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Updated: Aug 21, 2026

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
Published on: November 2, 2014
ANXA1/FPR Signaling Contribute to Paclitaxel Resistance in Ovarian Cancer Through PI3K/AKT-Associated PGC1α
Zhou Li1, Jiang Mingrui1, Zhou Yueyang1
1Department of Obstetrics and Gynecology, The First Hospital of Jilin University, Changchun, Jilin, China.
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.
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