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LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2

SPRY4‐intronic transcript 1 has been found in several kinds of cancers, but the role of SPRY4‐IT1 in breast cancer stem cells has not been studied. We investigated whether SPRY4‐IT1 is involved in the promotion of breast cancer stem cells (BCSCs). We used qRT‐PCR to detect the expression of SPRY4‐IT...

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Autores principales: Song, Xinyue, Zhang, Xiaoxue, Wang, Xinnan, Chen, Lianze, Jiang, Longyang, Zheng, Ang, Zhang, Ming, Zhao, Lin, Wei, Minjie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6933354/
https://www.ncbi.nlm.nih.gov/pubmed/31736268
http://dx.doi.org/10.1111/jcmm.14786
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author Song, Xinyue
Zhang, Xiaoxue
Wang, Xinnan
Chen, Lianze
Jiang, Longyang
Zheng, Ang
Zhang, Ming
Zhao, Lin
Wei, Minjie
author_facet Song, Xinyue
Zhang, Xiaoxue
Wang, Xinnan
Chen, Lianze
Jiang, Longyang
Zheng, Ang
Zhang, Ming
Zhao, Lin
Wei, Minjie
author_sort Song, Xinyue
collection PubMed
description SPRY4‐intronic transcript 1 has been found in several kinds of cancers, but the role of SPRY4‐IT1 in breast cancer stem cells has not been studied. We investigated whether SPRY4‐IT1 is involved in the promotion of breast cancer stem cells (BCSCs). We used qRT‐PCR to detect the expression of SPRY4‐IT1 in MCF‐7 cells and MCF‐7 cancer stem cells (MCF‐7 CSCs). The effects of SPRY4‐IT1 on the proliferation and renewal ability of breast cancer cells were investigated by in vitro and in vivo assays (ie in situ hybridization, colony formation assay, sphere formation assay, flow cytometry assay, western blotting, xenograft model and immunohistochemistry). The mechanism of SPPRY4‐IT1 as a ceRNA was studied by a dual‐luciferase reporter assay and bioinformatic analysis. In our study, SPRY4‐IT1 was up‐regulated in MCF‐7 CSCs compared with MCF‐7 cells, and high SPRY4‐IT1 expression was related to reduced breast cancer patient survival. Furthermore, SPRY4‐IT1 overexpression promoted breast cancer cell proliferation and stemness in vitro and in vivo. In addition, SPRY4‐IT1 knockdown suppressed BCSC renewal ability and stemness maintenance in vivo and in vitro. The dual‐luciferase reporter assays indicated that SPRY4‐IT1 as a sponge for miR‐6882‐3p repressed transcription factor 7‐like 2 (TCF7L2) expression. Taken together, these findings demonstrated that SPRY4‐IT1 promotes proliferation and stemness of breast cancer cells as well as renewal ability and stemness maintenance of BCSCs by increasing the expression of TCF7L2 through targeting miR‐6882‐3p.
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spelling pubmed-69333542020-01-01 LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2 Song, Xinyue Zhang, Xiaoxue Wang, Xinnan Chen, Lianze Jiang, Longyang Zheng, Ang Zhang, Ming Zhao, Lin Wei, Minjie J Cell Mol Med Original Articles SPRY4‐intronic transcript 1 has been found in several kinds of cancers, but the role of SPRY4‐IT1 in breast cancer stem cells has not been studied. We investigated whether SPRY4‐IT1 is involved in the promotion of breast cancer stem cells (BCSCs). We used qRT‐PCR to detect the expression of SPRY4‐IT1 in MCF‐7 cells and MCF‐7 cancer stem cells (MCF‐7 CSCs). The effects of SPRY4‐IT1 on the proliferation and renewal ability of breast cancer cells were investigated by in vitro and in vivo assays (ie in situ hybridization, colony formation assay, sphere formation assay, flow cytometry assay, western blotting, xenograft model and immunohistochemistry). The mechanism of SPPRY4‐IT1 as a ceRNA was studied by a dual‐luciferase reporter assay and bioinformatic analysis. In our study, SPRY4‐IT1 was up‐regulated in MCF‐7 CSCs compared with MCF‐7 cells, and high SPRY4‐IT1 expression was related to reduced breast cancer patient survival. Furthermore, SPRY4‐IT1 overexpression promoted breast cancer cell proliferation and stemness in vitro and in vivo. In addition, SPRY4‐IT1 knockdown suppressed BCSC renewal ability and stemness maintenance in vivo and in vitro. The dual‐luciferase reporter assays indicated that SPRY4‐IT1 as a sponge for miR‐6882‐3p repressed transcription factor 7‐like 2 (TCF7L2) expression. Taken together, these findings demonstrated that SPRY4‐IT1 promotes proliferation and stemness of breast cancer cells as well as renewal ability and stemness maintenance of BCSCs by increasing the expression of TCF7L2 through targeting miR‐6882‐3p. John Wiley and Sons Inc. 2019-11-17 2020-01 /pmc/articles/PMC6933354/ /pubmed/31736268 http://dx.doi.org/10.1111/jcmm.14786 Text en © 2019 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Song, Xinyue
Zhang, Xiaoxue
Wang, Xinnan
Chen, Lianze
Jiang, Longyang
Zheng, Ang
Zhang, Ming
Zhao, Lin
Wei, Minjie
LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2
title LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2
title_full LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2
title_fullStr LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2
title_full_unstemmed LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2
title_short LncRNA SPRY4‐IT1 regulates breast cancer cell stemness through competitively binding miR‐6882‐3p with TCF7L2
title_sort lncrna spry4‐it1 regulates breast cancer cell stemness through competitively binding mir‐6882‐3p with tcf7l2
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6933354/
https://www.ncbi.nlm.nih.gov/pubmed/31736268
http://dx.doi.org/10.1111/jcmm.14786
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