Yong Chen1, Hanying Wang1, Shuangmei Zhu1, Xiang Lan2. 1. Department of Radiation Oncology, Lishui People's Hospital, China. 2. Department of Radiation Oncology, Lishui People's Hospital, China. Electronic address: LL_XX1978@163.com.
Abstract
OBJECTIVES: miR-483-5p has been reported to be an oncogene of various cancers, but its functional and regulatory mechanisms in esophageal cancer (EC) remain unclear. This study aimed to investigate the functional and molecular mechanisms of miR-483-5p in EC so as to provide a theoretical basis for exploring the therapeutic target for EC. METHODS: miRNA expression profiles were downloaded from the TCGA-ESCA dataset to screen the target miRNA. Real-time quantitative PCR was performed to detect the transcriptional levels of miR-483-5p and KCNQ1 in EC cells. Western blot was conducted to determine the protein expression of KCNQ1. Cell Counting Kit-8 assay was carried out to assess cell proliferation. Transwell assay was performed to evaluate cell migration and invasion. Dual-luciferase reporter assay was conducted to verify the targeting relationship between miR-483-5p and KCNQ1. RESULTS: miR-483-5p was up-regulated in EC cells and could bind to the 3'-untranslational region of KCNQ1. Over-expressing miR-483-5p suppressed KCNQ1 expression. Besides, miR-483-5p over-expression facilitated EC cell proliferation, migration and invasion, while its down-regulation triggered opposite result. Over-expressing miR-483-5p and KCNQ1 simultaneously could weaken the promoting effect of miR-483-5p over-expression on EC cell proliferation, migration and invasion. CONCLUSION: miR-483-5p as an oncogene facilitated EC cell proliferation, migration and invasion by targeted silencing KCNQ1, which is likely to provide a basis for further exploring the molecular mechanism of EC progression.
OBJECTIVES:miR-483-5p has been reported to be an oncogene of various cancers, but its functional and regulatory mechanisms in esophageal cancer (EC) remain unclear. This study aimed to investigate the functional and molecular mechanisms of miR-483-5p in EC so as to provide a theoretical basis for exploring the therapeutic target for EC. METHODS: miRNA expression profiles were downloaded from the TCGA-ESCA dataset to screen the target miRNA. Real-time quantitative PCR was performed to detect the transcriptional levels of miR-483-5p and KCNQ1 in EC cells. Western blot was conducted to determine the protein expression of KCNQ1. Cell Counting Kit-8 assay was carried out to assess cell proliferation. Transwell assay was performed to evaluate cell migration and invasion. Dual-luciferase reporter assay was conducted to verify the targeting relationship between miR-483-5p and KCNQ1. RESULTS:miR-483-5p was up-regulated in EC cells and could bind to the 3'-untranslational region of KCNQ1. Over-expressing miR-483-5p suppressed KCNQ1 expression. Besides, miR-483-5p over-expression facilitated EC cell proliferation, migration and invasion, while its down-regulation triggered opposite result. Over-expressing miR-483-5p and KCNQ1 simultaneously could weaken the promoting effect of miR-483-5p over-expression on EC cell proliferation, migration and invasion. CONCLUSION:miR-483-5p as an oncogene facilitated EC cell proliferation, migration and invasion by targeted silencing KCNQ1, which is likely to provide a basis for further exploring the molecular mechanism of EC progression.