High expression of TBRG4 in relation to unfavorable outcome and cell ferroptosis in hepatocellular carcinoma
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View abstract on PubMed
Summary
This summary is machine-generated.Transforming growth factor beta regulator 4 (TBRG4) is highly expressed in hepatocellular carcinoma (HCC), promoting tumor proliferation, invasion, and metastasis. Targeting TBRG4 may offer a new therapeutic strategy for HCC treatment.
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- Hepatocellular carcinoma (HCC) is a prevalent liver malignancy with a poor patient prognosis.
- Understanding the molecular drivers of HCC progression is crucial for developing effective therapies.
Purpose Of The Study
- To investigate the expression of transforming growth factor beta regulator 4 (TBRG4) in HCC.
- To elucidate the role of TBRG4 in HCC cell proliferation, invasion, and metastasis.
- To analyze the underlying molecular mechanisms, including signaling pathways and potential interactions.
Main Methods
- Utilized TCGA database for bioinformatics analysis of TBRG4 expression and clinical relevance in HCC.
- Performed Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA).
- Conducted in vitro functional assays (cell counting, scratch, Transwell), apoptosis, ROS, and ferroptosis assessments, alongside Western blot, RT-PCR, and co-immunoprecipitation.
Main Results
- TBRG4 was significantly upregulated in HCC tissues, correlating with poor prognosis and metastasis.
- TBRG4 knockdown inhibited HCC cell proliferation, migration, and invasion.
- TBRG4 influences HCC progression via the DDX56/p-AKT/GSK3β pathway and interacts with Beclin1 to modulate ferroptosis.
Conclusions
- TBRG4 is a potential oncoprotein in HCC, linked to adverse outcomes.
- Targeting the DDX56/p-AKT/GSK3β pathway and TBRG4-Beclin1 interaction may represent novel therapeutic strategies for HCC.
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