http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
- 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
- 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
RISS 인기검색어
- 검색키워드
- 주제어 : Breast cancer · TMEM106C · PI3K/AKT/mTOR pathway · Migration · Apoptosis · Proliferation (검색결과 1 건)
- 무료
- 기관 내 무료
- 유료
-
Shang Jian,Liu Xiu,Bi Yanqing,Yan LiXia,Tian Cuiping,Guan Yu 대한독성 유전단백체 학회 2023 Molecular & cellular toxicology Vol.19 No.1
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 740YP. 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.
연관 검색어 추천
이 검색어로 많이 본 자료
활용도 높은 자료
