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MRPL42 Knockdown Suppresses the Malignant Functions of Hepatocellular Carcinoma by Regulating Oxidative
Jun Lv1, Fu-Yuan Gan2, Ming-Hao Li2
1Department of Hepatobiliary Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, China. lvjun1996@163.com.
Objective:
The diagnosis and treatment of hepatocellular carcinoma (HCC) remain unsatisfactory, underscoring the urgent need to explore new regulatory factors. This study aimed to uncover the regulatory role of mitochondrial ribosomal protein L42 (MRPL42) in HCC development and assess its clinical potential as a therapeutic target and prognostic biomarker.
Methods:
MRPL42 expression in HCC was analyzed in datasets obtained from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) databases. MRPL42 expression was detected via reverse transcription quantitative polymerase chain reaction and immunohistochemistry, and its diagnostic and prognostic abilities were assessed via receiver operating characteristic (ROC) curves and Kaplan-Meier curves. Cell proliferation was assessed via the Cell Counting Kit-8 assay, migration via the wound healing assay, and invasion via Transwell experiments. The molecular mechanisms underlying MRPL42 knockdown-mediated suppression of HCC progression were analyzed via transcriptome sequencing. Western blot analysis was used to measure protein levels. The ATP content and mitochondrial respiratory chain complex I activity were determined via commercial reagent kits.
Results:
MRPL42 overexpression predicted HCC occurrence and poor prognosis. MRPL42 knockdown suppressed the malignant functions of HCC. Transcriptomic analysis revealed that differentially expressed genes after MRPL42 knockdown were closely linked to oxidative phosphorylation (OXPHOS). MRPL42 knockdown inhibited the protein expression of the mitochondrial activity markers PGC-1α and MT-ND1 and reduced ATP content and mitochondrial respiratory chain complex I activity, indicating that MRPL42 deficiency impaired mitochondrial OXPHOS. Furthermore, MRPL42 knockdown suppressed the malignant functions of HCC cells by regulating OXPHOS.
Conclusion:
MRPL42 is overexpressed in HCC and is a potential biomarker for HCC diagnosis and prognosis. In regulating OXPHOS, MRPL42 knockdown suppressed HCC malignant function, highlighting its potential as a therapeutic target.
Insights
Mitochondrial ribosomal protein L42 (MRPL42) is overexpressed in hepatocellular carcinoma (HCC), driving tumor growth. Targeting MRPL42 and its regulation of oxidative phosphorylation (OXPHOS) shows potential for HCC diagnosis and treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Hepatocellular carcinoma (HCC) diagnosis and treatment require novel strategies.
- Mitochondrial ribosomal protein L42 (MRPL42) role in HCC is unexplored.
Purpose of the Study:
- Investigate MRPL42's regulatory role in HCC.
- Evaluate MRPL42 as a diagnostic/prognostic biomarker and therapeutic target.
Main Methods:
- Analyzed TCGA and GEO datasets for MRPL42 expression.
- Performed RT-qPCR, IHC, CCK-8, wound healing, and Transwell assays.
- Conducted transcriptome sequencing, Western blot, and measured ATP/mitochondrial activity.
Main Results:
- MRPL42 overexpression correlated with HCC occurrence and poor prognosis.
- MRPL42 knockdown suppressed HCC cell proliferation, migration, and invasion.
- MRPL42 regulates HCC malignancy via oxidative phosphorylation (OXPHOS).
Conclusions:
- MRPL42 is an overexpressed biomarker in HCC.
- MRPL42 knockdown inhibits HCC progression by modulating OXPHOS.
- MRPL42 presents a potential therapeutic target for HCC.
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