한빛사논문
- 조회286
Hwa Jin Kim1,2, Sue Jin Moon1,2 and Jeong Hoon Kim 1,2,*
1Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, South Korea.
2Research Institute for Future Medicine, Samsung Medical Center, Seoul 06351, South Korea.
*Corresponding author: correspondence to Jeong Hoon Kim
Abstract
Cell cycle and apoptosis regulator 2 (CCAR2), also known as deleted in breast cancer 1 (DBC1), has been recently identified as a master regulator of transcriptional processes and plays diverse roles in physiology and pathophysiology, including as a regulator of apoptosis, DNA repair, metabolism, and tumorigenesis. CCAR2 functions as a coregulator of various transcription factors and a critical regulator of numerous epigenetic modifiers. Based on its ability to stimulate apoptosis by activating and stabilizing p53, CCAR2 was initially considered to be a tumor suppressor. However, an increasing number of studies have shown that CCAR2 also functions as a tumor-promoting coregulator by activating oncogenic transcription factors and regulating the enzymatic activity of epigenetic modifiers, indicating that CCAR2 may play a dual role in cancer progression by acting as a tumor suppressor and tumor promoter. Here, we review recent progress in understanding the dual tumor-suppressing and oncogenic roles of CCAR2 in cancer. We discuss CCAR2 domain structures, its interaction partners, and the molecular mechanisms by which it regulates the activities of transcription factors and epigenetic modifiers.
논문정보
- Review Paper
- 2023년 08월 (BRIC 등록일 2023-08-03)
- 국내 연구진
- 생명과학 > 유전자발현
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