ZNF143-mediated upregulation of MEX3C promotes hepatocellular carcinoma progression
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View abstract on PubMed
Summary
This summary is machine-generated.Zinc finger protein 143 (ZNF143) promotes hepatocellular carcinoma (HCC) cell migration and invasion. ZNF143 upregulates MEX3C expression by binding to its promoter, driving aggressive tumor behavior.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Research
Background
- Microvascular invasion is a key indicator of aggressive hepatocellular carcinoma (HCC) and recurrence.
- Zinc finger protein 143 (ZNF143) is a transcription factor with diverse biological roles.
- The specific function of ZNF143 in HCC cell migration and invasion requires elucidation.
Purpose Of The Study
- To investigate the biological role and underlying mechanism of ZNF143 in HCC cell migration and invasion.
- To determine the relationship between ZNF143 expression and patient prognosis in HCC.
- To identify downstream targets of ZNF143 involved in HCC progression.
Main Methods
- Analysis of ZNF143 and MEX3C expression in HCC tissues and correlation with prognosis.
- In vitro assays (wound-healing, Matrigel transwell) to assess cell migration and invasion.
- mRNA profiling, dual luciferase assays, and chromatin immunoprecipitation (ChIP) to elucidate molecular mechanisms.
Main Results
- ZNF143 overexpression in HCC correlates with poor prognosis, higher tumor grade, and microvascular invasion.
- ZNF143 significantly enhances HCC cell migration and invasion.
- ZNF143 directly activates MEX3C transcription, and MEX3C knockdown reverses ZNF143-induced invasion.
Conclusions
- ZNF143 promotes HCC cell migration and invasion.
- ZNF143 exerts its function by directly activating MEX3C transcription.
- Targeting the ZNF143-MEX3C axis may offer therapeutic strategies for HCC.
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