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Updated: Jul 22, 2025
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
Long non-coding RNA MIR22HG inhibits the proliferation and migration, and promotes apoptosis by targeting
Shanwei Wang1, Yanli Wang2, Sheng Li2
1Department of Pathology, Xi'an Medical College, Xi'an City, 710021, P.R. China. wshanwei3@163.com.
Background:
This study aims to determine the role of long non-coding RNA (LncRNA) MIR22HG in small cell lung cancer (SCLC), and to explore its relevant mechanism.
Methods And Results:
The expressions of genes and proteins in SCLC cells were examined applying qRT-PCR and western blot. Cell proliferation estimation was implemented utilizing cell counting kit-8 (CCK-8) and colony formation assays; the assessment of cell migration and invasion was operated employing Wound healing and Transwell; apoptosis evaluation was conducted adopting flow cytometric assay. Binding relationships was confirmed by luciferase reporter assay. Moreover, SCLC animal model was established to explore the role of MIR22HG in vivo. It was found that MIR22HG was declined and miR-9-3p was elevated in five SCLC cell lines (NCI-H446, NCI-H69, SHP-77, DMS79 and NCI-H345) in comparison with normal human bronchial epithelial cell line (NHBE). More interestingly, overexpression of MIR22HG resulted in decreased cell viability, declined colony formation, diminished capacities of cell migration and invasion in NCI-H446 and NCI-H345 cells but induced more apoptotic cells. However, these impacts were reversed by miR-9-3p upregulation. Meanwhile, MIR22HG could bind to miR-9-3p and negatively regulate its expression in SCLC. What's more, LncRNA MIR22HG overexpression was also testified to elevate SOCS1 via downregulating miR-9-3p expression. Furthermore, in vivo study further confirmed the role of MIR22HG/miR-9-3p in tumor regulation of SCLC.
Conclusions:
In conclusion, MIR22HG in SCLC was found to modulate miR-9-3p level and might act as a possible biomarker for SCLC treatment.
Insights
Long non-coding RNA MIR22HG is downregulated in small cell lung cancer (SCLC). Overexpression of MIR22HG inhibits SCLC progression by modulating miR-9-3p, suggesting its potential as a therapeutic biomarker.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- Small cell lung cancer (SCLC) remains a significant challenge in oncology.
- The role of long non-coding RNAs (LncRNAs) in SCLC pathogenesis is increasingly recognized.
- MIR22HG is a novel LncRNA with potential implications in cancer development.
Purpose of the Study:
- To investigate the functional role of LncRNA MIR22HG in SCLC.
- To elucidate the underlying molecular mechanisms of MIR22HG in SCLC.
- To assess MIR22HG as a potential therapeutic target or biomarker for SCLC.
Main Methods:
- Gene and protein expression analysis using qRT-PCR and Western blot.
- Cellular assays including CCK-8, colony formation, wound healing, Transwell, and flow cytometry.
- In vivo studies using a SCLC animal model and luciferase reporter assays to confirm interactions.
Main Results:
- MIR22HG expression was significantly decreased in SCLC cell lines compared to normal cells.
- MIR22HG overexpression inhibited SCLC cell proliferation, migration, and invasion while promoting apoptosis.
- MIR22HG directly targets and downregulates miR-9-3p, and its overexpression upregulates SOCS1.
Conclusions:
- MIR22HG plays a crucial role in regulating SCLC progression by modulating the miR-9-3p/SOCS1 axis.
- MIR22HG acts as a tumor suppressor in SCLC.
- MIR22HG holds promise as a potential biomarker and therapeutic target for SCLC treatment.
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