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METTL7B Is Required for Cancer Cell Proliferation and Tumorigenesis in Non-Small Cell Lung Cancer
Dongcheng Liu1,2, Wei Li1,3, Fuhua Zhong1
1Department of Clinical Medical Research Center, The Second Clinical Medical College of Jinan University, the First Affiliated Hospital of Southern University of Science and Technology, Shenzhen People's Hospital, Shenzhen, China.
Abstract:
Lung cancer remains a leading cause of cancer-associated mortality worldwide, however, molecular mechanisms underlying lung cancer tumorigenesis and progression remain unknown. Here, we report evidence showing that one member of the mammalian methyltransferase-like family (METTL), METTL7B, is a potential molecular target for treatment of non-small cell lung cancer (NSCLC). METTL7B expression was elevated in the majority of NSCLC comparing to normal tissues. Increased expression of METTL7B contributed to advanced stages of tumor development and poor survival in NSCLC patients. Lentivirus-mediated shRNA silencing of METTL7B suppressed proliferation and tumorigenesis of cancer cells in vitro and in vivo. Investigation on gene expression profiles of NSCLC cells revealed that abundant cell cycle related genes were downregulated in the absence of METTL7B. Pathway enrichment analysis indicated that METTL7B participated in cell cycle regulation. Notably, CCND1, a key regulator for G1/S transition, was significantly decreased with the depletion of METTL7B, resulting in G0/G1 arrest, indicating that METTL7B is critical for cell cycle progression. Taken together, our findings implicate that METTL7B is essential for NSCLC development and progression. METTL7B might serve as a potential therapeutic target for NSCLC.
Insights
The methyltransferase-like 7B (METTL7B) protein promotes non-small cell lung cancer (NSCLC) growth and progression. Inhibiting METTL7B could be a new therapeutic strategy for treating lung cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Lung cancer is a major cause of cancer mortality globally.
- The molecular drivers of lung cancer development and progression are not fully understood.
- Identifying novel therapeutic targets is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the role of methyltransferase-like 7B (METTL7B) in non-small cell lung cancer (NSCLC).
- To evaluate METTL7B as a potential therapeutic target for NSCLC treatment.
Main Methods:
- Gene expression analysis comparing NSCLC and normal tissues.
- Functional studies using lentivirus-mediated shRNA to silence METTL7B.
- In vitro and in vivo assays to assess cell proliferation and tumorigenesis.
- Gene expression profiling and pathway enrichment analysis.
Main Results:
- METTL7B expression is elevated in most NSCLC tissues and correlates with advanced stages and poor survival.
- Silencing METTL7B inhibits NSCLC cell proliferation and tumorigenesis.
- METTL7B depletion leads to downregulation of cell cycle genes and G0/G1 cell cycle arrest.
- CCND1 expression is significantly reduced upon METTL7B depletion.
Conclusions:
- METTL7B plays a critical role in NSCLC cell cycle progression and tumorigenesis.
- METTL7B is essential for NSCLC development and progression.
- METTL7B represents a promising molecular target for NSCLC therapy.
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