ArticleOncogene2019
ATM-dependent activation of SIM2s regulates homologous recombination and epithelial-mesenchymal transition.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Loss of STING impairs lactogenic differentiation.Development (Cambridge, England) · 2024Article
- Large-scale analysis of CDH1 mutations defines a distinctive molecular subset with treatment implications in gastric cancer.NPJ precision oncology · 2024Article
- SIM2s directed Parkin-mediated mitophagy promotes mammary epithelial cell differentiation.Cell death and differentiation · 2023Article
- Noncanonical role of singleminded-2s in mitochondrial respiratory chain formation in breast cancer.Experimental & molecular medicine · 2023Article
- CircMAN1A2 contributes to nasopharyngeal carcinoma progression via enhancing the ubiquitination of ATMIN through miR-135a-3p/UBR5 axis.Human cell · 2023Article
- The Emerging Roles of Rad51 in Cancer and Its Potential as a Therapeutic Target.Frontiers in oncology · 2022Review
- Chromatin-directed proteomics-identified network of endogenous androgen receptor in prostate cancer cells.Oncogene · 2021Article
- Article
- Polymorphism of XRCC3 in Egyptian Breast Cancer Patients.Pharmacogenomics and personalized medicine · 2020Article
- Cross-talk between SIM2s and NFκB regulates cyclooxygenase 2 expression in breast cancer.Breast cancer research : BCR · 2019Article
- Loss of SIM2s inhibits RAD51 binding and leads to unresolved replication stress.Breast cancer research : BCR · 2019Article
- Silencing of RAD51AP1 suppresses epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.Thoracic cancer · 2019Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
There is increasing evidence that genomic instability is a prerequisite for cancer progression. Here we show that SIM2s, a member of the bHLH/PAS family of transcription factors, regulates DNA damage repair through enhancement of homologous recombination (HR), and prevents epithelial-mesenchymal transitions (EMT) in an Ataxia-telangiectasia mutated (ATM)-dependent manner. Mechanistically, we found that SIM2s interacts with ATM and is stabilized through ATM-dependent phosphorylation in response to IR. Once stabilized, SIM2s interacts with BRCA1 and supports RAD51 recruitment to the site of DNA damage. Loss of SIM2s through the introduction of shSIM2 or the mutation of SIM2s at one of the predicted ATM phosphorylation sites (S115) reduces HR efficiency through disruption of RAD51 recruitment, resulting in genomic instability and induction of EMT. The EMT induced by the mutation of S115 is characterized by a decrease in E-cadherin and an induction of the basal marker, K14, resulting in increased invasion and metastasis. Together, these results identify a novel player in the DNA damage repair pathway and provides a link in ductal carcinoma in situ progression to invasive ductal carcinoma through loss of SIM2s, increased genomic instability, EMT, and metastasis.
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Registered trials
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