Cancer reports (Hoboken, N.J.) · 2026
ANXA1/FPR Signaling Contribute to Paclitaxel Resistance in Ovarian Cancer Through PI3K/AKT-Associated PGC1α Regulation.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li Zhou, Mingrui Jiang, Yueyang Zhou, Hang Qi, Qing Liu, Xiaoyu Yan, Huimei Yu, Meihui Xia
Аннотация
BACKGROUND: Ovarian cancer has the highest mortality among gynecologic malignancies, and acquired resistance to paclitaxel severely limits its clinical efficacy.
AIMS: This 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 RESULTS: Using 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.
CONCLUSION: Our findings suggest that the ANXA1/FPR/PI3K/AKT/PGC1α axis may represent a potential therapeutic target for overcoming paclitaxel resistance in ovarian cancer.
AIMS: This 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 RESULTS: Using 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.
CONCLUSION: Our findings suggest that the ANXA1/FPR/PI3K/AKT/PGC1α axis may represent a potential therapeutic target for overcoming paclitaxel resistance in ovarian cancer.
Предметные рубрики MeSH
FemaleHumansPaclitaxelDrug Resistance, NeoplasmOvarian NeoplasmsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesAnnexin A1Antineoplastic Agents, PhytogenicCell Line, TumorGene Expression Regulation, Neoplastic