Related Experiment Video
Updated: Mar 10, 2026
Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
MiR-101-3p Regulates the Viability of Lung Squamous Carcinoma Cells via Targeting EZH2
1Department of Radiation Oncology, The Third Affiliated Hospital of Kunming Medical University, Cancer Hospital of Yunnan Province, Kunming 650118, P.R.China.
Abstract:
The aim of this study was to investigate the effects of miR-101-3p on the viability, migration, invasion, and mitosis of lung squamous carcinoma cells by inhibiting EZH2. In this study, RT-qPCR was used to detect the expression of miR-101-3p and EZH2 in both tissues and cells at RNA level. The dual luciferase reporter gene system was used to determine whether there was targeting relationship between miR-101-3p and EZH2-3'UTR. Western Blot was used to detect the expression of EZH2 as well as the proliferation and invasion related proteins. The CCK-8 assay, Transwell invasion assay, wound healing assay and flow cytometry were conducted to test the cell viability, invasion, migration and apoptosis. The results of RT-qPCR and Western blot showed that miR-101-3p was low-expressed and EZH2 was overexpressed in lung squamous cell carcinoma tissues and cells. Meanwhile the Western blot confirmed the effects of EZH2 expression on the proliferation and invasion of carcinoma cells. The results of luciferase assay and RT-qPCR showed that miR-101-3p had a negative regulation effect on EZH2. The CCK-8 assay, Transwell invasion assay, wound healing assay and flow cytometry results showed that the inhibition of EZH2 or the up-regulation of miR-101-3p inhibited the viability, migration, invasion and cell cycle but promoted cell apoptosis of lung squamous cell carcinoma. MiR-101-3p could inhibit the viability, migration, invasion, and cell cycle of lung squamous carcinoma cells by inhibiting the EZH2. J. Cell. Biochem. 118: 3142-3149, 2017. © 2016 Wiley Periodicals, Inc.
Insights
MicroRNA-101-3p (miR-101-3p) inhibits lung squamous cell carcinoma progression by targeting EZH2. Upregulating miR-101-3p or inhibiting EZH2 reduces cancer cell viability, migration, and invasion.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Lung squamous cell carcinoma (LSCC) is a major subtype of lung cancer.
- Dysregulation of microRNAs and epigenetic modifiers like EZH2 is implicated in LSCC pathogenesis.
- Understanding the molecular mechanisms driving LSCC is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of miR-101-3p in LSCC.
- To determine if miR-101-3p affects LSCC cell viability, migration, invasion, and mitosis by inhibiting EZH2.
- To elucidate the therapeutic potential of targeting the miR-101-3p/EZH2 axis in LSCC.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to assess miR-101-3p and EZH2 expression.
- Dual-luciferase reporter assay to confirm the targeting relationship between miR-101-3p and EZH2.
- Western blot to analyze protein expression levels.
- Cell Counting Kit-8 (CCK-8), Transwell invasion, wound healing, and flow cytometry assays to evaluate cell viability, invasion, migration, and apoptosis.
Main Results:
- miR-101-3p was significantly downregulated, while EZH2 was upregulated in LSCC tissues and cells.
- miR-101-3p directly targeted and inhibited EZH2 expression.
- Inhibition of EZH2 or upregulation of miR-101-3p suppressed LSCC cell viability, migration, invasion, and cell cycle progression.
- Upregulation of miR-101-3p or inhibition of EZH2 promoted LSCC cell apoptosis.
Conclusions:
- miR-101-3p acts as a tumor suppressor in LSCC by inhibiting EZH2.
- The miR-101-3p/EZH2 pathway represents a potential therapeutic target for LSCC treatment.
- Modulating miR-101-3p levels could offer a novel strategy for combating lung squamous cell carcinoma.
Related Concept Videos
01:22MicroRNAs
01:22MicroRNAs
02:23Abnormal Proliferation