Curcumin in ovarian cancer: mechanistic insights and translational potential.

Abstract

Ovarian cancer remains the most fatal gynecological malignancy, primarily due to delayed diagnosis, rapid progression, and resistance to standard chemotherapy. Curcumin, a natural polyphenol from Curcuma longa, has been investigated for its potential anticancer properties through the modulation of multiple molecular pathways. This systematic review examines the mechanistic and therapeutic roles of curcumin and its nanoformulations in preclinical models of ovarian cancer. Evaluation of 21 studies indicates that curcumin may influence key signaling pathways such as phosphoinositide 3-kinase (PI3K)/ protein kinase B (Akt)/ mechanistic target of rapamycin (mTOR), nuclear factor kappa β (NF-κβ), Janus kinase (JAK) /signal transducer and activator of transcription 3 (STAT3), and Wnt/β-catenin. Preliminary evidence also suggests that curcumin may modulate the tumor microenvironment through changes in tumor-associated macrophage polarization, although this finding is currently supported by limited evidence. These interactions are associated with increased apoptosis, reduced proliferation, inhibition of epithelial-to-mesenchymal transition (EMT), and enhanced sensitivity to chemotherapeutic agents like cisplatin and paclitaxel. Nanoformulations-such as micelles, dendrosomes, liposomes, and core-shell nanoparticles-have been shown to improve curcumin's bioavailability and therapeutic performance compared to its free form. While these preclinical findings suggest potential benefits, further clinical studies are necessary to confirm curcumin's role as a supportive treatment in ovarian cancer.