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Published on: October 27, 2014
MiR-542-3p exerts tumor suppressive functions in non-small cell lung cancer cells by upregulating FTSJ2
Bin Liu1, Jing Li2, Min Zheng1
1Department of Medical Oncology, Sichuan Cancer Hospital, Chengdu, China.
Aims:
Up-regulation or down-regulation of microRNAs (miRNAs) has been found in non-small cell lung cancer (NSCLC). However, the role and mechanism of regulation of miR-542-3p in NSCLC is still unclear. This study aimed at investigating the primary biological function of miR-542-3p and FTSJ2 in NSCLC tumorigenesis and the correlation of miR-542-3p and FTSJ2 in NSCLC.
Main Methods:
Our present results showed that miR-542-3p was down-regulated in NSCLC tissues and cancer cells. Overexpression of miR-542-3p inhibited cell proliferation, cell migration, cell cycle, EMT process and tumor growth in vitro, and induced cell apoptosis by MTT assay, colony formation assay, transwell migration assay, flow cytometry assay, RT-qPCR assay, western blot experiment and vivo model assay; miR-542-3p directly bound to the 3'UTR of FTSJ2 and upregulated FTSJ2 both mRNA and protein level by EGFP reporter assay, RT-qPCR and western blot analysis in NSCLC cells. FTSJ2 also reduced the aggressiveness of NSCLC cells.
Key Findings:
In short, miR-542-3p functions as a suppressor gene by targeting and upregulating FTSJ2, thus inhibiting the malignancy of NSCLC cells.
Significance:
According to the results, miRNA-542-3p and its targeted FTSJ2 may be indispensable as a predictive biomarker of the response to the treatment in patients with NSCLC.
Insights
MicroRNA-542-3p acts as a tumor suppressor in non-small cell lung cancer (NSCLC) by targeting FTSJ2. This finding suggests miR-542-3p and FTSJ2 could be biomarkers for NSCLC treatment response.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) play crucial roles in cancer development, with altered expression observed in non-small cell lung cancer (NSCLC).
- The specific function and regulatory mechanisms of miR-542-3p in NSCLC remain largely unelucidated.
- Understanding miRNA involvement is key to developing novel therapeutic strategies for NSCLC.
Purpose of the Study:
- To investigate the biological function of miR-542-3p in NSCLC tumorigenesis.
- To elucidate the regulatory relationship between miR-542-3p and FTSJ2 in NSCLC.
- To assess the potential of miR-542-3p and FTSJ2 as predictive biomarkers for NSCLC treatment.
Main Methods:
- Down-regulation of miR-542-3p in NSCLC tissues and cells was confirmed.
- Functional assays (MTT, colony formation, Transwell, flow cytometry) assessed the impact of miR-542-3p overexpression on NSCLC cell behavior.
- EGFP reporter assays, RT-qPCR, and Western blot analyses were employed to determine the direct interaction between miR-542-3p and FTSJ2, and their expression levels.
Main Results:
- Overexpression of miR-542-3p significantly inhibited NSCLC cell proliferation, migration, cell cycle progression, epithelial-mesenchymal transition (EMT), and tumor growth in vitro and in vivo.
- miR-542-3p directly targets the 3'UTR of FTSJ2, leading to the upregulation of FTSJ2 at both mRNA and protein levels.
- FTSJ2 was found to reduce the aggressiveness of NSCLC cells.
Conclusions:
- miR-542-3p functions as a tumor suppressor gene in NSCLC by targeting and upregulating FTSJ2, thereby inhibiting cancer cell malignancy.
- miR-542-3p and its target FTSJ2 hold potential as indispensable predictive biomarkers for treatment response in NSCLC patients.
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