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KMID : 1034820230190010099
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Molecular & Cellular Toxicology
2023 Volume.19 No. 1 p.99 ~ p.108
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Transmembrane protein 106C accelerates the progression of breast cancer through the activation of PI3K/AKT/mTOR signaling
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Jian Shang
Xiu Liu
Yanqing Bi
LiXia Yan
Cuiping Tian
Yu Guan
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Abstract
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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.
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KEYWORD
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Breast cancer, TMEM106C, PI3K/AKT/mTOR pathway, Migration, Apoptosis, Proliferation
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