{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Han Y"],"funding":["Young Scientists Fund","Natural Science Foundation of Shandong Province","National Natural Science Foundation of China"],"pagination":["17"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6587274"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["20(1)"],"pubmed_abstract":["<h4>Background</h4>The 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.<h4>Results</h4>In 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 cause"],"journal":["BMC molecular and cell biology"],"pubmed_title":["New STAT3-FOXL2 pathway and its function in cancer cells."],"pmcid":["PMC6587274"],"funding_grant_id":["81501683","ZR2015HL057","31570941","ZR2019MH047","81870237"],"pubmed_authors":["Wu J","Yang W","Zhang T","Wang D","Han Y","Cheng M"],"additional_accession":[]},"is_claimable":false,"name":"New STAT3-FOXL2 pathway and its function in cancer cells.","description":"<h4>Background</h4>The 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.<h4>Results</h4>In 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 cause","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Jun","modification":"2025-04-04T18:57:59.517Z","creation":"2019-07-24T07:25:13Z"},"accession":"S-EPMC6587274","cross_references":{"pubmed":["31221094"],"doi":["10.1186/s12860-019-0206-3"]}}