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Background Breast cancer (BC) continues to be a significant global health issue, with a rising number of cases requiring ongoing research and innovation in treatment strategies. Curcumin (CUR), a natural compound derived from Curcuma longa, and similar compounds have shown potential in targeting the STAT3 signaling pathway, which plays a crucial role in BC progression. Aims The aim of this study was to investigate the effects of curcumin and its analogues on BC based on cellular and molecular mechanisms. Materials & Methods The literature search conducted for this study involved utilizing the Scopus, ScienceDirect, PubMed, and Google Scholar databases in order to identify pertinent articles. Results This narrative review explores the potential of CUR and similar compounds in inhibiting STAT3 activation, thereby suppressing the proliferation of cancer cells, inducing apoptosis, and inhibiting metastasis. The review demonstrates that CUR directly inhibits the phosphorylation of STAT3, preventing its movement into the nucleus and its ability to bind to DNA, thereby hindering the survival and proliferation of cancer cells. CUR also enhances the effectiveness of other therapeutic agents and modulates the tumor microenvironment by affecting tumor‐associated macrophages (TAMs). CUR analogues, such as hydrazinocurcumin (HC), FLLL11, FLLL12, and GO‐Y030, show improved bioavailability and potency in inhibiting STAT3, resulting in reduced cell proliferation and increased apoptosis. Conclusion CUR and its analogues hold promise as effective adjuvant treatments for BC by targeting the STAT3 signaling pathway. These compounds provide new insights into the mechanisms of action of CUR and its potential to enhance the effectiveness of BC therapies. The figure is a graphical illustrating the effects of curcumin and its derivatives on various breast cancer cell lines, including MCF‐7, MCF10A, and MDA‐MB‐231 cells. Curcumin is shown to inhibit the proliferation of MDA‐MB‐231 cells and enhance the effects of IFN‐β/RA on breast cancer cells by up‐regulating GRIM‐19. It also inhibits STAT3 activation in MCF10A cells and increases the ratio of Bax to Bcl‐2 proteins while decreasing the activation of STAT3 in MCF‐7 cells. Hydrazino curcumin specifically inhibits STAT3 activation in MCF‐7 cells. Additionally, FLLL11 and FLLL12 inhibit AKT and STAT3 phosphorylation in breast cancer cells.

Ovarian cancer is an aggressive and heterogeneous malignancy characterized by genetic diversity, clonal evolution, and rapid development of therapeutic resistance, representing a major global clinical challenge. Neutrophils actively drive disease progression by fostering tumor growth, angiogenesis, immune evasion, and metastasis through the formation of neutrophil extracellular traps (NETs). NETs accelerate epithelial-to-mesenchymal transition (EMT), remodel the extracellular matrix (ECM), and prime pre-metastatic niches, creating a permissive environment for metastatic dissemination. Elevated NET levels correlate with advanced disease and poor prognosis, positioning them as powerful diagnostic and prognostic biomarkers. To exploit this vulnerability, we propose a multifunctional nanoparticle platform co-delivering GSK484, a selective anti-NETosis agent, alongside a potent cytotoxic drug. Engineered for tumor-selective targeting and pH-responsive release, this system dismantles the NET-rich tumor microenvironment while directly eradicating cancer cells, maximizing local efficacy and minimizing systemic toxicity. By simultaneously neutralizing the NET-modified niche and attacking tumor cells, this strategy has the potential to overcome chemoresistance, block metastatic spread, and enable precision-guided therapy. Implementation of this approach could refine patient stratification, enhance response rates, reduce recurrence, and translate into tangible survival benefits. This review highlights NETs as central orchestrators of ovarian cancer progression and presents a translationally actionable nanomedicine strategy poised to transform clinical outcomes in a malignancy long plagued by therapeutic failure. Highlights NETs are central drivers of ovarian cancer progression, promoting tumor growth, invasion, and pre-metastatic niche formation, particularly in the omentum. NET-induced immunosuppression and chemoresistance significantly compromise therapy effectiveness, and current treatment doses fail to adequately counter NET-mediated tumor progression. NETs serve as promising diagnostic and prognostic biomarkers for early detection and disease monitoring in ovarian cancer. Pharmacologic inhibition of NET formation can enhance the efficacy of standard therapies and improve patient survival. NETs facilitate epithelial-to-mesenchymal transition (EMT), promoting tumor cell migration and metastatic dissemination. Our multifunctional nanoparticle targets the tumor microenvironment, suppresses NETosis via PAD4 inhibition, and delivers a cytotoxic anticancer agent, offering a dual-action strategy to overcome current therapeutic limitations and maximize efficacy.