Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 531, Issue 4, Pages 615-621Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2020.07.037
Keywords
Esophageal cancer; miR-483-5p; KCNQ1; Proliferation; Migration; Invasion
Categories
Funding
- Zhejiang Medical Association Clinical Research Fund Project [20192YC-A68]
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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 30-untranslational region of KCNQ1. Over-expressing miR-483-5p suppressed KCNQ1 expression. Besides, miR-483-5p overexpression 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. (C) 2020 Elsevier Inc. All rights reserved.
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