Ming Wang1, Liang Wang2, Mingyun Zhang3, Xingde Li3, Zhongcheng Zhu3, HaiYan Wang3. 1. Department of Radiation Therapy, Cangzhou Central Hospital, Cangzhou, China. Electronic address: wangmingcz1@163.com. 2. Department of Endoscopic Professional, Cangzhou Central Hospital, Cangzhou, China. 3. Department of Radiation Therapy, Cangzhou Central Hospital, Cangzhou, China.
Abstract
BACKGROUND: Dysregulation of microRNA(miRNAs) expression was reported in human esophageal squamous cell carcinoma (ESCC). MiR-214 has been found to acts as a tumor suppressor in some tumors including ESCC. The objective of the study was to investigate the functional effect of miR-214 on the regulation of human ESCC progression. METHODS: The expression levels of miR-214 in 57 paired human ESCC tissues and adjacent normal tissues were examined by qRT-PCR. The capacities of cell proliferation and invasion were determined after up-regulation or down-regulation of miR-214 by performing cell viability assay, colony formation assay and transwell assay. Dual luciferase assays, Western blot analysis and qRT-PCR assay were used to demonstrate the association between CDC25B and miR-214. Western blot analysis assessed relative CDC25B protein expression. RESULTS: We observed that miR-214 expression exhibited a frequent down-regulation in ESCC tissues and cells, compared to adjacent normal tissues and cells, respectively. Furthermore, up-regulation of miR-214 significantly inhibited cell proliferation and colony formation and cell invasion capacities in Eca9706 and Eca109 cells. However, down-regulation of miR-214 exhibited an opposite effects. Dual luciferase assays showed that CDC25B was identified as a direct target of miR-214. Meanwhile, up-regulation of miR-214 decreased CDC25B expression, whereas, down-regulation of miR-214 increased the CDC25B expression in Eca9706 and Eca109 cells. Moreover, we demonstrated that miR-214 inhibited Eca9706 and Eca109 cells proliferation and invasion through CDC25B. CONCLUSION: Our results indicate that miR-214 function as a tumor suppressor and may be potential therapeutic target for ESCC.
BACKGROUND: Dysregulation of microRNA(miRNAs) expression was reported in humanesophageal squamous cell carcinoma (ESCC). MiR-214 has been found to acts as a tumor suppressor in some tumors including ESCC. The objective of the study was to investigate the functional effect of miR-214 on the regulation of human ESCC progression. METHODS: The expression levels of miR-214 in 57 paired human ESCC tissues and adjacent normal tissues were examined by qRT-PCR. The capacities of cell proliferation and invasion were determined after up-regulation or down-regulation of miR-214 by performing cell viability assay, colony formation assay and transwell assay. Dual luciferase assays, Western blot analysis and qRT-PCR assay were used to demonstrate the association between CDC25B and miR-214. Western blot analysis assessed relative CDC25B protein expression. RESULTS: We observed that miR-214 expression exhibited a frequent down-regulation in ESCC tissues and cells, compared to adjacent normal tissues and cells, respectively. Furthermore, up-regulation of miR-214 significantly inhibited cell proliferation and colony formation and cell invasion capacities in Eca9706 and Eca109 cells. However, down-regulation of miR-214 exhibited an opposite effects. Dual luciferase assays showed that CDC25B was identified as a direct target of miR-214. Meanwhile, up-regulation of miR-214 decreased CDC25B expression, whereas, down-regulation of miR-214 increased the CDC25B expression in Eca9706 and Eca109 cells. Moreover, we demonstrated that miR-214 inhibited Eca9706 and Eca109 cells proliferation and invasion through CDC25B. CONCLUSION: Our results indicate that miR-214 function as a tumor suppressor and may be potential therapeutic target for ESCC.