Background: Dysregulation of microRNAs (miRNAs) figures prominently in the radio-
sensitivity of non-small cell lung cancer (NSCLC). MiR-129-5p can block the development of
a variety of tumors. However, whether miR-129-5p modulates radio-sensitivity of NSCLC cells remains
Objective: This study was aimed to explore the role and the underlying mechanism of miR-129-5p
in the radiosensitivity of NSCLC.
Methods: Radio-resistant NSCLC cell lines (A549-R and H1299-R) were constructed using A549
and H1299 cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to
quantify miR-129-5p, SRY-box transcription factor 4 (SOX4) mRNA, and RUNX family transcription
factor 1 (RUNX1) mRNA expression levels. Cell apoptosis and cell cycle were detected by
flow cytometry. Cell counting kit-8 (CCK-8) assay and colony formation experiments were used to
measure cell proliferation. γ-H2AX was examined by Western blot to confirm DNA injury. Dual-
luciferase reporter experiments were applied to analyze the interactions among miR-129-5p,
RUNX1, and SOX4.
Results: In A549-R and H1299-R cells, compared with the wild-type cell lines, miR-129-5p expression
was remarkably reduced while SOX4 and RUNX1 expressions were increased. The transfection
of miR-129-5p into NSCLC cell lines markedly induced cell apoptosis, DNA injury, cell cycle
arrest, and inhibited cell proliferation and colony formation. RUNX1 and SOX4 were validated as
target genes of miR-129-5p, and the restoration of RUNX1 or SOX4 could counteract the influence
of miR-129-5p on A549-R cells.
Conclusions: MiR-129-5p sensitizes A549-R and H1299-R cells to radiation by targeting RUNX1