COA6 deficiency inhibits hepatocellular carcinoma progression by regulating cuproptosis through the JAK/STAT signaling pathway
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View abstract on PubMed
Summary
This summary is machine-generated.High COA6 expression in hepatocellular carcinoma (HCC) correlates with poor prognosis. Silencing COA6 inhibits tumor growth by blocking the JAK-STAT pathway and activating cuproptosis, suggesting COA6 as a therapeutic target for HCC.
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- Hepatocellular carcinoma (HCC) presents limited therapeutic options.
- COA6, a mitochondria-associated protein, regulates tumor cuproptosis but its role in HCC is uncharacterized.
Purpose Of The Study
- To investigate the expression and functional role of COA6 in HCC.
- To elucidate the underlying molecular mechanisms of COA6 in HCC progression.
Main Methods
- Analysis of TCGA-LIHC database for differentially expressed cuproptosis-related genes (CRGs) and prognostic value.
- In vitro and in vivo assays (CCK8, flow cytometry, wound healing, transwell, subcutaneous graft tumor) to assess COA6 function.
- Western blot, RNA-sequencing, Co-immunoprecipitation, and immunofluorescence to determine molecular mechanisms and COA6-NDUFA4L2 interaction.
Main Results
- COA6 is significantly overexpressed in HCC tissues and cell lines, correlating with poor prognosis.
- Silencing COA6 inhibited HCC cell proliferation, migration, and tumor growth.
- COA6 knockdown promoted ROS accumulation, activated cuproptosis, and inhibited the JAK-STAT signaling pathway.
Conclusions
- COA6 is highly expressed in HCC and promotes malignant phenotypes.
- Silencing COA6 activates cuproptosis and inhibits the JAK-STAT pathway, leading to reduced HCC progression.
- Targeting COA6 represents a potential therapeutic strategy for HCC.
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