The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3

Objective To study the effect of miR-16-5p on lung cancer cell injury and apoptosis, and its mechanism.Methods LPS induced lung cancer cell A549 injury; qRT-PCR method was applied to detect the expression of miR-16-5p and CXCR3 in A549 cells. Con (without LPS treatment), LPS + miR-NC group (transfec...

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Main Authors: Guo-Pan Liu, Wei-Wei Wang, Wen-Ying Lu, An-Quan Shang
Format: Article
Language:English
Published: Taylor & Francis Group 2019-12-01
Series:Artificial Cells, Nanomedicine, and Biotechnology
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Online Access:https://www.tandfonline.com/doi/10.1080/21691401.2019.1593998
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author Guo-Pan Liu
Wei-Wei Wang
Wen-Ying Lu
An-Quan Shang
author_facet Guo-Pan Liu
Wei-Wei Wang
Wen-Ying Lu
An-Quan Shang
author_sort Guo-Pan Liu
collection DOAJ
description Objective To study the effect of miR-16-5p on lung cancer cell injury and apoptosis, and its mechanism.Methods LPS induced lung cancer cell A549 injury; qRT-PCR method was applied to detect the expression of miR-16-5p and CXCR3 in A549 cells. Con (without LPS treatment), LPS + miR-NC group (transfected negative control samples), LPS + miR-16-5p group (transfected miR-16-5p mimics); LPS + si-NC group (transfected negative control samples), LPS + si-CXCR3 group (transfected si-CXCR3); LPS + miR-16-5p + pcDNA3.1 group (co-transfected miR-16-5p mimics and pcDNA3.1), LPS + miR-16-5p + pcDNA3.1-CXCR3 group (co-transfected miR-16-5p mimics and pcDNA3.1-CXCR3) were transfected into A549 cells by liposome method. Western blot was used to detect protein expression of CXCR3, IL-6 and TNF-α in A549 cells; apoptosis of A549 cells was detected by flow cytometry.Results Compared with the control group, the expression of miR-16-5p mRNA was significantly decreased in A549 cells in LPS group, and the mRNA and protein expression of CXCR3 were significantly increased (p < .05). Overexpression of miR-16-5p and knockdown of CXCR3 both can down-regulated protein expression of IL-6 and TNF-α, and up-regulated apoptosis in LPS-induced A549 cell; CXCR3 is a target of miR-16-5p. Overexpression of CXCR3 rescued the protective effect of miR-16-5p on LPS-induced A549 cell injury.Conclusion miR-16-5p can protect LPS-induced A549 cell injury, and its mechanism may be related to the targeted regulation of CXCR3, which could provide a new target for targeted therapy of lung cancer.
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spelling doaj-art-def4e5a23e9b47e890a34e22b4eb6dd82025-07-21T21:25:01ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2019-12-014711200120610.1080/21691401.2019.1593998The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3Guo-Pan Liu0Wei-Wei Wang1Wen-Ying Lu2An-Quan Shang3College of Clinical Medicine, Ningxia Medical University, Yinchuan, P.R. ChinaDepartment of Pathology, The Sixth People’s Hospital of Yancheng City, Yancheng, P.R. ChinaDepartment of Pathology, The Sixth People’s Hospital of Yancheng City, Yancheng, P.R. ChinaDepartment of Laboratory Medicine, Tongji Hospital of Tongji University, Shanghai, P.R. ChinaObjective To study the effect of miR-16-5p on lung cancer cell injury and apoptosis, and its mechanism.Methods LPS induced lung cancer cell A549 injury; qRT-PCR method was applied to detect the expression of miR-16-5p and CXCR3 in A549 cells. Con (without LPS treatment), LPS + miR-NC group (transfected negative control samples), LPS + miR-16-5p group (transfected miR-16-5p mimics); LPS + si-NC group (transfected negative control samples), LPS + si-CXCR3 group (transfected si-CXCR3); LPS + miR-16-5p + pcDNA3.1 group (co-transfected miR-16-5p mimics and pcDNA3.1), LPS + miR-16-5p + pcDNA3.1-CXCR3 group (co-transfected miR-16-5p mimics and pcDNA3.1-CXCR3) were transfected into A549 cells by liposome method. Western blot was used to detect protein expression of CXCR3, IL-6 and TNF-α in A549 cells; apoptosis of A549 cells was detected by flow cytometry.Results Compared with the control group, the expression of miR-16-5p mRNA was significantly decreased in A549 cells in LPS group, and the mRNA and protein expression of CXCR3 were significantly increased (p < .05). Overexpression of miR-16-5p and knockdown of CXCR3 both can down-regulated protein expression of IL-6 and TNF-α, and up-regulated apoptosis in LPS-induced A549 cell; CXCR3 is a target of miR-16-5p. Overexpression of CXCR3 rescued the protective effect of miR-16-5p on LPS-induced A549 cell injury.Conclusion miR-16-5p can protect LPS-induced A549 cell injury, and its mechanism may be related to the targeted regulation of CXCR3, which could provide a new target for targeted therapy of lung cancer.https://www.tandfonline.com/doi/10.1080/21691401.2019.1593998miR-16-5pCXCR3lung cancerapoptosis
spellingShingle Guo-Pan Liu
Wei-Wei Wang
Wen-Ying Lu
An-Quan Shang
The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3
Artificial Cells, Nanomedicine, and Biotechnology
miR-16-5p
CXCR3
lung cancer
apoptosis
title The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3
title_full The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3
title_fullStr The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3
title_full_unstemmed The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3
title_short The mechanism of miR-16-5p protection on LPS-induced A549 cell injury by targeting CXCR3
title_sort mechanism of mir 16 5p protection on lps induced a549 cell injury by targeting cxcr3
topic miR-16-5p
CXCR3
lung cancer
apoptosis
url https://www.tandfonline.com/doi/10.1080/21691401.2019.1593998
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