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miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells

PURPOSE: This study was done to investigate the inhibition effects of miR-30a-3p on mitotic arrest deficient 2 like 1 (MAD2L1) expression and the proliferation of gastric cancer cells. PATIENTS AND METHODS: Cluster analysis and the TCGA database were used to screen the key genes highly expressed in...

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Autores principales: Wang, Yu, Wang, Fenghui, He, Jing, Du, Juan, Zhang, Huahua, Shi, Haiyan, Chen, Yani, Wei, Yameng, Xue, Wanjuan, Yan, Jing, Feng, Yun, Gao, Yi, Li, Dan, Han, Jiming, Zhang, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927793/
https://www.ncbi.nlm.nih.gov/pubmed/31908496
http://dx.doi.org/10.2147/OTT.S222854
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author Wang, Yu
Wang, Fenghui
He, Jing
Du, Juan
Zhang, Huahua
Shi, Haiyan
Chen, Yani
Wei, Yameng
Xue, Wanjuan
Yan, Jing
Feng, Yun
Gao, Yi
Li, Dan
Han, Jiming
Zhang, Jing
author_facet Wang, Yu
Wang, Fenghui
He, Jing
Du, Juan
Zhang, Huahua
Shi, Haiyan
Chen, Yani
Wei, Yameng
Xue, Wanjuan
Yan, Jing
Feng, Yun
Gao, Yi
Li, Dan
Han, Jiming
Zhang, Jing
author_sort Wang, Yu
collection PubMed
description PURPOSE: This study was done to investigate the inhibition effects of miR-30a-3p on mitotic arrest deficient 2 like 1 (MAD2L1) expression and the proliferation of gastric cancer cells. PATIENTS AND METHODS: Cluster analysis and the TCGA database were used to screen the key genes highly expressed in gastric cancer. Based on the LinkedOmics website, the correlation between the miR-30a-3p and the cell cycle-related target gene MAD2L1 in gastric cancer was analyzed. The mRNA and protein expression levels were detected with the quantitative real-time PCR and Western blot analysis. The cell proliferation and cell cycle were also detected and analyzed. RESULTS: Bioinformatics analysis showed that MAD2L1 was highly expressed in tumor tissues compared with normal tissues. Compared with normal tissues, the miR-30a-3p was significantly decreased in the gastric cancer tissues. Moreover, MAD2L1 was significantly negatively correlated with the miR-30a-3p expression. Furthermore, over-expression of miR-30a-3p decreased the expression of MAD2L1 at the protein level, which inhibited the proliferation of AGS and BGC-823 gastric cancer cells. In addition, the cell cycles of AGS and BGC-823 cells were arrested at the G0/G1 phase. CONCLUSION: MAD2L1 is a pro-oncogene which is up-regulated in gastric cancer. The miR-30a-3p can down-regulate the MAD2L1 expression, inhibiting the proliferation of gastric cancer cells and affect the cell cycle.
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spelling pubmed-69277932020-01-06 miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells Wang, Yu Wang, Fenghui He, Jing Du, Juan Zhang, Huahua Shi, Haiyan Chen, Yani Wei, Yameng Xue, Wanjuan Yan, Jing Feng, Yun Gao, Yi Li, Dan Han, Jiming Zhang, Jing Onco Targets Ther Original Research PURPOSE: This study was done to investigate the inhibition effects of miR-30a-3p on mitotic arrest deficient 2 like 1 (MAD2L1) expression and the proliferation of gastric cancer cells. PATIENTS AND METHODS: Cluster analysis and the TCGA database were used to screen the key genes highly expressed in gastric cancer. Based on the LinkedOmics website, the correlation between the miR-30a-3p and the cell cycle-related target gene MAD2L1 in gastric cancer was analyzed. The mRNA and protein expression levels were detected with the quantitative real-time PCR and Western blot analysis. The cell proliferation and cell cycle were also detected and analyzed. RESULTS: Bioinformatics analysis showed that MAD2L1 was highly expressed in tumor tissues compared with normal tissues. Compared with normal tissues, the miR-30a-3p was significantly decreased in the gastric cancer tissues. Moreover, MAD2L1 was significantly negatively correlated with the miR-30a-3p expression. Furthermore, over-expression of miR-30a-3p decreased the expression of MAD2L1 at the protein level, which inhibited the proliferation of AGS and BGC-823 gastric cancer cells. In addition, the cell cycles of AGS and BGC-823 cells were arrested at the G0/G1 phase. CONCLUSION: MAD2L1 is a pro-oncogene which is up-regulated in gastric cancer. The miR-30a-3p can down-regulate the MAD2L1 expression, inhibiting the proliferation of gastric cancer cells and affect the cell cycle. Dove 2019-12-19 /pmc/articles/PMC6927793/ /pubmed/31908496 http://dx.doi.org/10.2147/OTT.S222854 Text en © 2019 Wang 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
Wang, Yu
Wang, Fenghui
He, Jing
Du, Juan
Zhang, Huahua
Shi, Haiyan
Chen, Yani
Wei, Yameng
Xue, Wanjuan
Yan, Jing
Feng, Yun
Gao, Yi
Li, Dan
Han, Jiming
Zhang, Jing
miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells
title miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells
title_full miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells
title_fullStr miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells
title_full_unstemmed miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells
title_short miR-30a-3p Targets MAD2L1 and Regulates Proliferation of Gastric Cancer Cells
title_sort mir-30a-3p targets mad2l1 and regulates proliferation of gastric cancer cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927793/
https://www.ncbi.nlm.nih.gov/pubmed/31908496
http://dx.doi.org/10.2147/OTT.S222854
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