ANXA1
/
FPR
Signaling Contribute to Paclitaxel Resistance in Ovarian Cancer Through
PI3K
/
A
Zhou Li, Jiang Mingrui, Zhou Yueyang, Qi Hang, Liu Qing, Yan Xiaoyu, Yu Huimei, Xia Meihui ABSTRACT
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.