ArticleBMC molecular and cell biology2019
New STAT3-FOXL2 pathway and its function in cancer cells.
Article in BMC molecular and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- FOXL2 + cancer-associated fibroblasts enhances epithelial ovarian cancer development via TGFβ/Smad signaling.BMC cancer · 2025Article
- Plectin, a novel regulator in migration, invasion and adhesion of ovarian cancer.Cell & bioscience · 2025Article
- Deciphering Aflatoxin B1 affected critical molecular pathways governing cancer: A bioinformatics study using CTD and PANTHER databases.Mycotoxin research · 2025Article
- STAT3 mediates ECM stiffness-dependent progression in ovarian cancer.Molecular and cellular biochemistry · 2025Article
- pSTAT3 activation ofProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Integration of gene expression and DNA methylation data using MLA-GNN for liver cancer biomarker mining.Frontiers in genetics · 2024Article
- Article
- Reduced RBPMS Levels Promote Cell Proliferation and Decrease Cisplatin Sensitivity in Ovarian Cancer Cells.International journal of molecular sciences · 2022Article
- Advances in the Regulation of Mammalian Follicle-Stimulating Hormone Secretion.Animals : an open access journal from MDPI · 2021Review
- Article
- Expressions and clinical significances of STAT3 and Grim19 in epithelial ovarian cancer.3 Biotech · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe forkhead transcription factor (FOXL2) plays a crucial role in blepharophimosis-ptosis-epicanthus inversus syndrome (BPES), sex determination, ovary growth and development, and cell cycle regulation. Emerging investigations have focused on the downstream targets of FOXL2, while little is known about its upstream regulation.
resultsIn this study, we show that FOXL2 could be regulated by STAT3 in cancer cells and that STAT3 binds to FOXL2 at the 5'- GCCTGATGTTTGTCTTCCCAGTCTGTGGCAA-3' site using EMSA and ChIP. We further found that knockdown of STAT3 or FOXL2 could significantly induce cancer cell apoptosis, indicating the importance of these two genes in cancer cell growth and apoptosis. Our data also indicated that the increased apoptotic cell rate may be caused by changes in apoptosis-related genes, such as TNF, TRAIL and GnRHR.
conclusionThis study presents a new upstream regulator of FOXL2 and demonstrats that this new STAT3-FOXL2 pathway has an important function in HeLaHeLa cell apoptosis, providing new insights regarding the targeting of FOXL2 for cancer prevention and treatment.
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Registered trials
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