BCL10 in cell survival after DNA damage

Yichen Luo; Jing Wu; Juan Zou; Yijing Cao; Yan He; Hui Ling; Tiebing Zeng

doi:10.1016/j.cca.2019.04.077

BCL10 in cell survival after DNA damage

Clin Chim Acta. 2019 Aug:495:301-308. doi: 10.1016/j.cca.2019.04.077. Epub 2019 Apr 29.

Authors

Yichen Luo¹, Jing Wu¹, Juan Zou¹, Yijing Cao¹, Yan He², Hui Ling³, Tiebing Zeng⁴

Affiliations

¹ Key Laboratory of Tumor Cellular & Molecular Pathology, College of Hunan Province, Cancer Research Institute, University of South China，Hengyang, Hunan 421001, China; Hunan Provincial Education Department document (Approval number: 2014-405], Hunan Province Cooperative innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan 421001, China.
² Key Laboratory of Tumor Cellular & Molecular Pathology, College of Hunan Province, Cancer Research Institute, University of South China，Hengyang, Hunan 421001, China; Department of Pathology, Longgang Central Hospital, Shenzhen, Guangdong 518000, China.
³ Key Laboratory of Tumor Cellular & Molecular Pathology, College of Hunan Province, Cancer Research Institute, University of South China，Hengyang, Hunan 421001, China; Hunan Provincial Education Department document (Approval number: 2014-405], Hunan Province Cooperative innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan 421001, China. Electronic address: nhdxlh@126.com.
⁴ Hunan Provincial Education Department document (Approval number: 2014-405], Hunan Province Cooperative innovation Center for Molecular Target New Drug Study, University of South China, Hengyang, Hunan 421001, China; Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, University of South China, Hengyang, Hunan 421001, China. Electronic address: nhdxztb@126.com.

PMID: 31047877
DOI: 10.1016/j.cca.2019.04.077

Abstract

The complex defense mechanism of the DNA damage response (DDR) developed by cells during long-term evolution is an important mechanism for maintaining the stability of the genome. Defects in the DDR pathway can lead to the occurrence of various diseases, including tumor development. Most cancer treatments cause DNA damage and apoptosis. However, cancer cells have the natural ability to repair this damage and inhibit apoptosis, ultimately leading to the development of drug resistance. Therefore, investigating the mechanism of DNA damage may contribute markedly to the future treatment of cancer. The CARMA-BCL10-MALT1 (CBM) complex formed by B cell lymphoma/leukemia 10 (BCL10) regulates apoptosis by activating NF-κB signaling. BCL10 is involved in the formation of complexes that antagonize apoptosis and contribute to cell survival after DNA damage, with cytoplasmic BCL10 entering the nucleus to promote DNA damage repair, including histone ubiquitination and the recruitment of homologous recombination (HR) repair factors. This article reviews the role of BCL10 in cell survival following DNA damage.

Keywords: BCL10; DDR; HR; NF-κB; RNF8/RNF168.

Publication types

Review

MeSH terms

B-Cell CLL-Lymphoma 10 Protein / physiology*
Cell Nucleus / metabolism
Cell Survival
DNA Damage*
DNA Repair

Substances

B-Cell CLL-Lymphoma 10 Protein
BCL10 protein, human