ArticleMolecular therapy. Nucleic acids2026
Nitric oxide-dependent stabilization of vimentin confers chemoresistance in ovarian cancer.
Article in Molecular therapy. Nucleic acids, 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
High-grade serous ovarian carcinoma (HGSC) is often diagnosed at an advanced stage and is characterized by an immunosuppressive tumor microenvironment that facilitates disease progression, therapeutic resistance, and poor survival. We recently demonstrated that nitric oxide (NO) blockade enhances the response of metaplastic breast cancer to PI3K inhibition and taxane therapy by reducing S-nitrosylation-mediated activation of the JNK/c-Jun pathway, thereby promoting tumor differentiation, suppressing stemness, and improving survival in patient-derived xenograft models. Here, we demonstrate that inducible nitric oxide synthase (iNOS) is constitutively expressed in HGSC and that pharmacologic inhibition of NO signaling with the pan-NOS inhibitor NG-monomethyl-L-arginine (L-NMMA) enhances cisplatin efficacy by reprogramming the tumor microenvironment. By targeting NO signaling with either L-NMMA or through CRISPR-Cas9-mediated iNOS knockout and iNOS small interfering RNA (siRNA), we impaired epithelial-to-mesenchymal transition (EMT) by inhibiting NO-mediated stabilizing effects on vimentin in both
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