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Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway
PURPOSE: Circular RNA_0101692 (circ_0101692) is overexpressed in clear cell renal cell carcinoma (ccRCC) by microarray analyses. However, its function and action mechanism in ccRCC tumorigenesis is still elusive. METHODS: Western blotting and qRT-PCR were executed to assess the circ_0101692, miR-384...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Neoplasia Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9813697/ https://www.ncbi.nlm.nih.gov/pubmed/36608542 http://dx.doi.org/10.1016/j.tranon.2022.101612 |
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author | Zhang, Huan Ma, Ming |
author_facet | Zhang, Huan Ma, Ming |
author_sort | Zhang, Huan |
collection | PubMed |
description | PURPOSE: Circular RNA_0101692 (circ_0101692) is overexpressed in clear cell renal cell carcinoma (ccRCC) by microarray analyses. However, its function and action mechanism in ccRCC tumorigenesis is still elusive. METHODS: Western blotting and qRT-PCR were executed to assess the circ_0101692, miR-384 and FN1 expression in ccRCC cells and tissues. Target relationships among them were determined via dual luciferase reporter and/or RNA immunoprecipitation assays. Cell proliferation was evaluated by CCK-8 assay. Caspase-3 activity assay was utilized to analyze cell apoptosis. To find out whether ccRCC cells might migrate, a transwell assay was performed. To assess the effects of circ_0101692 on tumor development in vivo, a mouse xenograft model was used. RESULTS: High expression of circ_0101692 and FN1, and decreased miR-384 were determined in ccRCC. Cell growth, migration and viability were decreased whereas cell apoptosis was stimulated when circ_0101692 was knockdown. miR-384 inhibitor transfection attenuated the inhibiting impacts of circ_0101692 silencing on ccRCC cell progression. FN1 deletion further inverted the cancer-promoting effect of miR-384 downregulation on cell viability and migration. In addition, circ_0101692 could sponge miR-384 to relieve the inhibition of miR-384 on FN1 in ccRCC. CONCLUSIONS: Circ_0101692 targeted miR-384/FN1 axis to facilitate cell proliferation, migration and repress apoptosis, thereby accelerating the development of ccRCC. This points out that circ_0101692/miR-384/FN1 axis might be a prospective target implemented for the future treatment of ccRCC. |
format | Online Article Text |
id | pubmed-9813697 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Neoplasia Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-98136972023-01-09 Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway Zhang, Huan Ma, Ming Transl Oncol Original Research PURPOSE: Circular RNA_0101692 (circ_0101692) is overexpressed in clear cell renal cell carcinoma (ccRCC) by microarray analyses. However, its function and action mechanism in ccRCC tumorigenesis is still elusive. METHODS: Western blotting and qRT-PCR were executed to assess the circ_0101692, miR-384 and FN1 expression in ccRCC cells and tissues. Target relationships among them were determined via dual luciferase reporter and/or RNA immunoprecipitation assays. Cell proliferation was evaluated by CCK-8 assay. Caspase-3 activity assay was utilized to analyze cell apoptosis. To find out whether ccRCC cells might migrate, a transwell assay was performed. To assess the effects of circ_0101692 on tumor development in vivo, a mouse xenograft model was used. RESULTS: High expression of circ_0101692 and FN1, and decreased miR-384 were determined in ccRCC. Cell growth, migration and viability were decreased whereas cell apoptosis was stimulated when circ_0101692 was knockdown. miR-384 inhibitor transfection attenuated the inhibiting impacts of circ_0101692 silencing on ccRCC cell progression. FN1 deletion further inverted the cancer-promoting effect of miR-384 downregulation on cell viability and migration. In addition, circ_0101692 could sponge miR-384 to relieve the inhibition of miR-384 on FN1 in ccRCC. CONCLUSIONS: Circ_0101692 targeted miR-384/FN1 axis to facilitate cell proliferation, migration and repress apoptosis, thereby accelerating the development of ccRCC. This points out that circ_0101692/miR-384/FN1 axis might be a prospective target implemented for the future treatment of ccRCC. Neoplasia Press 2023-01-04 /pmc/articles/PMC9813697/ /pubmed/36608542 http://dx.doi.org/10.1016/j.tranon.2022.101612 Text en © 2023 Published by Elsevier Inc. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Original Research Zhang, Huan Ma, Ming Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway |
title | Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway |
title_full | Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway |
title_fullStr | Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway |
title_full_unstemmed | Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway |
title_short | Circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through miR-384/FN1 pathway |
title_sort | circ_0101692 knockdown retards the development of clear cell renal cell carcinoma through mir-384/fn1 pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9813697/ https://www.ncbi.nlm.nih.gov/pubmed/36608542 http://dx.doi.org/10.1016/j.tranon.2022.101612 |
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