FOXL2 + cancer-associated fibroblasts enhances epithelial ovarian cancer development via TGFβ/Smad signaling.

Lei Zhao, Jingqi Nie, Jinming Wang, Dongliang Li, Xuewei Hao

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Article in BMC cancer, 2025. 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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5 authors.

Lei Zhao *College of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, No. 39 Xinyang Road, Daqing, 163319, Heilongjiang, China. zhaolei@hmudq.edu.cn.

Jingqi Nie *College of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, No. 39 Xinyang Road, Daqing, 163319, Heilongjiang, China.

Jinming WangCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, No. 39 Xinyang Road, Daqing, 163319, Heilongjiang, China.

Dongliang LiCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, No. 39 Xinyang Road, Daqing, 163319, Heilongjiang, China.

Xuewei HaoCollege of Medical Laboratory Science and Technology, Harbin Medical University at Daqing, No. 39 Xinyang Road, Daqing, 163319, Heilongjiang, China.

Funding

Heilongjiang Provincial Natural Science Foundation Project LH2022109

6 · The paper itself

Abstract

backgroundFOXL2, a key regulator of ovarian development, is linked to ovarian disorders, but its role in epithelial ovarian cancer (EOC) remains unclear. EOC progression is driven by cancer-associated fibroblasts (CAFs), and our data show FOXL2-expressing CAFs in EOC correlate with poor prognosis (high grade, lymphatic metastasis, advanced stage). METHODS AND

resultsPrimary CAFs were isolated from 10 patient EOC tissues via collagenase/hyaluronidase digestion. Experiments used these CAFs and A2780 cells, with in vitro assays in 3 replicates and in vivo studies with 5 mice/group. String analysis predicted a strong FOXL2-SUMO1 interaction, validated by Ni2+ NTA pull-down showing SUMO1 as the primary FOXL2 modifier (higher than SUMO2/3, p < 0.001). UBC9 enhanced FOXL2 SUMOylation (indicating UBC9 dependence), and SUMOylation stabilized FOXL2 by reducing ubiquitination. SUMOylated FOXL2 in CAFs promoted EOC cell proliferation, invasion, and migration. FOXL2 + CAFs activated TGF-β/Smad signaling via TGF-β secretion, and the inhibitor SB431542 reduced in vivo tumor growth induced by A2780 cells and FOXL2 + CAFs.

conclusionOur results cumulatively indicate that FOXL2 SUMOylation can maintain the FOXL2 stability in CAFs, thus accelerating tumorigenesis in ovarian cancer. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

Cancer-Associated FibroblastsCarcinoma, Ovarian EpithelialForkhead Box Protein L2Ovarian NeoplasmsSmad ProteinsTransforming Growth Factor betaAnimalsBenzamidesCell Line, TumorCell MovementCell ProliferationDioxolesFemaleHumansMicePrognosis4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamideBenzamidesDioxolesForkhead Box Protein L2FOXL2 protein, humanSmad ProteinsSUMO-1 ProteinSUMO1 protein, humanTransforming Growth Factor betaUbiquitin-Conjugating EnzymesUbiquitin-Conjugating Enzyme UBC9Cancer-associated fibroblastsFOXL2Ovarian cancerSUMOylationTGFβ/Smad signaling

Identifiers

PMID41436983

DOI10.1186/s12885-025-15364-6

PMCPMC12853930

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LicenceCC BY-NC-ND

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.