Abnormal expression of CDC25C in NSCLC is influenced by transcriptional and RNA N6‑methyladenosine‑mediated post‑transcriptional regulation

Non‑small cell lung Cancer (NSCLC) exhibits a high incidence and mortality rate worldwide. Elevated cytokinesis cyclin 25 homologous protein C (CDC25C) expression is correlated with a poor prognosis in patients with NSCLC. Transcriptional regulation and post‑transcriptional modification are critical mechanisms governing gene expression, with aberrations in these processes increasingly recognized as pivotal contributors to Cancer pathogenesis. The present study elucidated that the transcriptional activator, signal transducer and activator of transcription 3, directly interacts with the CDC25C promoter, thereby modulating its expression. Moreover, multi‑omics analysis was employed to identify the genes involved in the N6‑methyladenosine (m⁶A) methylation‑mediated post‑transcriptional regulation of CDC25C. The findings indicated that downregulation of alkB homolog 5 RNA demethylase in NSCLC leads to a marked increase in the m⁶A modification of CDC25C mRNA. It was also shown that YTH N6‑methyladenosine RNA binding protein (YTHDF) 3 and YTHDF2 compete to bind to CDC25C mRNA, thereby promoting or inhibiting its expression. Thus, the present study revealed that dysregulated expression of the CDC25C gene in NSCLC is influenced by multifaceted regulatory layers encompassing both transcriptional and post‑transcriptional mechanisms.

N6‑methyladenosine; YTH N6‑methyladenosine RNA binding proteins; alkB homolog 5 RNA demethylase; cytokinesis cyclin 25 homologous protein C; non‑small cell lung cancer.