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Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53

Background: Epithelial–mesenchymal transition (EMT), a phenotypic conversion of the epithelial to mesenchymal state, contributes to cancer progression. Currently, several microRNAs (miRNAs) are associated with EMT-mediated cancer progression, but the contribution of miR-34a to EMT in cancer cells re...

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Autores principales: Kawami, Masashi, Takenaka, Shinnosuke, Akai, Mizuki, Yumoto, Ryoko, Takano, Mikihisa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8699678/
https://www.ncbi.nlm.nih.gov/pubmed/34944497
http://dx.doi.org/10.3390/biom11121853
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author Kawami, Masashi
Takenaka, Shinnosuke
Akai, Mizuki
Yumoto, Ryoko
Takano, Mikihisa
author_facet Kawami, Masashi
Takenaka, Shinnosuke
Akai, Mizuki
Yumoto, Ryoko
Takano, Mikihisa
author_sort Kawami, Masashi
collection PubMed
description Background: Epithelial–mesenchymal transition (EMT), a phenotypic conversion of the epithelial to mesenchymal state, contributes to cancer progression. Currently, several microRNAs (miRNAs) are associated with EMT-mediated cancer progression, but the contribution of miR-34a to EMT in cancer cells remains controversial. The present study aimed to clarify the role of miR-34a in the EMT-related phenotypes of human non-small cell lung cancer (NSCLC) cell lines, A549 (p53 wild-type) and H1299 (p53-deficient). Methods: The miR-34a mimic and p53 small interfering RNA (siRNA) were transfected into the cells using Lipofectamine, and the obtained total RNA and cell lysates were used for real-time polymerase chain reaction and Western blotting analysis, respectively. Results: The introduction of the miR-34a mimic led to an increase in the mRNA and protein expression levels of α-smooth muscle actin (α-SMA), a mesenchymal marker gene, in A549, but not in H1299 cells. Additionally, miR-34a-induced the upregulation of p53 activity and migration was observed in A549, but not in H1299 cells. However, under the p53-knockdown condition, only α-SMA upregulation by miR-34a was abolished. Conclusion: These findings indicate a close relationship between p53 and miR-34a-induced EMT in p53-wild type NSCLC cells, which provides novel insights about the role of miR-34a in EMT-like phenotypic changes in NSCLC.
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spelling pubmed-86996782021-12-24 Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53 Kawami, Masashi Takenaka, Shinnosuke Akai, Mizuki Yumoto, Ryoko Takano, Mikihisa Biomolecules Article Background: Epithelial–mesenchymal transition (EMT), a phenotypic conversion of the epithelial to mesenchymal state, contributes to cancer progression. Currently, several microRNAs (miRNAs) are associated with EMT-mediated cancer progression, but the contribution of miR-34a to EMT in cancer cells remains controversial. The present study aimed to clarify the role of miR-34a in the EMT-related phenotypes of human non-small cell lung cancer (NSCLC) cell lines, A549 (p53 wild-type) and H1299 (p53-deficient). Methods: The miR-34a mimic and p53 small interfering RNA (siRNA) were transfected into the cells using Lipofectamine, and the obtained total RNA and cell lysates were used for real-time polymerase chain reaction and Western blotting analysis, respectively. Results: The introduction of the miR-34a mimic led to an increase in the mRNA and protein expression levels of α-smooth muscle actin (α-SMA), a mesenchymal marker gene, in A549, but not in H1299 cells. Additionally, miR-34a-induced the upregulation of p53 activity and migration was observed in A549, but not in H1299 cells. However, under the p53-knockdown condition, only α-SMA upregulation by miR-34a was abolished. Conclusion: These findings indicate a close relationship between p53 and miR-34a-induced EMT in p53-wild type NSCLC cells, which provides novel insights about the role of miR-34a in EMT-like phenotypic changes in NSCLC. MDPI 2021-12-09 /pmc/articles/PMC8699678/ /pubmed/34944497 http://dx.doi.org/10.3390/biom11121853 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kawami, Masashi
Takenaka, Shinnosuke
Akai, Mizuki
Yumoto, Ryoko
Takano, Mikihisa
Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53
title Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53
title_full Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53
title_fullStr Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53
title_full_unstemmed Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53
title_short Characterization of miR-34a-Induced Epithelial–Mesenchymal Transition in Non-Small Lung Cancer Cells Focusing on p53
title_sort characterization of mir-34a-induced epithelial–mesenchymal transition in non-small lung cancer cells focusing on p53
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8699678/
https://www.ncbi.nlm.nih.gov/pubmed/34944497
http://dx.doi.org/10.3390/biom11121853
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