Open AccessARL2 is required for homologous recombination repair and colon cancer stem cell survival
Author(s) -
Lee Hani,
Choi SeokGyeong,
Ha Sojung,
Yoon Sukjoon,
Kim WooYoung
Publication year - 2022
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.13438
Subject(s) - homologous recombination , rad51 , microbiology and biotechnology , dna repair , chromatin , cancer research , cell cycle checkpoint , cancer stem cell , chemistry , colorectal cancer , cell , biology , stem cell , cell cycle , gene , cancer , genetics
ARL2 regulates the dynamics of cytological components and is highly expressed in colon cancer tissues. Here, we report novel roles of ARL2 in the cell nucleus and colon cancer stem cells (CSCs). ARL2 is expressed at relatively low levels in K‐RAS active colon cancer cells, but its expression is induced in CSCs. Depletion of ARL2 results in M phase arrest exclusively in non‐CSC cultured cells; in addition, DNA break stress accumulates in CSCs leading to apoptosis. ARL2 expression is positively associated with the expression of all six RAD51 family genes, which are essential for homologous recombination repair (HRR). Furthermore, ARL2 is required for HRR and detected within chromatin compartments. These results demonstrate the requirement of ARL2 in colon CSC maintenance, which possibly occurs through mediating double‐strand break DNA repair in the nucleus.