Effects of miR-138-5p and miR-204-5p on the migration and proliferation of gastric cancer cells by targeting EGFR

GC (gastric cancer) remains one of the most lethal malignancies worldwide. EGFR (epidermal growth factor receptor) plays an important role in the malignant process of GC, therefore, the present study addressed the relationship between EGFR and its potential regulators and examined their regulatory mechanisms in GC. We examined differences in the expression levels of EGFR in GC and adjacent non-cancerous tissues. Bioinformatics analyses and dual luciferase reporter assays were used to confirm the putative relationship between miR-138 or miR-204 and EGFR, and their relationship was further detected using western blotting, RT-PCR, and a series of cell studies. EGFR proteins were abundantly expressed in GC tissues, however EGFR mRNA levels remained indistinctive. Consequently, EGFR was revealed as a putative target of miR-138 and miR-204 which bound to the 3′UTR of EGFR mRNA. Further analysis revealed that miR-138 and miR-204 were significantly downregulated in GC tissues and the overexpression of miR-138 and miR-204 in GC cell lines resulted in the significant inhibition of EGFR protein levels and GC cell proliferation and metastasis. Rescue experiments confirmed that the roles of the two microRNAs were specific to EGFR. EGFR is a pivotal oncogene in GC progression that may be regulated by miR-138 and miR-204.