Related Experiment Video
Updated: Jan 2, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
miR-1305 Inhibits The Progression Of Non-Small Cell Lung Cancer By Regulating MDM2
Yuxing Cai1, Yi Hao2, HaiFeng Ren3
1Department of Respiratory Medicine, Baoji Central Hospital, Baoji, 721008, People's Republic of China.
Background:
Increasing evidence has suggested the critical implication of microRNAs (miRNAs) in the initiation and progression of non-small cell lung cancer (NSCLC). Previous studies have shown the tumor-suppressive function of miR-1305 in cancer; however, the role of miR-1305 in NSCLC has not been fully understood.
Methods:
The expression of miR-1305 in NSCLC was detected by RT-qPCR. The influence of miR-1305 on the growth of NSCLC cells was determined via Cell Counting Kit 8 (CCK-8), colony formation and FACS analysis. The targets of miR-1305 were predicted with the miRDB database. Luciferase reporter assay was performed to investigate the binding between miR-1305 and 3'-UTR of MDM2. Western blot was applied to check the expression of MDM2 with miR-1305.
Results:
Here, we found that miR-1305 was down-regulated in NSCLC tissues and cell lines. Decreased miR-1305 was significantly correlated with the metastasis and poor prognostics of NSCLC patients. Overexpression of miR-1305 inhibited the proliferation and migration and promoted the apoptosis of NSCLC cells. Bioinformatics and luciferase assay uncovered that the mouse/murine double minute 2 (MDM2) was a target of miR-1305. miR-1305 bound the 3'-untranslated region (UTR) of MDM2 and decreased the expression of MDM2 in NSCLC cells. As MDM2 was a negative regulator of p53, decreased MDM2 by miR-1305 up-regulated the abundance of p53 in NSCLC cells. Restoration of MDM2 markedly attenuated the suppressive role of miR-1305 in the proliferation and migration of NSCLC cells.
Conclusion:
The findings provided novel mechanism of miR-1305/MDM2 signaling in regulating the progression of NSCLC, suggesting miR-1305 as a promising target for the treatment of NSCLC.
Insights
MicroRNA 1305 (miR-1305) is downregulated in non-small cell lung cancer (NSCLC), inhibiting tumor progression. Restoring miR-1305 suppresses NSCLC growth by targeting MDM2, offering a potential therapeutic strategy.
Area of Science:
- Molecular Biology
- Oncology
- Gene Regulation
Background:
- MicroRNAs (miRNAs) play a critical role in non-small cell lung cancer (NSCLC) development.
- The tumor-suppressive function of miR-1305 is known in cancer, but its specific role in NSCLC requires further elucidation.
Purpose of the Study:
- To investigate the expression and function of miR-1305 in NSCLC.
- To identify the molecular targets and signaling pathways regulated by miR-1305 in NSCLC.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) for miR-1305 expression.
- Cell proliferation, colony formation, and flow cytometry assays to assess cellular effects.
- Bioinformatic prediction and luciferase reporter assays to identify and validate miR-1305 targets.
- Western blot analysis for protein expression (MDM2, p53).
Main Results:
- miR-1305 expression is significantly decreased in NSCLC tissues and cell lines.
- Downregulation of miR-1305 correlates with metastasis and poor prognosis in NSCLC patients.
- Overexpression of miR-1305 inhibits NSCLC cell proliferation and migration, and promotes apoptosis.
- MDM2 was identified as a direct target of miR-1305, with miR-1305 binding to the 3'-UTR of MDM2.
- miR-1305 reduces MDM2 levels, leading to increased p53 abundance and subsequent suppression of NSCLC progression.
Conclusions:
- A novel mechanism involving the miR-1305/MDM2/p53 signaling axis in NSCLC progression was identified.
- miR-1305 demonstrates potential as a therapeutic target for NSCLC treatment.
More Related Videos
09:45An In Vitro Protocol for Evaluating MicroRNA Levels, Functions, and Associated Target Genes in Tumor Cells
Published on: May 21, 2019
06:51Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
Related Concept Videos
Abnormal Proliferation
MicroRNAs
MicroRNAs
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Mitogens and the Cell Cycle
Inhibition of Cdk Activity