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Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A
OBJECTIVE: Gastric cancer (GC) is a gastrointestinal tumor. This study is aimed to explore the regulatory mechanism of long non-coding RNA BLACAT1 (BLACAT1)/microRNA-149-5p (miR-149-5p)/KIF2A cascade on GC. METHODS: The expression of BLACAT1, miR-149-5p and KIF2A in GC was detected by qRT-PCR. The p...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402705/ https://www.ncbi.nlm.nih.gov/pubmed/32801897 http://dx.doi.org/10.2147/CMAR.S258178 |
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author | Wang, Zhengkun Liu, Xichun Liu, Xiaolei Niu, Dongguang |
author_facet | Wang, Zhengkun Liu, Xichun Liu, Xiaolei Niu, Dongguang |
author_sort | Wang, Zhengkun |
collection | PubMed |
description | OBJECTIVE: Gastric cancer (GC) is a gastrointestinal tumor. This study is aimed to explore the regulatory mechanism of long non-coding RNA BLACAT1 (BLACAT1)/microRNA-149-5p (miR-149-5p)/KIF2A cascade on GC. METHODS: The expression of BLACAT1, miR-149-5p and KIF2A in GC was detected by qRT-PCR. The proliferation, migration and invasion of GC cells in vitro were analyzed by MTT, wound-healing and transwell assay, respectively. The xenograft tumor model was constructed in nude mice to confirm the inhibition effect of BLACAT1 knockdown on GC in vivo. Then, dual-luciferase reporter assay was used to detect the interactions among BLACAT1, miR-149-5p and KIF2A. Western blot assay was performed to determine the protein expression of KIF2A. RESULTS: The expression of BLACAT1 and KIF2A was up-regulated in GC, but miR-149-5p expression was down-regulated. Silencing of BLACAT1 retarded the proliferation, migration and invasion of GC cells in vitro and the growth of tumor xenograft in vivo. Moreover, BLACAT1 acted as the molecular sponge of miR-149-5p to up-regulate KIF2A expression. At last, feedback experiments suggested that BLACAT1 accelerated the proliferation, migration and invasion of GC cells by regulating miR-149-5p/KIF2A axis. CONCLUSION: BLACAT1 facilitated the tumorigenesis of GC through regulating miR-149-5p/KIF2A axis, which indicated BLACAT1/miR-149-5p/KIF2A cascade may be a new therapeutic target. |
format | Online Article Text |
id | pubmed-7402705 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-74027052020-08-14 Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A Wang, Zhengkun Liu, Xichun Liu, Xiaolei Niu, Dongguang Cancer Manag Res Original Research OBJECTIVE: Gastric cancer (GC) is a gastrointestinal tumor. This study is aimed to explore the regulatory mechanism of long non-coding RNA BLACAT1 (BLACAT1)/microRNA-149-5p (miR-149-5p)/KIF2A cascade on GC. METHODS: The expression of BLACAT1, miR-149-5p and KIF2A in GC was detected by qRT-PCR. The proliferation, migration and invasion of GC cells in vitro were analyzed by MTT, wound-healing and transwell assay, respectively. The xenograft tumor model was constructed in nude mice to confirm the inhibition effect of BLACAT1 knockdown on GC in vivo. Then, dual-luciferase reporter assay was used to detect the interactions among BLACAT1, miR-149-5p and KIF2A. Western blot assay was performed to determine the protein expression of KIF2A. RESULTS: The expression of BLACAT1 and KIF2A was up-regulated in GC, but miR-149-5p expression was down-regulated. Silencing of BLACAT1 retarded the proliferation, migration and invasion of GC cells in vitro and the growth of tumor xenograft in vivo. Moreover, BLACAT1 acted as the molecular sponge of miR-149-5p to up-regulate KIF2A expression. At last, feedback experiments suggested that BLACAT1 accelerated the proliferation, migration and invasion of GC cells by regulating miR-149-5p/KIF2A axis. CONCLUSION: BLACAT1 facilitated the tumorigenesis of GC through regulating miR-149-5p/KIF2A axis, which indicated BLACAT1/miR-149-5p/KIF2A cascade may be a new therapeutic target. Dove 2020-07-30 /pmc/articles/PMC7402705/ /pubmed/32801897 http://dx.doi.org/10.2147/CMAR.S258178 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Wang, Zhengkun Liu, Xichun Liu, Xiaolei Niu, Dongguang Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A |
title | Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A |
title_full | Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A |
title_fullStr | Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A |
title_full_unstemmed | Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A |
title_short | Long Non-Coding RNA BLACAT1 Promotes the Tumorigenesis of Gastric Cancer by Sponging microRNA-149-5p and Targeting KIF2A |
title_sort | long non-coding rna blacat1 promotes the tumorigenesis of gastric cancer by sponging microrna-149-5p and targeting kif2a |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7402705/ https://www.ncbi.nlm.nih.gov/pubmed/32801897 http://dx.doi.org/10.2147/CMAR.S258178 |
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