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LncRNA SNHG9 is Downregulated in Non-Small Cell Lung Cancer and Suppressed miR-21 Through Methylation to Promote Cell
Dingxue Wang1, Xiaoqing Cao2, Yi Han2
1Department of Oncology, The First Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, 550001, People's Republic of China.
Background:
LncRNA SNHG9 has been shown to be an oncogenic lncRNA in glioblastoma, while its role in other cancers is unknown. The aim of this study was to investigate the role of SNHG9 in non-small cell lung cancer (NSCLC).
Methods:
The differential expression of SNHG9 in NSCLC was first explored by analyzing the TCGA dataset, followed by measuring the expression levels of SNHG9 in paired NSCLC and non-tumor tissues by RT-qPCR. Expression of miR-21 was also determined by RT-qPCR. Correlations were analyzed by linear regression. The interaction between miR-21 and SNHG9 was detected using RNA pull-down. The expression relationship between SNHG9 and miR-21 was analyzed by SNHG9 or miR-21 overexpression experiments. The effects of overexpression of SNHG9 on the methylation of miR-21 were analyzed by methylation-specific PCR (MSP). Cell proliferation was evaluated by CCK-8 assay.
Results:
By analyzing the TCGA dataset, we observed downregulation of SNHG9 in NSCLC, which was confirmed by measuring the expression levels of SNHG9 in paired NSCLC tumor tissues and non-tumor tissues from NSCLC patients involved in this study. MiR-21 was upregulated in NSCLC tumor tissues and inversely correlated with SNHG9 in cancer tissues but not in non-tumor tissues. The interaction between SNHG9 and miR-21 was predicted by bioinformatic analyses, which was further verified by RNA pull-down. In NSCLC cells, overexpression of SNHG9 led to downregulated miR-21 and increased methylation of miR-21 gene. In contrast, miR-21 did not affect the expression of SNHG9. In addition, overexpression of SNHG9 attenuated the enhancing effects of miR-21 on NSCLC proliferation.
Conclusion:
SNHG9 might downregulate miR-21 through methylation to suppress cancer cell proliferation.
Insights
Long non-coding RNA SNHG9 is downregulated in non-small cell lung cancer (NSCLC) and may suppress proliferation by downregulating miR-21 through methylation.
Area of Science:
- Oncology
- Molecular Biology
- Gene Regulation
Background:
- Long non-coding RNA SNHG9 (small nucleolar RNA host gene 9) is implicated as an oncogene in glioblastoma.
- The role of SNHG9 in non-small cell lung cancer (NSCLC) remains largely unexplored.
Purpose of the Study:
- To investigate the expression and function of SNHG9 in non-small cell lung cancer (NSCLC).
- To elucidate the regulatory relationship between SNHG9 and miR-21 in NSCLC.
Main Methods:
- Differential expression analysis of SNHG9 in NSCLC using TCGA dataset and RT-qPCR.
- Assessment of miR-21 expression and its correlation with SNHG9.
- RNA pull-down assay to confirm SNHG9-miR-21 interaction.
- Methylation-specific PCR (MSP) to analyze miR-21 gene methylation.
- Cell proliferation assays (CCK-8) to evaluate functional impact.
Main Results:
- SNHG9 was found to be downregulated in NSCLC tissues compared to non-tumor tissues.
- MiR-21 was upregulated in NSCLC and inversely correlated with SNHG9 expression.
- SNHG9 overexpression led to decreased miR-21 levels and increased miR-21 gene methylation.
- SNHG9 overexpression attenuated miR-21-induced proliferation in NSCLC cells.
Conclusions:
- SNHG9 plays a suppressive role in NSCLC progression.
- SNHG9 may downregulate miR-21 via methylation, thereby inhibiting NSCLC cell proliferation.
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