MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1

Abstract This study was aimed at the investigation of the effects of miR‐21 on drug resistance, invasion, migration, and epithelial–mesenchymal transition (EMT) of lung adenocarcinoma cells and the related molecular mechanisms. Cell viability of A549 cell line was measured by MTT assay. Wound healin...

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Main Authors: Chongyu Su, Xu Cheng, Yunsong Li, Yi Han, Xiaoyun Song, Daping Yu, Xiaoqing Cao, Zhidong Liu
Format: Article
Language:English
Published: Wiley 2018-06-01
Series:Cancer Medicine
Subjects:
Online Access:https://doi.org/10.1002/cam4.1294
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author Chongyu Su
Xu Cheng
Yunsong Li
Yi Han
Xiaoyun Song
Daping Yu
Xiaoqing Cao
Zhidong Liu
author_facet Chongyu Su
Xu Cheng
Yunsong Li
Yi Han
Xiaoyun Song
Daping Yu
Xiaoqing Cao
Zhidong Liu
author_sort Chongyu Su
collection DOAJ
description Abstract This study was aimed at the investigation of the effects of miR‐21 on drug resistance, invasion, migration, and epithelial–mesenchymal transition (EMT) of lung adenocarcinoma cells and the related molecular mechanisms. Cell viability of A549 cell line was measured by MTT assay. Wound healing assay and transwell assay were, respectively, employed to examine cell migration and invasion abilities. The cells were transfected with miR‐21 mimic or inhibitor using Lipofectamine 3000. The target relationship between miR‐21 and HBP1 was confirmed by luciferase reporter gene assay. Western blot and qRT‐PCR were used to examine the expression of HBP1 and EMT‐related molecules. Compared with A549 cells, drug resistance of A549/PTX cells and A549/DDP cells were obviously stronger. A549/PTX cells and A549/DDP cells had stronger ability of migration and invasion compared with parental A549 cells. Meanwhile, EMT of A549/PTX and A549/DDP was significantly higher than that of A549 cells. MiR‐21 promoted migration, invasion, and EMT of human lung adenocarcinoma cancer cells. Our experiment also verified the target relationship between miR‐21 and HBP1. MiR‐21 may affect migration and invasion ability of drug‐resistant lung adenocarcinoma cells by targeting HBP1, therefore modulating EMT.
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spelling doaj-art-9cea9fe465734684aba91057cdba37582025-08-20T03:15:03ZengWileyCancer Medicine2045-76342018-06-01762485250310.1002/cam4.1294MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1Chongyu Su0Xu Cheng1Yunsong Li2Yi Han3Xiaoyun Song4Daping Yu5Xiaoqing Cao6Zhidong Liu7Department of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaDepartment of Thoracic Surgery Beijing Chest Hospital Capital Medical University Beijing 101149 ChinaAbstract This study was aimed at the investigation of the effects of miR‐21 on drug resistance, invasion, migration, and epithelial–mesenchymal transition (EMT) of lung adenocarcinoma cells and the related molecular mechanisms. Cell viability of A549 cell line was measured by MTT assay. Wound healing assay and transwell assay were, respectively, employed to examine cell migration and invasion abilities. The cells were transfected with miR‐21 mimic or inhibitor using Lipofectamine 3000. The target relationship between miR‐21 and HBP1 was confirmed by luciferase reporter gene assay. Western blot and qRT‐PCR were used to examine the expression of HBP1 and EMT‐related molecules. Compared with A549 cells, drug resistance of A549/PTX cells and A549/DDP cells were obviously stronger. A549/PTX cells and A549/DDP cells had stronger ability of migration and invasion compared with parental A549 cells. Meanwhile, EMT of A549/PTX and A549/DDP was significantly higher than that of A549 cells. MiR‐21 promoted migration, invasion, and EMT of human lung adenocarcinoma cancer cells. Our experiment also verified the target relationship between miR‐21 and HBP1. MiR‐21 may affect migration and invasion ability of drug‐resistant lung adenocarcinoma cells by targeting HBP1, therefore modulating EMT.https://doi.org/10.1002/cam4.1294Drug resistanceepithelial–mesenchymal transitionHBP1lung adenocarcinomamiRNA‐21
spellingShingle Chongyu Su
Xu Cheng
Yunsong Li
Yi Han
Xiaoyun Song
Daping Yu
Xiaoqing Cao
Zhidong Liu
MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1
Cancer Medicine
Drug resistance
epithelial–mesenchymal transition
HBP1
lung adenocarcinoma
miRNA‐21
title MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1
title_full MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1
title_fullStr MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1
title_full_unstemmed MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1
title_short MiR‐21 improves invasion and migration of drug‐resistant lung adenocarcinoma cancer cell and transformation of EMT through targeting HBP1
title_sort mir 21 improves invasion and migration of drug resistant lung adenocarcinoma cancer cell and transformation of emt through targeting hbp1
topic Drug resistance
epithelial–mesenchymal transition
HBP1
lung adenocarcinoma
miRNA‐21
url https://doi.org/10.1002/cam4.1294
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