TMEM106C accelerated the malignant phenotypes of MCF7 cells, while TMEM106C silencing displayed the opposite outcomes in MDA-MB-231 cells. Furthermore, TMEM106C over-expression activated PI3K/AKT/mTOR signaling, which reversed by Wortmannin. Similarly, TMEM106C silencing inhibited PI3K/AKT/mTOR signaling, which abolished by 740Y-P. Moreover, we also confirmed that 740Y-P significantly reversed the function of TMEM106C silencing on the malignant phenotypes of MDA-MB-231 cells. Conclusion This study indicated that TMEM106C could promote the malignant phenotypes of breast cancer cells by activating PI3K/AKT/mTOR signaling.