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Updated: Jun 13, 2026

Transplantation Into the Mouse Ovarian Fat Pad
Published on: September 7, 2016
IGF2BP3 promotes epithelial ovarian cancer progression by regulating FASN expression
Danting Sun1, Yuance Xu2, Jiaze Gao1
1Department of Gynecology, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, China.
Abstract:
Ovarian cancer (OC) is the most lethal disease among female reproductive system tumors, particularly epithelial ovarian cancer (EOC). N6-methyladenosine (m6A) is the most abundant internal modification in eukaryotic RNA and is involved in gene expression regulation. In OC, high expression of the m6A reader protein IGF2BP3 predicts a poor prognosis, but the target molecules and mechanisms underlying this association remain unclear. This study demonstrates that IGF2BP3 promotes EOC progression by recognizing and stabilizing m6A-modified FASN mRNA, thereby activating the WNT/β-catenin signaling pathway. This activation enhances lipid synthesis, increases mitochondrial membrane potential, shortens S-phase duration, and promotes cell proliferation and metastasis. Mechanistically, IGF2BP3 binds to m6A-modified FASN mRNA to enhance its stability, and pharmacological inhibition of FASN by orlistat reverses IGF2BP3-mediated oncogenic effects and WNT/β-catenin activation. In vivo and in vitro experiments confirm that knocking down either IGF2BP3 or FASN reverses these malignant phenotypes. These findings highlight a novel m6A-dependent IGF2BP3-FASN-WNT axis that drives EOC progression, providing a potential biomarker for targeted therapy.
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