OBJECTIVE: To explore the role and mechanism of microRNA185 (miR-185) on proliferation, migration and invasion of esophageal squamous cell carcinoma (ESCC). METHODS: Samples were obtained from 23 ESCC patients undergoing surgery whose were confirmed by pathological diagnosis of esophageal carcinoma from 2002 to 2012,at Department of Thoracic Surgery,Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College. Real-time PCR was used to measure the expression of miR-185. The xCELLigence RTCA MP system and Transwell assay were performed to detect the effect of miR-185 on proliferation, migration and invasion of ESCC respectively. After transfecting of miR-185 mimic into KYSE150, the expression of Six1's downstream gene cyclin A1 was evaluated by real-time PCR. After transfection of miR-185 inhibitor into KYSE30, the expression of E-cadherin, a downstream protein of Six1, was observed under confocal microscope. RESULTS: The expression level of miR-185 was down-regulated in ESCC compared with adjacent normal tissue (0.006 vs 0.039,P = 0.016). After transfection of miR-185 mimic, miR-185 significantly inhibited proliferation, migration and invasion of ESCC.Transwell assay showed, in comparison with the control group, the number of KYSE150 metastatic and invasive cells was respectively decreased(146 ± 15 vs 64 ± 11, 110 ± 12 vs 67 ± 5, both P < 0.05). And the expression level of cyclin A1 decreased. After transfection of miR-185 inhibitor,the expression level of E-cadherin decreased. CONCLUSION: miR-185 may inhibit proliferation, migration and invasion of ESCC through its target gene Six1.
OBJECTIVE: To explore the role and mechanism of microRNA185 (miR-185) on proliferation, migration and invasion of esophageal squamous cell carcinoma (ESCC). METHODS: Samples were obtained from 23 ESCC patients undergoing surgery whose were confirmed by pathological diagnosis of esophageal carcinoma from 2002 to 2012,at Department of Thoracic Surgery,Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College. Real-time PCR was used to measure the expression of miR-185. The xCELLigence RTCA MP system and Transwell assay were performed to detect the effect of miR-185 on proliferation, migration and invasion of ESCC respectively. After transfecting of miR-185 mimic into KYSE150, the expression of Six1's downstream gene cyclin A1 was evaluated by real-time PCR. After transfection of miR-185 inhibitor into KYSE30, the expression of E-cadherin, a downstream protein of Six1, was observed under confocal microscope. RESULTS: The expression level of miR-185 was down-regulated in ESCC compared with adjacent normal tissue (0.006 vs 0.039,P = 0.016). After transfection of miR-185 mimic, miR-185 significantly inhibited proliferation, migration and invasion of ESCC.Transwell assay showed, in comparison with the control group, the number of KYSE150 metastatic and invasive cells was respectively decreased(146 ± 15 vs 64 ± 11, 110 ± 12 vs 67 ± 5, both P < 0.05). And the expression level of cyclin A1 decreased. After transfection of miR-185 inhibitor,the expression level of E-cadherin decreased. CONCLUSION:miR-185 may inhibit proliferation, migration and invasion of ESCC through its target gene Six1.