Che-1 in Tumor Proliferation and Apoptosis
10.13865/j.cnki.cjbmb.2020.09.1359
- Author:
Mu-Hua CHEN
1
;
Xiao-Feng LIU
1
;
Bao-Cai XING
1
Author Information
1. Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education / Beijing), Hepatopancreatobiliary Surgery Department I, Peking University Cancer Hospital & Institute
- Publication Type:Journal Article
- Keywords:
apoptosis;
apoptosis-antagonizing transcription factor(AATF/ Che-1);
proliferation;
tumor
- From:
Chinese Journal of Biochemistry and Molecular Biology
2021;37(3):310-315
- CountryChina
- Language:Chinese
-
Abstract:
Tumor is a type of most common diseases in clinical practice. The classical treatments of tumors mainly include surgical resection, radiotherapy and chemotherapy. In recent years, the methods of tumor treatment have been developing continuously, but many advanced tumors still have no particularly effective treatment. New treatments are urgently needed. Sustaining proliferation and resisting cell death are important characteristics of tumor cells. Therefore, the identification of genes involved in the proliferation and apoptosis of tumor cells will provide potential targets for tumor therapy. Apoptosis-antagonizing transcription factor (AATF), is also called Che-1, the earliest discovered to interact with RNA polymerase Ⅱ and Rb. Moreover, Che-1 restrains the activity of Rb and supports cell growth. It is found that Che-1 also binds to RNA polymerase I, thereby promoting RNA polymerase I-dependent transcription and affecting ribosome synthesis. Under cellular stress, the localization and stability of Che-1 are regulated by post-translational modification. In response to DNA damage, apoptosis stimulation and other stress, Che-1 regulates the occurrence and development of tumors by regulating genes associated with proliferation and apoptosis. In addition, the expression of Che-1 is regulated by a negative feedback mechanism. In this review, we highlight the advances in the roles of Che-1 in tumor development and progression.
