MicroRNA-148a-3p suppresses cell proliferation and migration of esophageal carcinoma by targeting CEP55
This study evaluated microRNA-148a-3p in esophageal carcinoma cells. The prediction of bioinformatics analysis revealed that microRNA-148a-3p may target CEP55. qRT-PCR and western blot showed that CEP55 level in esophageal carcinoma cells and tissue was dramatically higher than that of normal cells...
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Published in | Cellular & molecular biology letters Vol. 26; no. 1; p. 54 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
England
BioMed Central
24.12.2021
BMC |
Subjects | |
Online Access | Get full text |
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Summary: | This study evaluated microRNA-148a-3p in esophageal carcinoma cells. The prediction of bioinformatics analysis revealed that microRNA-148a-3p may target CEP55. qRT-PCR and western blot showed that CEP55 level in esophageal carcinoma cells and tissue was dramatically higher than that of normal cells and tissue, while microRNA-148a-3p was the opposite. Forced expression of microRNA-148a-3p restrained cell malignant behaviors of esophageal carcinoma, and repression of microRNA-148a-3p resulted in the converse results in terms of cell function. Dual-luciferase assay confirmed that microRNA-148a-3p targeted CEP55. CEP55 attenuated the suppressive effect of microRNA-148a-3p on proliferation and migration of esophageal carcinoma cells, demonstrating that microRNA-148a-3p regulated function of esophageal carcinoma cells via decreasing CEP55 level. Microscopy observation indicated that cell morphology was also affected by the microRNA-148a-3p/CEP55 axis. Furthermore, western blot analysis revealed that the PI3K/AKT signaling pathway could be suppressed by activating the microRNA-148a-3p/CEP55 axis. Finally, in vivo experiments confirmed the effects of microRNA-148a-3p on tumorigenesis. Thus, microRNA-148a-3p could act as a repressor in esophageal carcinoma via binding to CEP55. |
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Bibliography: | SourceType-Other Sources-1 content type line 63 ObjectType-Correspondence-1 |
ISSN: | 1425-8153 1689-1392 |
DOI: | 10.1186/s11658-021-00298-1 |