ArticleCell death & disease2026
ROR1-PI3K/AKT signaling drives adaptive resistance to cell cycle blockade in TP53 mutated ovarian cancer.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Effect of 6-gingerol on proliferation and apoptosis of ovarian cancer cells by the PI3K/AKT/mTOR pathway.Biochemistry and biophysics reports · 2026Article
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- The Art of Domesticating Proteins: How Cancer Cells Adapt to Therapeutic and Environmental Stressors.International journal of molecular sciences · 2026Review
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Authors and funding
12 authors.
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Abstract
Drug resistance remains a major challenge to durable responses in ovarian cancer, the fifth leading cause of cancer-related death among women. In this study, we developed long-term resistant (lt-res, several months) pre-clinical models of two drugs inducing mitotic arrest in TP53-mutated cells: adavosertib (ADA), an investigational WEE1 inhibitor targeting the DNA damage response and currently evaluated in clinical trials, and paclitaxel (PTX), a widely used chemotherapeutic agent in cancer care targeting microtubules. Through integrated multi-omics functional profiling, we identify a shared PI3K/AKT-regulated signaling node that governs drug adaptation across all lt-res models. This node modulates the activity of DNA-damage responses and genotoxic stress to toggle between two adaptive states: activated PI3K/AKT driving a proliferative "fast-bypass" program with sustained cell cycle progression and mitotic evasion, or reduced PI3K/AKT signaling initiating a "slow-repair" state characterized by DNA damage checkpoint engagement, replication slowdown, and increased drug efflux. Notably, upregulation of receptor tyrosine kinases, such as ROR1, was observed in both ADA and PTX lt-res models with activated PI3K/AKT signaling. Targeting ROR1 with zilovertamab-vedotin, a monoclonal antibody-drug conjugate, resulted in enhanced cytotoxicity, demonstrating a new approach against recurrent drug-resistant ovarian cancer.
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