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microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9
MicroRNAs (miRNAs) regulate the progression of human malignancy by targeting oncogenes or tumor suppressors, which are 12 promising targets for cancer treatment. Increasing evidence has suggested the aberrant expression and tumor-suppressive function of miR-1298 in cancers, however, the regulatory m...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7729294/ https://www.ncbi.nlm.nih.gov/pubmed/33146718 http://dx.doi.org/10.1042/BSR20201215 |
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author | Chen, Weili Lu, Qing Li, Siyu Zhang, Xinyue Xue, Xiaohong |
author_facet | Chen, Weili Lu, Qing Li, Siyu Zhang, Xinyue Xue, Xiaohong |
author_sort | Chen, Weili |
collection | PubMed |
description | MicroRNAs (miRNAs) regulate the progression of human malignancy by targeting oncogenes or tumor suppressors, which are 12 promising targets for cancer treatment. Increasing evidence has suggested the aberrant expression and tumor-suppressive function of miR-1298 in cancers, however, the regulatory mechanism of miR-1298 in breast cancer (BC) remains unclear. Here, our findings showed that miR-1298 was down-regulated in BC tissues and cell lines. Lower level of miR-1298 was significantly correlated with the advanced progression of BC patients. Experimental study showed that overexpression of miR-1298 inhibited the proliferation, induced apoptosis and cell cycle arrest in BC cells. The in vivo xenograft mice model showed that highly expressed miR-1298 significantly reduced the tumor growth and metastasis. Further mechanism analysis revealed that miR-1298 bound the 3′-untranslated region (UTR) of a disintegrin and metalloproteinase 9 domain (ADAM9) and suppressed the expression of ADAM9 in BC cells. ADAM9 was overexpressed in BC tissues and inversely correlated with miR-1298. Down-regulation of ADAM9 induced apoptosis and cell cycle arrest of BC cells. Moreover, ectopic expression of ADAM9 by transiently transfecting with vector encoding the full coding sequence of ADAM9 attenuated the inhibitory effects of miR-1298 on the proliferation and cell cycle progression of BC cells. Collectively, our results illustrated that miR-1298 played a suppressive role in regulating the phenotype of BC cells through directly repressing ADAM9, suggesting the potential application of miR-1298 in the therapy of BC. |
format | Online Article Text |
id | pubmed-7729294 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-77292942020-12-17 microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 Chen, Weili Lu, Qing Li, Siyu Zhang, Xinyue Xue, Xiaohong Biosci Rep Cancer MicroRNAs (miRNAs) regulate the progression of human malignancy by targeting oncogenes or tumor suppressors, which are 12 promising targets for cancer treatment. Increasing evidence has suggested the aberrant expression and tumor-suppressive function of miR-1298 in cancers, however, the regulatory mechanism of miR-1298 in breast cancer (BC) remains unclear. Here, our findings showed that miR-1298 was down-regulated in BC tissues and cell lines. Lower level of miR-1298 was significantly correlated with the advanced progression of BC patients. Experimental study showed that overexpression of miR-1298 inhibited the proliferation, induced apoptosis and cell cycle arrest in BC cells. The in vivo xenograft mice model showed that highly expressed miR-1298 significantly reduced the tumor growth and metastasis. Further mechanism analysis revealed that miR-1298 bound the 3′-untranslated region (UTR) of a disintegrin and metalloproteinase 9 domain (ADAM9) and suppressed the expression of ADAM9 in BC cells. ADAM9 was overexpressed in BC tissues and inversely correlated with miR-1298. Down-regulation of ADAM9 induced apoptosis and cell cycle arrest of BC cells. Moreover, ectopic expression of ADAM9 by transiently transfecting with vector encoding the full coding sequence of ADAM9 attenuated the inhibitory effects of miR-1298 on the proliferation and cell cycle progression of BC cells. Collectively, our results illustrated that miR-1298 played a suppressive role in regulating the phenotype of BC cells through directly repressing ADAM9, suggesting the potential application of miR-1298 in the therapy of BC. Portland Press Ltd. 2020-12-10 /pmc/articles/PMC7729294/ /pubmed/33146718 http://dx.doi.org/10.1042/BSR20201215 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the . |
spellingShingle | Cancer Chen, Weili Lu, Qing Li, Siyu Zhang, Xinyue Xue, Xiaohong microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 |
title | microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 |
title_full | microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 |
title_fullStr | microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 |
title_full_unstemmed | microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 |
title_short | microRNA-1298 inhibits the malignant behaviors of breast cancer cells via targeting ADAM9 |
title_sort | microrna-1298 inhibits the malignant behaviors of breast cancer cells via targeting adam9 |
topic | Cancer |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7729294/ https://www.ncbi.nlm.nih.gov/pubmed/33146718 http://dx.doi.org/10.1042/BSR20201215 |
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