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miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN

Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)-224-5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription-quantitative PCR...

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Autores principales: Peng, Xiaobo, Guo, Chengtao, Wu, Yanjun, Ying, Mingzhen, Chang, Renxu, Song, Lele, Zhan, Lixing, Zhan, Xianbao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974333/
https://www.ncbi.nlm.nih.gov/pubmed/33760113
http://dx.doi.org/10.3892/mmr.2021.11985
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author Peng, Xiaobo
Guo, Chengtao
Wu, Yanjun
Ying, Mingzhen
Chang, Renxu
Song, Lele
Zhan, Lixing
Zhan, Xianbao
author_facet Peng, Xiaobo
Guo, Chengtao
Wu, Yanjun
Ying, Mingzhen
Chang, Renxu
Song, Lele
Zhan, Lixing
Zhan, Xianbao
author_sort Peng, Xiaobo
collection PubMed
description Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)-224-5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription-quantitative PCR was used to explorethe expression of miR-224-5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR-224-5p was assessed and verified by luciferase assay. miR-224-5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR-224-5p promoted the proliferation, migration and invasion of MCC and knockdown of miR-224-5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR-224-5p. The negative correlation between miR-224-5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR-224-5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR-224-5p was highly expressed and served an oncogenic role in MCC. miR-224-5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC.
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spelling pubmed-79743332021-03-24 miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN Peng, Xiaobo Guo, Chengtao Wu, Yanjun Ying, Mingzhen Chang, Renxu Song, Lele Zhan, Lixing Zhan, Xianbao Mol Med Rep Articles Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)-224-5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription-quantitative PCR was used to explorethe expression of miR-224-5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR-224-5p was assessed and verified by luciferase assay. miR-224-5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR-224-5p promoted the proliferation, migration and invasion of MCC and knockdown of miR-224-5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR-224-5p. The negative correlation between miR-224-5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR-224-5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR-224-5p was highly expressed and served an oncogenic role in MCC. miR-224-5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC. D.A. Spandidos 2021-05 2021-03-10 /pmc/articles/PMC7974333/ /pubmed/33760113 http://dx.doi.org/10.3892/mmr.2021.11985 Text en Copyright: © Peng 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
Peng, Xiaobo
Guo, Chengtao
Wu, Yanjun
Ying, Mingzhen
Chang, Renxu
Song, Lele
Zhan, Lixing
Zhan, Xianbao
miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN
title miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN
title_full miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN
title_fullStr miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN
title_full_unstemmed miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN
title_short miR-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN
title_sort mir-224-5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting pten
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7974333/
https://www.ncbi.nlm.nih.gov/pubmed/33760113
http://dx.doi.org/10.3892/mmr.2021.11985
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