ArticleInternational journal of toxicology
Cellular deficiency of Werner syndrome protein or RECQ1 promotes genotoxic potential of hydroquinone and benzo[a]pyrene exposure.
Article in International journal of toxicology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- RECQ1 expression is upregulated in response to DNA damage and in a p53-dependent manner.Oncotarget · 2017Article
- Different non-synonymous polymorphisms modulate the interaction of the WRN protein to its protein partners and its enzymatic activities.Oncotarget · 2016Article
- Site-directed mutants of human RECQ1 reveal functional importance of the zinc binding domain.Mutation research · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The 5 known RecQ helicases in humans (RECQ1, BLM, WRN, RECQL4, and RECQ5) have demonstrated roles in diverse genome maintenance mechanisms but their functions in safeguarding the genome from environmental toxicants are poorly understood. Here, we have evaluated a potential role of WRN (mutated in Werner syndrome) and RECQ1 (the most abundant homolog of WRN) in hydroquinone (HQ)- and benzo[a]pyrene (BaP)-induced genotoxicity. Silencing of WRN or RECQ1 expression in HeLa cells increased their sensitivity to HQ and BaP but elicited distinct DNA damage response. The RECQ1-depleted cells exhibited increased replication protein A phosphorylation, Chk1 activation, and DNA double-strand breaks (DSBs) as compared to control or WRN-depleted cells following exposure to BaP treatment. The BaP-induced DSBs in RECQ1-depleted cells were dependent on DNA-dependent protein kinase activity. Notably, loss of WRN in RECQ1-depleted cells ameliorated BaP toxicity. Collectively, our results provide first indication of nonredundant participation of WRN and RECQ1 in protection from the potentially carcinogenic effects of BaP and HQ.
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Registered trials
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