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FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy. | LitMetric

AI Article Synopsis

  • High-grade serous ovarian cancer (HGSOC) recurrence is linked to factors like gene copy number changes, tumor stemness, and resistance to platinum-based chemotherapy.
  • A new mouse model shows that certain gene gains contribute to aggressive cancer traits and resistance to cisplatin, a common chemotherapy drug.
  • Targeting FAK (focal adhesion kinase) with inhibitors can help overcome chemoresistance by inducing cell death in these cancer cells, highlighting FAK's role in supporting tumor growth and survival.

Article Abstract

Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in , and (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721800PMC
http://dx.doi.org/10.7554/eLife.47327DOI Listing

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