THAP3 recruits SMYD3 to OXPHOS genes and epigenetically promotes mitochondrial respiration in hepatocellular carcinoma
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View abstract on PubMed
Summary
This summary is machine-generated.Transcription factor THAP3 epigenetically regulates mitochondrial oxidative phosphorylation (OXPHOS) by recruiting SMYD3. This mechanism promotes liver cancer cell proliferation and is overexpressed in human liver cancer.
Area Of Science
- Molecular Biology
- Cellular Respiration
- Cancer Research
Background
- Mitochondria are crucial for cellular respiration via oxidative phosphorylation (OXPHOS).
- Transcriptional regulation of OXPHOS is not well understood.
- Identifying regulatory mechanisms is key to understanding cellular metabolism and cancer.
Purpose Of The Study
- To investigate the transcriptional regulation of OXPHOS.
- To identify novel factors involved in OXPHOS regulation and their role in liver cancer.
- To elucidate the mechanism by which THAP3 influences OXPHOS and cancer cell growth.
Main Methods
- Analysis of The Cancer Genome Atlas (TCGA) transcriptome data.
- Investigating the interaction between THAP3 and SMYD3.
- Assessing the epigenetic modifications (H3K4me3) and their impact on OXPHOS gene expression.
- Evaluating the role of THAP3 and SMYD3 in liver cancer cell proliferation and colony formation.
Main Results
- THAP3 is strongly associated with OXPHOS gene expression.
- THAP3 recruits SMYD3 to upregulate H3K4me3 and promote OXPHOS gene expression.
- THAP3 and SMYD3 levels are modulated by metabolic cues and collaboratively enhance liver cancer cell proliferation.
- Both THAP3 and SMYD3 are overexpressed in human liver cancer and correlate positively with OXPHOS gene expression.
Conclusions
- THAP3 epigenetically upregulates OXPHOS by recruiting SMYD3.
- The THAP3-SMYD3 complex drives liver cancer cell proliferation.
- THAP3 and SMYD3 represent potential therapeutic targets in liver cancer.
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