Circular RNA hsa_circ_0002024 suppresses cell proliferation, migration, and invasion in bladder cancer by sponging miR-197-3p
Circular RNA hsa_circ_0002024 has been reported to be underexpressed in bladder cancer (BC). However, the biological role of hsa_circ_0002024 in BC and its underlying molecular mechanisms remain unclear. In this study, the expression levels of hsa_circ_0002024 and miR-197-3p were examined by quantit...
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Published in | American journal of translational research Vol. 11; no. 3; pp. 1644 - 1652 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
e-Century Publishing Corporation
01.01.2019
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Subjects | |
Online Access | Get full text |
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Summary: | Circular RNA hsa_circ_0002024 has been reported to be underexpressed in bladder cancer (BC). However, the biological role of hsa_circ_0002024 in BC and its underlying molecular mechanisms remain unclear. In this study, the expression levels of hsa_circ_0002024 and miR-197-3p were examined by quantitative real-time polymerase chain reaction. The proliferation abilities of EJ and T24 cells were assessed by Cell Counting Kit-8 and 5-ethynyl-20-deoxyuridine assays. Cell migration and invasion were evaluated by transwell migration and invasion assays. Luciferase reporter assay and rescue experiments were conducted to elucidate the underlying mechanism of hsa_circ_0002024. We found that the expression of hsa_circ_0002024 was downregulated, but that of miR-197-3p was upregulated in BC tissues and cell lines. Upregulation of hsa_circ_0002024 suppressed the proliferation, migration, and invasion of EJ and T24 cells. Hsa_circ_0002024 was confirmed as a direct target of miR-197-3p. In addition, we found that restoration of miR-197-3p expression could abolish hsa_circ_0002024-mediated inhibition of BC cell proliferation, migration, and invasion. In conclusion, our data demonstrated that hsa_circ_0002024 suppresses cell proliferation, migration, and invasion in BC by sponging miR-197-3p. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1943-8141 1943-8141 |