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New STAT3-FOXL2 pathway and its function in cancer cells
Yangyang Han1, Jun Wu2, Weiwei Yang3
1School of Bioscience and Technology, Weifang Medical University, Weifang, Shandong, 261053, People's Republic of China. hanyy2009@163.com.
BMC Molecular and Cell Biology
|June 22, 2019
Summary
Signal transducer and activator of transcription 3 (STAT3) regulates the forkhead transcription factor (FOXL2) in cancer cells. This STAT3-FOXL2 pathway is crucial for regulating cancer cell apoptosis, offering new therapeutic targets.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- The forkhead transcription factor (FOXL2) is vital for blepharophimosis-ptosis-epicanthus inversus syndrome (BPES), sex determination, ovarian development, and cell cycle control.
- While FOXL2's downstream targets are studied, its upstream regulation remains largely unknown.
Purpose of the Study:
- To investigate the upstream regulation of FOXL2.
- To explore the role of STAT3 in regulating FOXL2.
- To determine the functional significance of the STAT3-FOXL2 interaction in cancer cell apoptosis.
Main Methods:
- Electrophoretic mobility shift assay (EMSA) to confirm STAT3 binding to FOXL2.
- Chromatin immunoprecipitation (ChIP) to identify the binding site of STAT3 on FOXL2.
- Gene knockdown experiments to assess the impact of STAT3 and FOXL2 on cancer cell apoptosis.
Main Results:
- STAT3 was identified as a regulator of FOXL2 in cancer cells.
- STAT3 directly binds to the FOXL2 gene promoter at a specific DNA sequence.
- Knockdown of either STAT3 or FOXL2 significantly increased cancer cell apoptosis.
- Apoptosis induction was associated with altered expression of apoptosis-related genes like TNF, TRAIL, and GnRHR.
Conclusions:
- This study identifies STAT3 as a novel upstream regulator of FOXL2.
- The STAT3-FOXL2 pathway plays a significant role in regulating apoptosis in HeLa cells.
- These findings provide new insights for targeting FOXL2 in cancer prevention and treatment strategies.
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