AIM: To identify whether miR-148a-3p interacts with DNA (cytosine-5)-methyltransferase 1 (DNMT1) in esophageal cancer. METHODS: A luciferase assay and immunoblotting were performed to detect the relationship between miR-148a-3p and DNMT1. The MTT method, Annexin V/propidium iodide staining, and Transwell assays were adopted to assess the biological behaviors in EC109 cells. The association between the expression level of miR-148a-3p, clinical features, and prognosis were evaluated by chi-square test and univariate survival analysis. RESULTS: In this study, DNMT1 was identified as a direct target of miR-148a-3p by luciferase assay and Western blot. Real-time quantitative PCR analyses showed that the relative expression levels of miR-148a-3p and DNMT1 were reduced in esophageal cancer samples compared with adjacent tissues; and a negative relationship between both was indicated. Upon overexpression of miR-148a-3p in esophageal cancer cells, proliferation and invasion were significantly suppressed, and apoptosis was promoted. A higher level of miR-148a-3p was correlated with better patient outcomes. CONCLUSIONS: Our study indicated that miR-148a-3p, by targeting DNMT1, likely regulates cell proliferation and invasion in esophageal cancer. miR-148a-3p might also be used prognostically in esophageal cancer and serve as a therapeutic target in the future.
AIM: To identify whether miR-148a-3p interacts with DNA (cytosine-5)-methyltransferase 1 (DNMT1) in esophageal cancer. METHODS: A luciferase assay and immunoblotting were performed to detect the relationship between miR-148a-3p and DNMT1. The MTT method, Annexin V/propidium iodide staining, and Transwell assays were adopted to assess the biological behaviors in EC109 cells. The association between the expression level of miR-148a-3p, clinical features, and prognosis were evaluated by chi-square test and univariate survival analysis. RESULTS: In this study, DNMT1 was identified as a direct target of miR-148a-3p by luciferase assay and Western blot. Real-time quantitative PCR analyses showed that the relative expression levels of miR-148a-3p and DNMT1 were reduced in esophageal cancer samples compared with adjacent tissues; and a negative relationship between both was indicated. Upon overexpression of miR-148a-3p in esophageal cancer cells, proliferation and invasion were significantly suppressed, and apoptosis was promoted. A higher level of miR-148a-3p was correlated with better patient outcomes. CONCLUSIONS: Our study indicated that miR-148a-3p, by targeting DNMT1, likely regulates cell proliferation and invasion in esophageal cancer. miR-148a-3p might also be used prognostically in esophageal cancer and serve as a therapeutic target in the future.