ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
RAD51 regulates CHK1 stability via autophagy to promote cell growth in esophageal squamous carcinoma cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Using network pharmacology approaches to identify treatment mechanisms for codonopsis in esophageal cancer.International journal of clinical and experimental pathology · 2022Article
- Combined Inhibition of Rad51 and Wee1 Enhances Cell Killing in HNSCC Through Induction of Apoptosis Associated With Excessive DNA Damage and Replication Stress.Molecular cancer therapeutics · 2021Article
- Epigenomic Analysis of RAD51 ChIP-seq Data RevealsCancers · 2021Article
- Identification of a Ten-Gene Signature of DNA Damage Response Pathways with Prognostic Value in Esophageal Squamous Cell Carcinoma.Journal of oncology · 2021Article
- Expression of RAD51 and Its Clinical Impact in Oral Squamous Cell Carcinoma.Analytical cellular pathology (Amsterdam) · 2020Article
- Roles for Autophagy in Esophageal Carcinogenesis: Implications for Improving Patient Outcomes.Cancers · 2019Review
- Selective Autophagy Regulates Cell Cycle in Cancer Therapy.Theranostics · 2019Review
- Autophagy Inhibition Stimulates Apoptosis in Oesophageal Squamous Cell Carcinoma Treated with Fasudil.Journal of Cancer · 2018Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
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Abstract
The serine/threonine protein kinase CHK1 has been reported to bind to the recombinase RAD51 and facilitates its assembly in DNA damage sites via phosphorylation. However, the role of RAD51 in regulating the expression of CHK1 has never been explored. Here, we show that RAD51 is highly upregulated in esophageal squamous tumor tissues and its DMC1 domain significantly promotes cell growth of esophageal cancer (EC) cells through CHK1. To gain the mechanistic insights, firstly, in the presence of 3-methyladenine (3MA), an autophagy inhibitor, we found that the reduction of CHK1 and the inhibition of cell growth in RAD51-deficient EC109 cells were strikingly restored. Subsequently, the autophagy-related experiments revealed that RAD51 negatively participated in autophagy. Moreover, results from in vitro clonogenic survival assays showed that RAD51 depletion greatly enabled EC cells to resist the autophagy inhibitors 3MA and hydroxychloroquine (HCQ) treatments. Above all, our studies firstly highlight a direct role of RAD51 in autophagy process and characterize its functional domain in cell growth regulation. Moreover, our data firstly shed insights into the possible application of autophagy inhibitors in treating RAD51 overexpressed EC patients.
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