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Published on: March 3, 2023
MRPL42 is activated by YY1 to promote lung adenocarcinoma progression
Wei Jiang1, Chengpeng Zhang1, Yunteng Kang1
1Department of Thoracic Surgery, the First Affiliated Hospital of Soochow, University, Suzhou, Jiangsu, China.
Abstract:
Mammalian mitochondrial ribosomal proteins are a group of protein factors encoded by nuclear genes, responsible for the synthesis of proteins in mitochondria. As a member of mitochondrial ribosomal proteins, MRPL42 (mitochondrial ribosomal protein L42) belongs to 28S and 39S subunits. The current literature showed that its role in lung adenocarcinoma (LUAD) was not clear. We found that MRPL42 was highly expressed in early-stage LUAD tissues and cell lines, and remarkably related to the prognosis of patients. Knockdown of MRPL42 could reduce the proliferation and colonization, promote cell cycle arrest in G1/S phase, and weaken the migration and invasion ability of LUAD cells in vitro. Moreover, depletion of MRPL42 also inhibited tumor growth in vivo. Bioinformatics analysis found that YY1 may bind to the promoter region upstream of the MRPL42 gene to promote the transcription of MRPL42, which was verified by the ChIP and Dual luciferase reporter assay. QRT-PCR confirmed that knocking down YY1 could attenuate the expression of MRPL42. In summary, MRPL42 acts as an oncogene in LUAD, and its expression level is regulated by YY1.
Insights
Mitochondrial ribosomal protein L42 (MRPL42) is highly expressed in lung adenocarcinoma (LUAD) and promotes tumor growth. Inhibiting MRPL42 reduces LUAD cell proliferation, migration, and invasion, suggesting it is an oncogene.
Area of Science:
- Molecular Biology
- Oncology
- Biochemistry
Background:
- Mitochondrial ribosomal proteins are crucial for mitochondrial protein synthesis.
- The specific role of MRPL42 (mitochondrial ribosomal protein L42) in lung adenocarcinoma (LUAD) remains unclear.
- Understanding MRPL42's function in LUAD is vital for developing targeted therapies.
Purpose of the Study:
- To investigate the role of MRPL42 in lung adenocarcinoma (LUAD).
- To elucidate the regulatory mechanism of MRPL42 expression in LUAD.
- To assess MRPL42 as a potential therapeutic target for LUAD.
Main Methods:
- Quantitative real-time PCR (QRT-PCR) to assess gene expression.
- In vitro assays to evaluate cell proliferation, cell cycle, migration, and invasion.
- In vivo studies to assess tumor growth inhibition.
- Bioinformatics analysis, Chromatin Immunoprecipitation (ChIP), and Dual Luciferase Reporter assays to determine gene regulation.
Main Results:
- MRPL42 is highly expressed in early-stage LUAD tissues and cell lines.
- MRPL42 expression correlates significantly with patient prognosis.
- MRPL42 knockdown inhibits LUAD cell proliferation, colonization, migration, and invasion, and promotes G1/S phase arrest.
- MRPL42 depletion suppresses tumor growth in vivo.
- YY1 transcription factor binds to the MRPL42 promoter, enhancing its transcription.
- Knockdown of YY1 attenuates MRPL42 expression.
Conclusions:
- MRPL42 functions as an oncogene in lung adenocarcinoma.
- MRPL42 expression is transcriptionally upregulated by YY1.
- MRPL42 represents a potential therapeutic target for LUAD treatment.
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