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Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
Published on: February 9, 2024
beta4GalT-II increases cisplatin-induced apoptosis in HeLa cells depending on its Golgi localization
Jianhai Jiang1, Jin Zhou, Yuanyan Wei
1Key Laboratory of Glycoconjuates Research, Ministry of Public Health and State Key Laboratory of Genetic Engineering and Gene Research Center, Shanghai Medical College of Fudan University, Shanghai 200032, People's Republic of China.
Abstract:
beta1,4-Galactosyltransferase II (beta4GalT-II) is one of the enzymes transferring galactose to the terminal N-acetylglucosamine of complex-type N-glycans and its expression is significantly altered during oncogenesis with unknown functions. Here, we reported for the first time the pro-apoptotic role of beta4GalT-II in tumor cells. The level of beta4GalT-II mRNA expression was obviously decreased during HeLa cell apoptosis induced by cisplatin. Interestingly, the ectopic expression of beta4GalT-II in HeLa cells markedly increased apoptosis and cleavage of PARP induced by cisplatin as well as the expression of pro-apoptotic protein Bax. Furthermore, deletion of Golgi localization domain abolished the apoptotic role of beta4GalT-II in HeLa cells. Collectively, these results suggest that beta4GalT-II increases HeLa cell apoptosis induced by cisplatin depending on its Golgi localization, which indicates that beta4GalT-II might contribute to the therapeutic efficiency of cisplatin for cervix cancer.