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As esophageal squamous cell carcinoma (ESCC) is one of the most frequently diagnosed cancers in Asia, it is crucial to uncover its underlying molecular mechanisms that support its development and progression. Several articles have reported that microRNA (miR)‑485‑5p inhibits the malignant phenotype in a number of cancer types, such as lung, gastric and breast cancer, but to the best of our knowledge, its function in ESCC has not been studied in depth until the present study. It is of great significance to probe the regulatory action and underlying mechanism of miR‑485‑5p in ESCC. In brief, this study identified that miR‑485‑5p expression in ESCC tissues was significantly lower than that in normal tissues. The decrease in miR‑485‑5p expression was associated with a larger tumour size and poor histology and stage. The expression of miR‑485‑5p was relatively high in Eca 109 and TE‑1 cells, but relatively low in KYSE 30. The overexpression of miR‑485‑5p inhibited cell proliferation, migration and invasion in vitro , whereas miR‑485‑5p knockdown did the opposite. Flotillin‑1 (FLOT‑1) can facilitate the malignant phenotype in various cancer types. The present study found that in ESCC tissue, the protein expression of FLOT‑1 was negatively correlated with miR‑485‑5p expression. Further experiments showed that miR‑485‑5p directly targeted the 3'‑untranslated region of FLOT‑1. The overexpression of miR‑485‑5p significantly suppressed the mRNA and protein expression levels of FLOT‑1, whereas knockdown had the reverse effects. Furthermore, overexpression of miR‑485‑5p restrained epithelial‑mesenchymal metastasis (EMT)‑related factors at both the mRNA and protein levels. At the same time, it also inhibited the growth of ESCC and restrained the EMT in vivo . In summary, miR‑485‑5p was found to be an inhibitor of ESCC and may have potential as a novel target candidate for ESCC treatment.

oncology reports

MicroRNA‑485‑5p suppresses the progression of esophageal squamous cell carcinoma by targeting flotillin‑1 and inhibits the epithelial‑mesenchymal transition