MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR

Background and objective Non-small cell lung cancer (NSCLC) is a kind of lung cancer, because its high incidence has been concerned. Therefore, it has great significance to reveal the pathogenesis of NSCLC. As a transcriptional regulatory factor, MATF-A plays an important role in the development of...

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Main Authors: Kun ZHANG, Yubin ZHOU, Gang FENG, Fuchun ZENG
Format: Article
Language:zho
Published: Chinese Anti-Cancer Association; Chinese Antituberculosis Association 2019-02-01
Series:Chinese Journal of Lung Cancer
Subjects:
Online Access:http://dx.doi.org/10.3779/j.issn.1009-3419.2019.02.02
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author Kun ZHANG
Yubin ZHOU
Gang FENG
Fuchun ZENG
author_facet Kun ZHANG
Yubin ZHOU
Gang FENG
Fuchun ZENG
author_sort Kun ZHANG
collection DOAJ
description Background and objective Non-small cell lung cancer (NSCLC) is a kind of lung cancer, because its high incidence has been concerned. Therefore, it has great significance to reveal the pathogenesis of NSCLC. As a transcriptional regulatory factor, MATF-A plays an important role in the development of multiple tumors, can regulate the migration process of a variety of tumor cells. HOTAIR is a long non-coding RNA (LncRNA) found in recent years, which expresses abnormally in multiple tumors and is involved in the proliferation and migration of multiple tumors. The aim of this study is to explore the role of MRTF-A through HOTAIR to regulate the proliferation and migration of NSCLC cell A549 cell. Methods We constructed the overexpression plasmid and interfering plasmid of MRTF-A, and detected the effect of MRTF-A on the proliferation and migration of A549 cells by CCK8 and wound healing methods respectively. Then, we designed the siRNA of HOTAIR to detect its effect on the proliferation and migration of A549 cells. Through qRT-PCR, we detected the effect of MRTF-A on HOTAIR expression. Finally, we constructed HOTAIR's promoter, and detect the effect of MRTF-A on HOTAIR promoter activity by luciferase reporter gene test. Results Overexpression of MRTF-A promotes the proliferation and migration of A549 cells, while silent MRTF-A inhibits its proliferation and migration. Next, we found that interfered HOTAIR expression inhibited the proliferation of A549 cells. We found that MRTF-A could influence the expression of HOTAIR and regulate the activity of HOTAIR promoter. Conclusion MRTF-A regulates the proliferation and migration of A549 cell through HOTAIR.
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spelling doaj.art-1a341d3426a34985ba9f1481c48f65152022-12-21T23:41:23ZzhoChinese Anti-Cancer Association; Chinese Antituberculosis AssociationChinese Journal of Lung Cancer1009-34191999-61872019-02-01222828910.3779/j.issn.1009-3419.2019.02.02MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIRKun ZHANG0Yubin ZHOU1Gang FENG2Fuchun ZENG3Department of Thoracic Surgery, Sichuan Provincial People's Hospital, Chengdu 610072, ChinaDepartment of Thoracic Surgery, Sichuan Provincial People's Hospital, Chengdu 610072, ChinaDepartment of Thoracic Surgery, Sichuan Provincial People's Hospital, Chengdu 610072, ChinaDepartment of Thoracic Surgery, Sichuan Provincial People's Hospital, Chengdu 610072, ChinaBackground and objective Non-small cell lung cancer (NSCLC) is a kind of lung cancer, because its high incidence has been concerned. Therefore, it has great significance to reveal the pathogenesis of NSCLC. As a transcriptional regulatory factor, MATF-A plays an important role in the development of multiple tumors, can regulate the migration process of a variety of tumor cells. HOTAIR is a long non-coding RNA (LncRNA) found in recent years, which expresses abnormally in multiple tumors and is involved in the proliferation and migration of multiple tumors. The aim of this study is to explore the role of MRTF-A through HOTAIR to regulate the proliferation and migration of NSCLC cell A549 cell. Methods We constructed the overexpression plasmid and interfering plasmid of MRTF-A, and detected the effect of MRTF-A on the proliferation and migration of A549 cells by CCK8 and wound healing methods respectively. Then, we designed the siRNA of HOTAIR to detect its effect on the proliferation and migration of A549 cells. Through qRT-PCR, we detected the effect of MRTF-A on HOTAIR expression. Finally, we constructed HOTAIR's promoter, and detect the effect of MRTF-A on HOTAIR promoter activity by luciferase reporter gene test. Results Overexpression of MRTF-A promotes the proliferation and migration of A549 cells, while silent MRTF-A inhibits its proliferation and migration. Next, we found that interfered HOTAIR expression inhibited the proliferation of A549 cells. We found that MRTF-A could influence the expression of HOTAIR and regulate the activity of HOTAIR promoter. Conclusion MRTF-A regulates the proliferation and migration of A549 cell through HOTAIR.http://dx.doi.org/10.3779/j.issn.1009-3419.2019.02.02Lung neoplasmsA549MRTF-AHOTAIRProliferationMigration
spellingShingle Kun ZHANG
Yubin ZHOU
Gang FENG
Fuchun ZENG
MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR
Chinese Journal of Lung Cancer
Lung neoplasms
A549
MRTF-A
HOTAIR
Proliferation
Migration
title MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR
title_full MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR
title_fullStr MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR
title_full_unstemmed MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR
title_short MRTF-A Regulates the Proliferation and Migration of Non-small Cell Lung Cancer Cells of A549 through HOTAIR
title_sort mrtf a regulates the proliferation and migration of non small cell lung cancer cells of a549 through hotair
topic Lung neoplasms
A549
MRTF-A
HOTAIR
Proliferation
Migration
url http://dx.doi.org/10.3779/j.issn.1009-3419.2019.02.02
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