ArticleDiscover oncology2025
CDCA5 knockdown potentiates olaparib sensitivity in BRCA1-mutated ovarian cancer through autophagy activation.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundBRCA1-mutated ovarian cancer poses substantial therapeutic hurdles due to its poor prognosis and resistance to traditional therapies. Although acquired resistance is still a significant obstacle, PARP inhibitors, e.g., olaparib, have demonstrated promise in prolonging progression-free survival (PFS) in these individuals. The therapeutic potential of CDCA5 silencing in conjunction with olaparib to improve treatment effectiveness for ovarian cancer with a BRCA1 mutation is examined in this study.
methodsUsing BRCA1-mutated ovarian cancer cell lines (UWB1.289 and SNU251) and xenograft models, we analyzed the effects of CDCA5 knockdown alone or combined with olaparib. Functional assays (CCK-8, immunofluorescence, TEM, western blot) evaluated proliferation, autophagy, DNA damage, and PI3K/AKT/mTOR signaling.
resultsCDCA5 knockdown inhibited proliferation, activated autophagy, and induced DNA damage in BRCA1-mutated cells. Moreover, combination with olaparib synergistically enhanced these effects, with significant tumor growth inhibition in vivo. Mechanistically, the combination suppressed the PI3K/AKT/mTOR pathway, promoting autophagy and exacerbating DNA damage. Pharmacological activation of PI3K/AKT/mTOR reversed these antitumor effects.
conclusionsThe anticancer effects of olaparib are enhanced by CDCA5 knockdown, which also promotes autophagy and exacerbates DNA damage via the PI3K/AKT/mTOR pathway. These findings provide a novel therapeutic approach for treating BRCA1-mutated ovarian cancer that overcomes PARP inhibitor resistance and enhances treatment results.
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