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MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12

Cervical cancer is the second most common type of cancer among women worldwide and a leading cause of mortality in women. Metastases reduce the overall survival rate in patients with cervical cancer. Thus, it is clinically urgent to investigate the molecular mechanism of cervical cancer metastasis....

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Detalles Bibliográficos
Autores principales: Tan, Dongmei, Zhou, Chao, Han, Sai, Hou, Xuetao, Kang, Shufang, Zhang, Youzhong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928611/
https://www.ncbi.nlm.nih.gov/pubmed/29488616
http://dx.doi.org/10.3892/mmr.2018.8645
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author Tan, Dongmei
Zhou, Chao
Han, Sai
Hou, Xuetao
Kang, Shufang
Zhang, Youzhong
author_facet Tan, Dongmei
Zhou, Chao
Han, Sai
Hou, Xuetao
Kang, Shufang
Zhang, Youzhong
author_sort Tan, Dongmei
collection PubMed
description Cervical cancer is the second most common type of cancer among women worldwide and a leading cause of mortality in women. Metastases reduce the overall survival rate in patients with cervical cancer. Thus, it is clinically urgent to investigate the molecular mechanism of cervical cancer metastasis. The aim of the present study was to investigate the mechanism of microRNA (miR)-378 in the metastasis of cervical cancer. In the present study, miR-378 expression levels were significantly upregulated in cervical cancer tissues and cervical intraepithelial neoplasia III tissues when compared with normal cervix tissues. Re-expression of miR-378 significantly promoted tumor migration and invasion in vitro, and metastasis in vivo, while downregulation of miR-378 suppressed the effect in vitro. Luciferase reporter assay revealed that autophagy-related protein 12 (ATG12) was a direct target of miR-378 and its expression was downregulated by miR-378. In cervical cancer tissues with lymph node metastasis, miR-378 was upregulated while ATG12 was downregulated when compared with lymph node negative cases. To the best of our knowledge, the present study is the first to provide evidence that miR-378 may be associated with ATG12. Collectively, the data of the present study suggested that miR-378 may function as an oncogene by promoting metastasis in cervical cancer. The finding that miR-378 targets ATG12 indicated that miR-378 may have a potential role in autophagy. These findings may provide novel insights into the mechanism of metastasis in cervical cancer and a novel therapeutic target for the treatment of cervical cancer.
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spelling pubmed-59286112018-05-07 MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12 Tan, Dongmei Zhou, Chao Han, Sai Hou, Xuetao Kang, Shufang Zhang, Youzhong Mol Med Rep Articles Cervical cancer is the second most common type of cancer among women worldwide and a leading cause of mortality in women. Metastases reduce the overall survival rate in patients with cervical cancer. Thus, it is clinically urgent to investigate the molecular mechanism of cervical cancer metastasis. The aim of the present study was to investigate the mechanism of microRNA (miR)-378 in the metastasis of cervical cancer. In the present study, miR-378 expression levels were significantly upregulated in cervical cancer tissues and cervical intraepithelial neoplasia III tissues when compared with normal cervix tissues. Re-expression of miR-378 significantly promoted tumor migration and invasion in vitro, and metastasis in vivo, while downregulation of miR-378 suppressed the effect in vitro. Luciferase reporter assay revealed that autophagy-related protein 12 (ATG12) was a direct target of miR-378 and its expression was downregulated by miR-378. In cervical cancer tissues with lymph node metastasis, miR-378 was upregulated while ATG12 was downregulated when compared with lymph node negative cases. To the best of our knowledge, the present study is the first to provide evidence that miR-378 may be associated with ATG12. Collectively, the data of the present study suggested that miR-378 may function as an oncogene by promoting metastasis in cervical cancer. The finding that miR-378 targets ATG12 indicated that miR-378 may have a potential role in autophagy. These findings may provide novel insights into the mechanism of metastasis in cervical cancer and a novel therapeutic target for the treatment of cervical cancer. D.A. Spandidos 2018-05 2018-02-27 /pmc/articles/PMC5928611/ /pubmed/29488616 http://dx.doi.org/10.3892/mmr.2018.8645 Text en Copyright: © Tan 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
Tan, Dongmei
Zhou, Chao
Han, Sai
Hou, Xuetao
Kang, Shufang
Zhang, Youzhong
MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
title MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
title_full MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
title_fullStr MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
title_full_unstemmed MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
title_short MicroRNA-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
title_sort microrna-378 enhances migration and invasion in cervical cancer by directly targeting autophagy-related protein 12
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928611/
https://www.ncbi.nlm.nih.gov/pubmed/29488616
http://dx.doi.org/10.3892/mmr.2018.8645
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