ArticleCancer reports (Hoboken, N.J.)2026
ANXA1/FPR Signaling Contribute to Paclitaxel Resistance in Ovarian Cancer Through PI3K/AKT-Associated PGC1α Regulation.
Article in Cancer reports (Hoboken, N.J.), 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
backgroundOvarian cancer has the highest mortality among gynecologic malignancies, and acquired resistance to paclitaxel severely limits its clinical efficacy.
aimsThis study aimed to investigate whether the ANXA1/FPR axis contributes to paclitaxel resistance in ovarian cancer and to elucidate the underlying molecular mechanisms. METHODS AND
resultsUsing the ANXA1 mimetic peptide Ac2-26 and the FPR antagonist Boc2, we provided pharmacological evidence that activation of the ANXA1/FPR axis promotes paclitaxel resistance in ovarian cancer cells. Mechanistically, ANXA1/FPR signaling activated the PI3K/AKT pathway and upregulated PGC1α, leading to enhanced mitochondrial biogenesis and adaptive energy metabolism remodeling, which in turn prevented paclitaxel-induced cell death.
conclusionOur findings suggest that the ANXA1/FPR/PI3K/AKT/PGC1α axis may represent a potential therapeutic target for overcoming paclitaxel resistance in ovarian cancer.
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