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Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells

OBJECTIVE: To explore the related influencing mechanism of miR-384 and miR-134-5p acting on Yin Yang 1 (YY1) signaling transduction on the biological function of gastric cancer (GC) cells. METHODS: miR-384, miR-134-5p and YY1 levels in human GC cell lines KATO III, MKN-45, SNU-1 and normal gastric c...

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Autores principales: Zhong, Bing-Zheng, Wang, Qiang, Liu, Feng, He, Jia-Li, Xiong, Yi, Cao, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7534049/
https://www.ncbi.nlm.nih.gov/pubmed/33061445
http://dx.doi.org/10.2147/OTT.S259988
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author Zhong, Bing-Zheng
Wang, Qiang
Liu, Feng
He, Jia-Li
Xiong, Yi
Cao, Jie
author_facet Zhong, Bing-Zheng
Wang, Qiang
Liu, Feng
He, Jia-Li
Xiong, Yi
Cao, Jie
author_sort Zhong, Bing-Zheng
collection PubMed
description OBJECTIVE: To explore the related influencing mechanism of miR-384 and miR-134-5p acting on Yin Yang 1 (YY1) signaling transduction on the biological function of gastric cancer (GC) cells. METHODS: miR-384, miR-134-5p and YY1 levels in human GC cell lines KATO III, MKN-45, SNU-1 and normal gastric cell line GES-1 were measured by polymerase chain reaction (PCR). Dual luciferase reporter (DLR) gene assay and Western blot (WB) were employed for correlation analysis between miR-384, miR-134-5p and YY1. miR-384-inhibitor, miR-384-mimics, empty plasmid (miRNA-NC) and sh-YY1 were transfected into KATO III cells. Cell proliferation was determined by 3-(4,5-Dimethylthiazolyl-2)-2,5-Diphenyl Tetrazolium Bromide (MTT), cell invasion was measured by Transwell, and apoptosis was analyzed by flow cytometry (FC). RESULTS: In KATO III, MKN-45 and SNU-1 cell lines, YY1 was upregulated while miR-384 and miR-134-5p were downregulated (P<0.001). The expression of miR-134-5p in the miR-134-5p-inhibitor group was significantly lower (P<0.001), while that in the miR-134-5p-mimics group was significantly higher (P<0.001). The expression of miR-384 in the miR-384-inhibitor group was significantly lower (P<0.001), and that in the miR-384-mimics group was significantly higher as compared to the NC group (P<0.001). Both miR-384 and miR-134-5p overexpression could inhibit cell proliferation and invasion, and promote apoptosis. As detected by WB, overexpressed miR-384 and miR-134-5p inhibited the expression of EMT-related molecular markers. Compared with sh-YY1, the number of cells in S phase decreased, the pro-apoptotic proteins boosted statistically, and the anti-apoptotic proteins declined notably after transfecting miR-134-5p-mimics/sh-YY1 or miR-384-mimics/sh-YY1 (P<0.05). The tumor growth rate of nude mice in miR-134-5p/sh-YY1 and miR-384/sh-YY1 groups were significantly lower than those in sh-YY1 group (all P<0.001). CONCLUSION: By targeting YY1 signaling transduction, miR-134-5p and miR-384 can alter the growth and apoptosis of GC cells, which are promising targets for new therapeutics of GC.
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spelling pubmed-75340492020-10-14 Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells Zhong, Bing-Zheng Wang, Qiang Liu, Feng He, Jia-Li Xiong, Yi Cao, Jie Onco Targets Ther Original Research OBJECTIVE: To explore the related influencing mechanism of miR-384 and miR-134-5p acting on Yin Yang 1 (YY1) signaling transduction on the biological function of gastric cancer (GC) cells. METHODS: miR-384, miR-134-5p and YY1 levels in human GC cell lines KATO III, MKN-45, SNU-1 and normal gastric cell line GES-1 were measured by polymerase chain reaction (PCR). Dual luciferase reporter (DLR) gene assay and Western blot (WB) were employed for correlation analysis between miR-384, miR-134-5p and YY1. miR-384-inhibitor, miR-384-mimics, empty plasmid (miRNA-NC) and sh-YY1 were transfected into KATO III cells. Cell proliferation was determined by 3-(4,5-Dimethylthiazolyl-2)-2,5-Diphenyl Tetrazolium Bromide (MTT), cell invasion was measured by Transwell, and apoptosis was analyzed by flow cytometry (FC). RESULTS: In KATO III, MKN-45 and SNU-1 cell lines, YY1 was upregulated while miR-384 and miR-134-5p were downregulated (P<0.001). The expression of miR-134-5p in the miR-134-5p-inhibitor group was significantly lower (P<0.001), while that in the miR-134-5p-mimics group was significantly higher (P<0.001). The expression of miR-384 in the miR-384-inhibitor group was significantly lower (P<0.001), and that in the miR-384-mimics group was significantly higher as compared to the NC group (P<0.001). Both miR-384 and miR-134-5p overexpression could inhibit cell proliferation and invasion, and promote apoptosis. As detected by WB, overexpressed miR-384 and miR-134-5p inhibited the expression of EMT-related molecular markers. Compared with sh-YY1, the number of cells in S phase decreased, the pro-apoptotic proteins boosted statistically, and the anti-apoptotic proteins declined notably after transfecting miR-134-5p-mimics/sh-YY1 or miR-384-mimics/sh-YY1 (P<0.05). The tumor growth rate of nude mice in miR-134-5p/sh-YY1 and miR-384/sh-YY1 groups were significantly lower than those in sh-YY1 group (all P<0.001). CONCLUSION: By targeting YY1 signaling transduction, miR-134-5p and miR-384 can alter the growth and apoptosis of GC cells, which are promising targets for new therapeutics of GC. Dove 2020-09-29 /pmc/articles/PMC7534049/ /pubmed/33061445 http://dx.doi.org/10.2147/OTT.S259988 Text en © 2020 Zhong 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
Zhong, Bing-Zheng
Wang, Qiang
Liu, Feng
He, Jia-Li
Xiong, Yi
Cao, Jie
Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells
title Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells
title_full Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells
title_fullStr Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells
title_full_unstemmed Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells
title_short Effects of miR-384 and miR-134-5p Acting on YY1 Signaling Transduction on Biological Function of Gastric Cancer Cells
title_sort effects of mir-384 and mir-134-5p acting on yy1 signaling transduction on biological function of gastric cancer cells
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7534049/
https://www.ncbi.nlm.nih.gov/pubmed/33061445
http://dx.doi.org/10.2147/OTT.S259988
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