MiR-601 inhibits the proliferation and metastasis of esophageal squamous cell carcinoma (ESCC) by targeting HDAC6.

OBJECTIVE: The aim of this study was to explore the role of microRNA-601 (miR-601) in the proliferation and invasion of esophageal squamous cell carcinoma (ESCC) cells, thereby providing new thoughts for prognosis evaluation and targeted therapy of ESCC. PATIENTS AND METHODS: 23 pairs of ESCC tissue samples and adjacent normal tissues were collected. and the expression level of miR-601 was detected. Biological information analysis and Luciferase report gene assay were used to verify the potential target genes of miR-601. Then, three groups were established in ESCC cell line (TE-1) to perform similar experiments, including the miR-NC group, the miR-601 mimics group and the mimics + HDAC6 group. Cell counting kit-8 (CCK-8) assay was used to detect cell proliferation ability. Meanwhile, transwell assay and scratch-wound assay were applied to observe the effect of miR-601 on cell invasion and migration. Quantitative reverse transcription Polymerase Chain Reaction (qPCR) and Western blot assay were applied to determine the mRNA and protein expression changes after transfection. RESULTS: Compared with normal adjacent tissues and normal esophageal epithelial cells, the expression of miR-601 was significantly decreased in ESCC tissues and cells. HDAC6 was identified as a target gene of miR-601. The expression of HDAC6 in esophageal carcinoma cells transfected with miR-601 mimics was significantly down-regulated. The negative correlation between miR-601 and HDAC6 expression was assessed by qPCR and Western blot (WB) assay. Furthermore. miR-601 remarkably suppressed the proliferation of ESCC cells. Meanwhile, cell invasion and migration were also found markedly restricted after transfection of miR-601 mimics. However, the overexpression of HDAC6 significantly counteracted the effects of miR-601. CONCLUSIONS: MiR-601 suppressed the proliferation, invasion and migration of esophagus carcinoma cells by down-regulating HDAC6 expression.