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MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1

MicroRNAs (miRs), which are a class of small non-coding RNAs, are key regulators of gene expression via induction of translational repression or mRNA degradation. However, the molecular mechanism of miR-22 underlying the malignant progression of breast cancer, remains to be elucidated. The present s...

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Autores principales: Zou, Quanqing, Tang, Qianli, Pan, Yinhua, Wang, Xuedi, Dong, Xiaofeng, Liang, Zhongxiao, Huang, Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526179/
https://www.ncbi.nlm.nih.gov/pubmed/28781618
http://dx.doi.org/10.3892/etm.2017.4590
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author Zou, Quanqing
Tang, Qianli
Pan, Yinhua
Wang, Xuedi
Dong, Xiaofeng
Liang, Zhongxiao
Huang, Dong
author_facet Zou, Quanqing
Tang, Qianli
Pan, Yinhua
Wang, Xuedi
Dong, Xiaofeng
Liang, Zhongxiao
Huang, Dong
author_sort Zou, Quanqing
collection PubMed
description MicroRNAs (miRs), which are a class of small non-coding RNAs, are key regulators of gene expression via induction of translational repression or mRNA degradation. However, the molecular mechanism of miR-22 underlying the malignant progression of breast cancer, remains to be elucidated. The present study aimed to explore the regulatory mechanism of miR-22 in breast cancer cell growth and metastasis. Reverse transcription-quantitative polymerase chain reaction data revealed that miR-22 was significantly downregulated in breast cancer tissues, compared with adjacent non-tumor tissues. Furthermore, the miR-22 levels were further decreased in stage III–IV, compared with stage I–II breast cancer. In addition, low miR-22 levels were significantly associated with the poor differentiation, metastasis and advanced clinical stages of breast cancer. Sirtuin1 (SIRT1) was demonstrated to act as a direct target gene of miR-22 and its protein expression negatively regulated by miR-22 in the MCF-7 breast cancer cell line. Furthermore, SIRT1 expression levels were significantly upregulated in breast cancer tissues, compared with adjacent non-tumor tissues. SIRT1 levels were observed to be increased in stage III–IV when compared with stage I–II breast cancer. miR-22 overexpression decreased the proliferation, migration and invasion of MCF-7 cells, whereas overexpression of SIRT1 eliminated the suppressive effects of the miR-22 overexpression on the malignant phenotype of MCF-7 cells. The results of the present study therefore suggested that miR-22 demonstrated suppressive effects on breast cancer growth and metastasis via targeting SIRT1, and thus the miR-22/SIRT1 axis may be used as a novel and potential therapeutic target for breast cancer in the future.
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spelling pubmed-55261792017-08-04 MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1 Zou, Quanqing Tang, Qianli Pan, Yinhua Wang, Xuedi Dong, Xiaofeng Liang, Zhongxiao Huang, Dong Exp Ther Med Articles MicroRNAs (miRs), which are a class of small non-coding RNAs, are key regulators of gene expression via induction of translational repression or mRNA degradation. However, the molecular mechanism of miR-22 underlying the malignant progression of breast cancer, remains to be elucidated. The present study aimed to explore the regulatory mechanism of miR-22 in breast cancer cell growth and metastasis. Reverse transcription-quantitative polymerase chain reaction data revealed that miR-22 was significantly downregulated in breast cancer tissues, compared with adjacent non-tumor tissues. Furthermore, the miR-22 levels were further decreased in stage III–IV, compared with stage I–II breast cancer. In addition, low miR-22 levels were significantly associated with the poor differentiation, metastasis and advanced clinical stages of breast cancer. Sirtuin1 (SIRT1) was demonstrated to act as a direct target gene of miR-22 and its protein expression negatively regulated by miR-22 in the MCF-7 breast cancer cell line. Furthermore, SIRT1 expression levels were significantly upregulated in breast cancer tissues, compared with adjacent non-tumor tissues. SIRT1 levels were observed to be increased in stage III–IV when compared with stage I–II breast cancer. miR-22 overexpression decreased the proliferation, migration and invasion of MCF-7 cells, whereas overexpression of SIRT1 eliminated the suppressive effects of the miR-22 overexpression on the malignant phenotype of MCF-7 cells. The results of the present study therefore suggested that miR-22 demonstrated suppressive effects on breast cancer growth and metastasis via targeting SIRT1, and thus the miR-22/SIRT1 axis may be used as a novel and potential therapeutic target for breast cancer in the future. D.A. Spandidos 2017-08 2017-06-13 /pmc/articles/PMC5526179/ /pubmed/28781618 http://dx.doi.org/10.3892/etm.2017.4590 Text en Copyright: © Zou et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zou, Quanqing
Tang, Qianli
Pan, Yinhua
Wang, Xuedi
Dong, Xiaofeng
Liang, Zhongxiao
Huang, Dong
MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1
title MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1
title_full MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1
title_fullStr MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1
title_full_unstemmed MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1
title_short MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1
title_sort microrna-22 inhibits cell growth and metastasis in breast cancer via targeting of sirt1
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5526179/
https://www.ncbi.nlm.nih.gov/pubmed/28781618
http://dx.doi.org/10.3892/etm.2017.4590
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