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Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145

BACKGROUND: Gastric cancer receives considerable attention not only because it is the most common cancer all through the world, but also because it’s on the top third leading reason for cancer-related death. Lidocaine is a well-documented local anesthetic that has been reported to suppress cancer de...

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Autores principales: Sui, Hongyang, Lou, Anfeng, Li, Zhisong, Yang, Jianjun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419442/
https://www.ncbi.nlm.nih.gov/pubmed/30876463
http://dx.doi.org/10.1186/s12885-019-5431-9
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author Sui, Hongyang
Lou, Anfeng
Li, Zhisong
Yang, Jianjun
author_facet Sui, Hongyang
Lou, Anfeng
Li, Zhisong
Yang, Jianjun
author_sort Sui, Hongyang
collection PubMed
description BACKGROUND: Gastric cancer receives considerable attention not only because it is the most common cancer all through the world, but also because it’s on the top third leading reason for cancer-related death. Lidocaine is a well-documented local anesthetic that has been reported to suppress cancer development. The study explored the effects of lidocaine on the growth, migration and invasion of the gastric carcinoma cell line MKN45 and the mechanism behind. METHODS: The effect of lidocaine on viability, proliferation and apoptosis of MKN45 cells were analyzed by Cell Counting Kit-8 assay, BrdU staining assay and flow cytometry, respectively. Moreover, cell migration and invasion were both examined by Transwell assay. The expression of apoptosis-, migration-, and invasion-related proteins were detected by western blot. The relative expression of miR-145 was determined by qRT-PCR. Moreover, the impact which lidocaine brought on MEK/ERK and NF-κB pathways were examined by western blot. RESULTS: Lidocaine inhibited viability, proliferation, migration, and invasion of MKN45 cells, while enhanced apoptosis. Moreover, miR-145 expression was enhanced by lidocaine; and transfection with miR-145 inhibitor increased cell viability, proliferation, migration, and invasion, but inhibited apoptosis. The up-regulation of miR-145 was partly contributed to the inhibitory effect of lidocaine on gastric cancer cell line MKN45. Finally, lidocaine inactivated MEK/ERK and NF-κB pathways via up-regulation of miR-145. CONCLUSIONS: Our results suggested that lidocaine decreased growth, migration and invasion of MKN45 cells via regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways.
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spelling pubmed-64194422019-03-27 Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145 Sui, Hongyang Lou, Anfeng Li, Zhisong Yang, Jianjun BMC Cancer Research Article BACKGROUND: Gastric cancer receives considerable attention not only because it is the most common cancer all through the world, but also because it’s on the top third leading reason for cancer-related death. Lidocaine is a well-documented local anesthetic that has been reported to suppress cancer development. The study explored the effects of lidocaine on the growth, migration and invasion of the gastric carcinoma cell line MKN45 and the mechanism behind. METHODS: The effect of lidocaine on viability, proliferation and apoptosis of MKN45 cells were analyzed by Cell Counting Kit-8 assay, BrdU staining assay and flow cytometry, respectively. Moreover, cell migration and invasion were both examined by Transwell assay. The expression of apoptosis-, migration-, and invasion-related proteins were detected by western blot. The relative expression of miR-145 was determined by qRT-PCR. Moreover, the impact which lidocaine brought on MEK/ERK and NF-κB pathways were examined by western blot. RESULTS: Lidocaine inhibited viability, proliferation, migration, and invasion of MKN45 cells, while enhanced apoptosis. Moreover, miR-145 expression was enhanced by lidocaine; and transfection with miR-145 inhibitor increased cell viability, proliferation, migration, and invasion, but inhibited apoptosis. The up-regulation of miR-145 was partly contributed to the inhibitory effect of lidocaine on gastric cancer cell line MKN45. Finally, lidocaine inactivated MEK/ERK and NF-κB pathways via up-regulation of miR-145. CONCLUSIONS: Our results suggested that lidocaine decreased growth, migration and invasion of MKN45 cells via regulating miR-145 expression and further inactivation of MEK/ERK and NF-κB signaling pathways. BioMed Central 2019-03-15 /pmc/articles/PMC6419442/ /pubmed/30876463 http://dx.doi.org/10.1186/s12885-019-5431-9 Text en © The Author(s). 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Sui, Hongyang
Lou, Anfeng
Li, Zhisong
Yang, Jianjun
Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145
title Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145
title_full Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145
title_fullStr Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145
title_full_unstemmed Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145
title_short Lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of miR-145
title_sort lidocaine inhibits growth, migration and invasion of gastric carcinoma cells by up-regulation of mir-145
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419442/
https://www.ncbi.nlm.nih.gov/pubmed/30876463
http://dx.doi.org/10.1186/s12885-019-5431-9
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