RAD51
Overview
RAD51 is a central mediator of homologous recombination (HR) DNA repair. In the context of ARID1A-deficient cancers, RAD51 is induced as part of a compensatory DNA damage response, making it a marker of replication stress and a potential therapeutic vulnerability when targeted alongside BET bromodomain inhibition.
Alterations observed in the corpus
- RAD51 expression is induced upon ARID1A depletion as part of the DNA damage response in small cell lung cancer (SCLC) cells; overexpression of ARID1A suppresses RAD51; JQ1 (BET inhibitor) treatment dose-dependently reduces RAD51 expression PMID:22037554
- Recruitment to DSBs requires TRMT10A pSer28-dependent BRCA1 loading; RAD51 foci reduced by TRMT10A or USP10 loss and by the USP10 inhibitor spautin-1 in mCRPC models PMID:28068672
Cancer types (linked)
- SCLC: RAD51 upregulation is a consequence of ARID1A loss and is suppressed by JQ1 BET bromodomain inhibition PMID:22037554
Co-occurrence and mutual exclusivity
- RAD51 induction co-occurs with PARP1 upregulation and phospho-CHK1 activation in ARID1A-deficient SCLC cells PMID:22037554
Therapeutic relevance
- Suppression of RAD51 by JQ1 (BET bromodomain inhibitor) contributes to synthetic lethality in ARID1A-low SCLC, impairing HR repair capacity PMID:22037554
Open questions
- Whether RAD51 suppression by BET inhibitors is a primary mechanism or secondary effect requires further mechanistic dissection.
Sources
This page was processed by entity-page-writer on 2026-05-06. - PMID:28068672
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