Abstract
Background
MicroRNA-17-5p (miR-17-5p) plays a pivotal role in the tumorigenesis and progression of non-small cell lung cancer (NSCLC) by regulating its target genes. Advances in molecular biology highlight the importance of long non-coding RNAs (lncRNAs) in cancer, yet the mechanistic interactions between miR-17-5p and lncRNAs in NSCLC remain underexplored.
Objective
This study investigated the regulatory interplay between miR-17-5p and lncRNA-FGD5-AS1 and evaluated their potential as targets for NSCLC therapy.
Methods
A comprehensive set of technologies, including cell transfection, quantitative real-time PCR (qRT-PCR), bioinformatics analysis, and functional assays (proliferation, migration, apoptosis), was employed to examine the role of miR-17-5p and lncRNA-FGD5-AS1 in NSCLC.
Results
Elevated lncRNA-FGD5-AS1 expression was observed in NSCLC cell lines A549 and H1299, correlating with poor patient prognosis. Functional assays revealed that miR-17-5p directly downregulates lncRNA-FGD5-AS1, thereby modulating key oncogenic processes. Overexpression of miR-17-5p reduced tumor cell proliferation and migration while inducing apoptosis. Conversely, miR-17-5p inhibition elevated lncRNA-FGD5-AS1 levels and reversed these effects.
Conclusion
The findings identify the miR-17-5p/lncRNA-FGD5-AS1 regulatory axis as a novel therapeutic target for NSCLC. By integrating molecular and technological approaches, this study offers insights into precision oncology and highlights the potential for advanced RNA-based interventions.
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