Liu Xian, Zhang Yanru, Zheng PengSheng, Cui Nan
Department of Reproductive Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, 710061 Xi'an, Shaanxi, PR China.
Section of Cancer Stem Cell Research, Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education of the People's Republic of China, 710061 Xi'an, Shaanxi, PR China.
J Cancer. 2021 Mar 1;12(8):2422-2429. doi: 10.7150/jca.52950. eCollection 2021.
Musashi-1 (Msi1) is an RNA binding protein that functions as a regulator in multiple carcinomas. Our previous study demonstrated that Msi1 could promote the proliferation of cervical cancer cells by targeting the cell cycle proteins P21, P27 and P53. However, the mechanisms by which Msi1 affects the survival of cervical cancer cells, such as apoptosis, are still unclear. In this study, we found that the expression of Msi1 inhibited cervical cancer cell apoptosis and . Furthermore, the expression of Msi1 downregulated the expression of PTEN, while AKT signaling was activated, which resulted in a reduction in the proapoptotic protein BAK. In addition, rescue the expression of BAK in Msi1 expressing cervical cancer cells induced the increase of apoptosis cells. These findings indicate that Msi1 regulates cervical cancer cell apoptosis by inhibiting PTEN and activating AKT signaling, which leads to the downregulation of BAK.
Musashi-1（Msi1）是一种RNA结合蛋白，在多种癌症中发挥调节作用。我们之前的研究表明，Msi1可通过靶向细胞周期蛋白P21、P27和P53促进宫颈癌细胞的增殖。然而，Msi1影响宫颈癌细胞存活的机制，如凋亡，仍不清楚。在本研究中，我们发现Msi1的表达抑制宫颈癌细胞凋亡。此外，Msi1的表达下调了PTEN的表达，同时激活了AKT信号通路，导致促凋亡蛋白BAK减少。此外，在表达Msi1的宫颈癌细胞中挽救BAK的表达可诱导凋亡细胞增加。这些发现表明，Msi1通过抑制PTEN和激活AKT信号通路来调节宫颈癌细胞凋亡，从而导致BAK的下调。
