DNA methylation‑regulated miR‑155‑5p depresses sensitivity of esophageal carcinoma cells to radiation and multiple chemotherapeutic drugs via suppression of MAP3K10.

Radiotherapy and chemotherapy are two major treatment options for esophageal carcinoma, and heterogeneous treatment effects are observed in the clinical setting to provide an overall 5‑year survival rate of ~20%. Hence, defining the molecular mechanisms that affect the chemoradiotherapy response is vital to achieve an optimal outcome. The present study revealed that miR‑155‑5p may be involved in esophageal squamous cell carcinoma (ESCC). By means of reverse transcription‑PCR, the present study defined its differential expression pattern in six ESCC cell lines that were associated with resistance to radiation. Ectopic expression of miR‑155‑5p promoted DNA damage repair and induced resistance against radiation by non‑homologous end joining repair. It also enhanced chemoresistance, proliferation, and migration and invasion of ESCC cells. By further screening its potential target genes, the present study identified MAP3K10 as the direct target gene to exert its anti‑chemoradiation functions. The results also demonstrated that its differential expression pattern was negatively regulated by the methylation status of the upstream CpG island. Overall, the results of the present study demonstrated that miR‑155‑5p is a key molecule for understanding the heterogeneous responses of ESCC to chemoradiotherapy, and may be used in personalized treatment plans for this high mortality tumor in the future.