ArticleBritish journal of cancer2020
BCAS2, a protein enriched in advanced prostate cancer, interacts with NBS1 to enhance DNA double-strand break repair.
Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- BCAS2 and hnRNPH1 orchestrate alternative splicing for DNA double-strand break repair and synapsis in meiotic prophase I.Cellular and molecular life sciences : CMLS · 2024Article
- Leveraging baseline transcriptional features and information from single-cell data to power the prediction of influenza vaccine response.Frontiers in cellular and infection microbiology · 2024Article
- DNA double-strand break genetic variants in patients with premature ovarian insufficiency.Journal of ovarian research · 2023Review
- BCAS2 regulates granulosa cell survival by participating in mRNA alternative splicing.Journal of ovarian research · 2023Article
- Breast carcinoma-amplified sequence 2 regulates adult neurogenesis via β-catenin.Stem cell research & therapy · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBreast cancer amplified sequence 2 (BCAS2) plays crucial roles in pre-mRNA splicing and androgen receptor transcription. Previous studies suggested that BCAS2 is involved in double-strand breaks (DSB); therefore, we aimed to characterise its mechanism and role in prostate cancer (PCa).
methodsWestern blotting and immunofluorescence microscopy were used to assay the roles of BCAS2 in the DSBs of PCa cells and apoptosis in Drosophila, respectively. The effect of BCAS2 dosage on non-homologous end joining (NHEJ) and homologous recombination (HR) were assayed by precise end-joining assay and flow cytometry, respectively. Glutathione-S-transferase pulldown and co-immunoprecipitation assays were used to determine whether and how BCAS2 interacts with NBS1. The expression of BCAS2 and other proteins in human PCa was determined by immunohistochemistry.
resultsBCAS2 helped repair radiation-induced DSBs efficiently in both human PCa cells and Drosophila. BCAS2 enhanced both NHEJ and HR, possibly by interacting with NBS1, which involved the BCAS2 N-terminus as well as both the NBS1 N- and C-termini. The overexpression of BCAS2 was significantly associated with higher Gleason and pathology grades and shorter survival in patients with PCa.
conclusionBCAS2 promotes two DSB repair pathways by interacting with NBS1, and it may affect PCa progression.
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