miR-144-5p Enhances the Radiosensitivity of Non-Small-Cell Lung Cancer Cells via Targeting ATF2

Area of Science:

• Molecular Biology
• Oncology
• Gene Regulation

Background:

• MicroRNAs (miRNAs) are key posttranscriptional regulators of gene expression.
• Dysregulation of miRNAs is implicated in various cancers, including non-small cell lung cancer (NSCLC).
• The specific role of miR-144-5p in NSCLC radiosensitivity remains largely unexplored.

Purpose of the Study:

• To investigate the role of miR-144-5p in the radiosensitivity of NSCLC.
• To identify the molecular targets and mechanisms underlying miR-144-5p's function in NSCLC.
• To evaluate the therapeutic potential of targeting the miR-144-5p pathway in NSCLC.

Main Methods:

• Quantitative analysis of miR-144-5p expression in NSCLC clinical specimens and cell lines.
• Assessment of miR-144-5p's effect on NSCLC cell radiosensitivity in vitro and in vivo xenograft models.
• Bioinformatics analysis and luciferase reporter assays to identify and validate ATF2 as a direct target of miR-144-5p.

Main Results:

• miR-144-5p was found to be significantly downregulated in NSCLC tissues and radiation-exposed NSCLC cells.
• Overexpression of miR-144-5p enhanced NSCLC cell radiosensitivity both in vitro and in vivo.
• Activating transcription factor 2 (ATF2) was identified as a direct functional target of miR-144-5p, and its restoration abrogated miR-144-5p's radiosensitizing effects.

Conclusions:

• The miR-144-5p/ATF2 axis plays a critical role in regulating NSCLC radiosensitivity.
• Downregulation of miR-144-5p contributes to radioresistance in NSCLC.
• Targeting the miR-144-5p/ATF2 pathway presents a promising therapeutic strategy for improving NSCLC radiosensitivity.