Reciprocal activation between PLK1 and Stat3 contributes to survival and proliferation of esophageal cancer cells
- 1State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
- 0State Key Laboratory of Molecular Oncology, Cancer Institute (Hospital), Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
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View abstract on PubMed
Summary
This summary is machine-generated.Signal transducer and activator of transcription 3 (Stat3) and polo-like kinase 1 (PLK1) form a positive feedback loop, driving esophageal squamous cell carcinoma (ESCC) progression. This mutual regulation enhances ESCC cell survival and proliferation.
Area Of Science
- Oncology
- Molecular Biology
- Cell Biology
Background
- Aberrant activation of signal transducer and activator of transcription 3 (Stat3) and overexpression of polo-like kinase 1 (PLK1) are implicated in cancer.
- The precise mechanisms and significance of Stat3 and PLK1 dysregulation in cancer, particularly esophageal squamous cell carcinoma (ESCC), remain incompletely understood.
Purpose Of The Study
- To investigate the relationship between Stat3 and PLK1 in ESCC.
- To elucidate the functional consequences of Stat3 and PLK1 dysregulation on ESCC cell proliferation and survival.
Main Methods
- Utilized immunoblot, quantitative reverse-transcription polymerase chain reaction, immunochemistry, chromatin immunoprecipitation, mobility shift, and reporter assays to examine the Stat3-PLK1 interaction.
- Employed colony formation, fluorescence-activated cell sorting, TUNEL assays, and xenograft tumor models to assess the impact of Stat3 and PLK1 on ESCC cell proliferation and survival.
Main Results
- Demonstrated that Stat3 directly activates PLK1 transcription in esophageal cancer cells and NIH3T3 cells.
- Revealed that PLK1 potentiates Stat3 expression, with beta-catenin mediating PLK1-dependent Stat3 transcriptional activation.
- Observed that this mutual Stat3-PLK1 regulation is essential for esophageal cancer cell proliferation and apoptosis resistance in vitro and in vivo.
- Found a correlation between Stat3 phosphorylation and PLK1 overexpression in a subset of ESCC samples.
Conclusions
- Established that Stat3 and PLK1 engage in a positive feedback loop, controlling each other's transcription and contributing to ESCC development.
- Concluded that elevated Stat3 activity and PLK1 overexpression significantly promote the survival and proliferation of ESCC cells, both in vitro and in mouse xenograft models.
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