miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer

Background Long non‐coding RNA‐urothelial carcinoma associated 1 (LncRNA‐UCA1) is a crucial oncogene that is deregulated in many types of cancers. However, the mechanism of UCA1 function, especially for its posttranscriptional regulation in lung cancer, remains unclear. Methods miRCode was used to p...

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Main Authors: Guangsu Xun, Ming Ma, Bing Li, Song Zhao
Format: Article
Language:English
Published: Wiley 2020-09-01
Series:Thoracic Cancer
Subjects:
Online Access:https://doi.org/10.1111/1759-7714.13605
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author Guangsu Xun
Ming Ma
Bing Li
Song Zhao
author_facet Guangsu Xun
Ming Ma
Bing Li
Song Zhao
author_sort Guangsu Xun
collection DOAJ
description Background Long non‐coding RNA‐urothelial carcinoma associated 1 (LncRNA‐UCA1) is a crucial oncogene that is deregulated in many types of cancers. However, the mechanism of UCA1 function, especially for its posttranscriptional regulation in lung cancer, remains unclear. Methods miRCode was used to predict potential miRNA candidates that might target UCA1. The targets of miR‐138 and miR‐193 on UCA1 and CDK6 were verified by luciferase reporter analysis. Western blotting was used to detect protein levels. The RNA level was evaluated using quantitative real‐time polymerase chain reaction (PCR). Proliferation, wound healing, and transwell invasion assays were performed to assess cell proliferation and invasion abilities. Correlations between miR‐138 or miR‐193 and UCA1 in lung cancer tissues was assessed using quantitative real‐time PCR. Results miR‐138 and miR‐193 specifically targeted and regulated lncRNA‐UCA1. MiR‐138 and miR‐193 both suppressed cell proliferation and cell cycle progression. Moreover, miR‐138 and miR‐193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR‐138 or miR‐193. Furthermore, miR‐138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR‐138 and miR‐193 common target. In human lung cancer tissues, our study showed a significant negative correlation between miR‐138 or miR‐193 and UCA1 in lung cancer tissues. Conclusions Our results demonstrated that miR‐138 and miR‐193 affect cell function by directly targeting and regulating UCA1 in lung cancer.
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spelling doaj.art-fc4540ad3a404303a747da71c52d76122022-12-21T18:38:01ZengWileyThoracic Cancer1759-77061759-77142020-09-011192681268910.1111/1759-7714.13605miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancerGuangsu Xun0Ming Ma1Bing Li2Song Zhao3Department of Thoracic Surgery The First Affiliated Hospital of Zhengzhou University Zhengzhou ChinaDepartment of Pharmacy The Second Affiliated Hospital of Henan University of Chinese Medicine Zhengzhou ChinaDepartment of Thoracic Surgery The First Affiliated Hospital of Zhengzhou University Zhengzhou ChinaDepartment of Thoracic Surgery The First Affiliated Hospital of Zhengzhou University Zhengzhou ChinaBackground Long non‐coding RNA‐urothelial carcinoma associated 1 (LncRNA‐UCA1) is a crucial oncogene that is deregulated in many types of cancers. However, the mechanism of UCA1 function, especially for its posttranscriptional regulation in lung cancer, remains unclear. Methods miRCode was used to predict potential miRNA candidates that might target UCA1. The targets of miR‐138 and miR‐193 on UCA1 and CDK6 were verified by luciferase reporter analysis. Western blotting was used to detect protein levels. The RNA level was evaluated using quantitative real‐time polymerase chain reaction (PCR). Proliferation, wound healing, and transwell invasion assays were performed to assess cell proliferation and invasion abilities. Correlations between miR‐138 or miR‐193 and UCA1 in lung cancer tissues was assessed using quantitative real‐time PCR. Results miR‐138 and miR‐193 specifically targeted and regulated lncRNA‐UCA1. MiR‐138 and miR‐193 both suppressed cell proliferation and cell cycle progression. Moreover, miR‐138 and miR‐193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR‐138 or miR‐193. Furthermore, miR‐138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR‐138 and miR‐193 common target. In human lung cancer tissues, our study showed a significant negative correlation between miR‐138 or miR‐193 and UCA1 in lung cancer tissues. Conclusions Our results demonstrated that miR‐138 and miR‐193 affect cell function by directly targeting and regulating UCA1 in lung cancer.https://doi.org/10.1111/1759-7714.13605Lung cancermiR‐138miR‐193proliferationUCA1
spellingShingle Guangsu Xun
Ming Ma
Bing Li
Song Zhao
miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer
Thoracic Cancer
Lung cancer
miR‐138
miR‐193
proliferation
UCA1
title miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer
title_full miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer
title_fullStr miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer
title_full_unstemmed miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer
title_short miR‐138 and miR‐193 target long non‐coding RNA UCA1 to inhibit cell proliferation, migration, and invasion of lung cancer
title_sort mir 138 and mir 193 target long non coding rna uca1 to inhibit cell proliferation migration and invasion of lung cancer
topic Lung cancer
miR‐138
miR‐193
proliferation
UCA1
url https://doi.org/10.1111/1759-7714.13605
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