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LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis
BACKGROUND: Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of several diseases, especially some kinds of cancer. This study aimed to investigate the expression of MTCP1-AS1 and its effects on endometrial cancer (EC). METHODS: MTCP1-AS1 expression level was determined in human...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868288/ https://www.ncbi.nlm.nih.gov/pubmed/33568915 http://dx.doi.org/10.2147/OTT.S240010 |
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author | Gao, Qin Huang, Qin Li, Fangbing Luo, Fang |
author_facet | Gao, Qin Huang, Qin Li, Fangbing Luo, Fang |
author_sort | Gao, Qin |
collection | PubMed |
description | BACKGROUND: Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of several diseases, especially some kinds of cancer. This study aimed to investigate the expression of MTCP1-AS1 and its effects on endometrial cancer (EC). METHODS: MTCP1-AS1 expression level was determined in human EC tissues and cell lines by qRT-PCR. The role of MTCP1-AS1 on EC cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) was detected by CCK8, wound-healing assay, transwell assay and Western blot, respectively. Moreover, luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were performed to verify the targeting relationship between miR-650, MCTP1-AS1 and SMAD7 in EC cells. RESULTS: Our data showed that MCTP1-AS1 expression was downregulated in EC tissues and cell lines. Overexpression of MCTP1-AS1 inhibited cell proliferation, migration, invasion and EMT process of EC cells. Moreover, MCTP1-AS1 was proved to be the target of miR-650 and reversely correlated with its expression. In addition, MCTP1-AS1 reversed the effect of miR-650 on the EC cells, which might be associated with the role of SMAD7. Moreover, Western blot showed siRNA-SMAD7 transfection could rescue the repressed TGF-β/SMAD pathway induced by MCTP1-AS1 in EC cells. CONCLUSION: Taken together, these data suggested that lncRNA MCTP1-AS1 inhibited cell proliferation, migration, invasion and EMT process of EC cells via targeting the miR-650/SMAD7 axis and it has the potential to be explored as a therapeutic target for the treatment of EC in the future. |
format | Online Article Text |
id | pubmed-7868288 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-78682882021-02-09 LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis Gao, Qin Huang, Qin Li, Fangbing Luo, Fang Onco Targets Ther Original Research BACKGROUND: Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of several diseases, especially some kinds of cancer. This study aimed to investigate the expression of MTCP1-AS1 and its effects on endometrial cancer (EC). METHODS: MTCP1-AS1 expression level was determined in human EC tissues and cell lines by qRT-PCR. The role of MTCP1-AS1 on EC cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) was detected by CCK8, wound-healing assay, transwell assay and Western blot, respectively. Moreover, luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were performed to verify the targeting relationship between miR-650, MCTP1-AS1 and SMAD7 in EC cells. RESULTS: Our data showed that MCTP1-AS1 expression was downregulated in EC tissues and cell lines. Overexpression of MCTP1-AS1 inhibited cell proliferation, migration, invasion and EMT process of EC cells. Moreover, MCTP1-AS1 was proved to be the target of miR-650 and reversely correlated with its expression. In addition, MCTP1-AS1 reversed the effect of miR-650 on the EC cells, which might be associated with the role of SMAD7. Moreover, Western blot showed siRNA-SMAD7 transfection could rescue the repressed TGF-β/SMAD pathway induced by MCTP1-AS1 in EC cells. CONCLUSION: Taken together, these data suggested that lncRNA MCTP1-AS1 inhibited cell proliferation, migration, invasion and EMT process of EC cells via targeting the miR-650/SMAD7 axis and it has the potential to be explored as a therapeutic target for the treatment of EC in the future. Dove 2021-02-03 /pmc/articles/PMC7868288/ /pubmed/33568915 http://dx.doi.org/10.2147/OTT.S240010 Text en © 2021 Gao et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Gao, Qin Huang, Qin Li, Fangbing Luo, Fang LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis |
title | LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis |
title_full | LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis |
title_fullStr | LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis |
title_full_unstemmed | LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis |
title_short | LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis |
title_sort | lncrna mctp1-as1 regulates emt process in endometrial cancer by targeting the mir-650/smad7 axis |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7868288/ https://www.ncbi.nlm.nih.gov/pubmed/33568915 http://dx.doi.org/10.2147/OTT.S240010 |
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