Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer
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View abstract on PubMed
Summary
This summary is machine-generated.Cell division cycle 25C (CDC25C) is a key prognostic marker in non-small cell lung cancer (NSCLC). Targeting the miR-142-3p/CDC25C axis impacts NSCLC cell proliferation, apoptosis, and autophagy.
Area Of Science
- Oncology
- Molecular Biology
- Bioinformatics
Background
- Non-small cell lung cancer (NSCLC) exhibits genetic diversity and heterogeneity, necessitating improved prognostic evaluation and targeted therapies.
- Understanding the molecular mechanisms driving NSCLC progression is crucial for developing effective treatment strategies.
Purpose Of The Study
- To identify key prognostic genes in NSCLC using bioinformatics analysis.
- To investigate the functional role of identified genes and regulatory pathways in NSCLC cell behavior.
- To explore the therapeutic potential of targeting specific molecular axes in NSCLC.
Main Methods
- Bioinformatics analysis of The Cancer Genome Atlas (TCGA)-NSCLC and GSE68571 datasets to identify differentially expressed genes (DEGs).
- Construction of protein-protein interaction (PPI) networks and identification of key prognostic genes.
- In vitro experiments assessing the phenotypic effects of cell division cycle 25C (CDC25C) on NSCLC cell lines, including proliferation, migration, invasion, apoptosis, and cell cycle analysis.
- Investigation of the miR-142-3p/CDC25C axis and its impact on autophagy and apoptosis, including the role of 3-methyladenine (3-MA).
Main Results
- CDC25C was identified as a significant prognostic marker in NSCLC, with elevated expression in tumor tissues.
- CDC25C knockdown suppressed NSCLC cell proliferation, migration, invasion, induced apoptosis, and caused cell cycle arrest.
- A reciprocal regulatory relationship was observed between CDC25C and miR-142-3p, with CDC25C counteracting miR-142-3p's inhibitory effects.
- Combined inhibition of miR-142-3p, CDC25C silencing, and 3-MA treatment synergistically regulated NSCLC cell proliferation, apoptosis, and autophagy.
Conclusions
- MiR-142-3p directly targets CDC25C, playing a critical role in regulating autophagy and apoptosis in NSCLC.
- The miR-142-3p/CDC25C axis represents a crucial regulatory pathway in NSCLC, offering potential therapeutic targets.
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