CRIP1 promotes docetaxel resistance and immune-associated cell death modulation in prostate cancer

Background: Docetaxel resistance is a major barrier to durable disease control in advanced and castration-resistant prostate cancer. There is a pharmacological need to identify biomarkers that not only stratify resistance risk but also nominate tractable regulators whose perturbation can restore taxane sensitivity and suppress resistant phenotypes. Methods: . Results: . In parallel, CRIP1 depletion was accompanied by changes in damage-associated and immune-related cell-death readouts under taxane stress, suggesting a potential role in linking drug tolerance to immune-relevant cell-death programs. Conclusion: These findings identify CRIP1 as a functionally validated, pharmacologically relevant mediator of docetaxel resistance in prostate cancer. While independent validation in taxane-treated clinical cohorts is warranted, our results support CRIP1 as a candidate therapeutic target and provide a mechanistic framework connecting taxane resistance with immune-associated cell-death modulation.