ArticleJournal of translational medicine2026
Mitochondria in situ releasing corosolic acid enhanced antitumor effects via activating mitophagy in castration-resistant prostate cancer.
Article in Journal of translational medicine, 2026. 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
backgroundCorosolic acid (CA) and its derivatives have shown promise as anticancer agents, but their effectiveness against resistant cancer types remains underexplored. Organelle-targeted drug delivery is a promising approach to enhance therapeutic efficacy and reduce side effects.
methodsA mitochondria-targeted prodrug, CA-TPP, was synthesized using an esterase-responsive phenolic ester bond, which enables the in situ release of CA within the mitochondria. The therapeutic efficacy of CA-TPP was assessed both in vitro (using DU145 cells) and in vivo. RNA sequencing was employed to investigate the molecular mechanisms, particularly focusing on the PINK1/Parkin-mediated mitophagy pathway.
resultsCA-TPP significantly reduced the required treatment dose of CA by 75%, maintaining its anticancer activity. In DU145 cells, CA-TPP induced cell death through the mitochondrial apoptosis pathway. RNA sequencing revealed that CA-TPP activated apoptosis through PINK1/Parkin-mediated mitophagy. Inhibition of mitophagy via PINK1 shRNA alleviated the cytotoxic effects of CA-TPP, confirming the role of mitophagy in its mechanism. Additionally, CA-TPP treatment resulted in elevated ROS production, leading to mitochondrial apoptosis and mitophagy.
conclusionsThe CA-TPP prodrug strategy enhances the specificity and anti-tumor effects of corosolic acid, offering a promising approach for targeted cancer therapy. This work opens new possibilities for mitochondria-targeted cancer treatments with reduced drug dosages. This study did not involve clinical trials, and thus trial registration is not applicable.
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