Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway
Autor(a) principal: | |
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Data de Publicação: | 2020 |
Outros Autores: | , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Genetics and Molecular Biology |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000600702 |
Resumo: | Abstract We attempted to explore the effect of Rho guanine nucleotide exchange factor 39 (ARHGEF39) on the phenotypes of clear cell renal cell carcinoma (ccRCC) cells and the underlying mechanism. Analyses of the data from The Cancer Genome Atlas (TCGA) illustrated that ARHGEF39 expression was upregulated in ccRCC and high ARHGEF39 expression was correlated with a worse prognosis. The mRNA and protein expression of ARHGEF39 in ccRCC and nontumorigenic cells was measured by qRT-PCR and western blotting, respectively. The results showed that ARHGEF39 expression was upregulated in ccRCC cells compared with nontumorigenic cells. CCK8 and clonogenic assays were used to measure the viability of ccRCC cells after knockdown or overexpression of ARHGEF39. Transwell assays were used to examine the changes in cell motility after alterations in ARHGEF39 expression and treatment with LY294002 (an AKT inhibitor) or PD98059 (an ERK inhibitor). ARHGEF39-mediated changes in the phosphorylation of AKT and ERK were measured by western blotting. The results indicated that ARHGEF39 promoted the viability, migration and invasion of ccRCC cells by regulating the activation of the AKT/ERK signaling pathway. Overall, our research suggested that ARHGEF39 was upregulated in ccRCC and possibly facilitated the malignant development of ccRCC by modulating the AKT/ERK signaling pathway. |
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Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathwayARHGEF39ccRCCmigrationviabilityAKT/ERK signalingAbstract We attempted to explore the effect of Rho guanine nucleotide exchange factor 39 (ARHGEF39) on the phenotypes of clear cell renal cell carcinoma (ccRCC) cells and the underlying mechanism. Analyses of the data from The Cancer Genome Atlas (TCGA) illustrated that ARHGEF39 expression was upregulated in ccRCC and high ARHGEF39 expression was correlated with a worse prognosis. The mRNA and protein expression of ARHGEF39 in ccRCC and nontumorigenic cells was measured by qRT-PCR and western blotting, respectively. The results showed that ARHGEF39 expression was upregulated in ccRCC cells compared with nontumorigenic cells. CCK8 and clonogenic assays were used to measure the viability of ccRCC cells after knockdown or overexpression of ARHGEF39. Transwell assays were used to examine the changes in cell motility after alterations in ARHGEF39 expression and treatment with LY294002 (an AKT inhibitor) or PD98059 (an ERK inhibitor). ARHGEF39-mediated changes in the phosphorylation of AKT and ERK were measured by western blotting. The results indicated that ARHGEF39 promoted the viability, migration and invasion of ccRCC cells by regulating the activation of the AKT/ERK signaling pathway. Overall, our research suggested that ARHGEF39 was upregulated in ccRCC and possibly facilitated the malignant development of ccRCC by modulating the AKT/ERK signaling pathway.Sociedade Brasileira de Genética2020-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000600702Genetics and Molecular Biology v.43 n.4 2020reponame:Genetics and Molecular Biologyinstname:Sociedade Brasileira de Genética (SBG)instacron:SBG10.1590/1678-4685-gmb-2019-0383info:eu-repo/semantics/openAccessWang,ShuzhongWang,YanmeiWang,Chuanyuneng2020-11-16T00:00:00Zoai:scielo:S1415-47572020000600702Revistahttp://www.gmb.org.br/ONGhttps://old.scielo.br/oai/scielo-oai.php||editor@gmb.org.br1678-46851415-4757opendoar:2020-11-16T00:00Genetics and Molecular Biology - Sociedade Brasileira de Genética (SBG)false |
dc.title.none.fl_str_mv |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
title |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
spellingShingle |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway Wang,Shuzhong ARHGEF39 ccRCC migration viability AKT/ERK signaling |
title_short |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
title_full |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
title_fullStr |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
title_full_unstemmed |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
title_sort |
Rho guanine nucleotide exchange factor 39 increases the viability, migration and invasion of clear cell renal cell carcinoma cells via the activation of the AKT/ERK signaling pathway |
author |
Wang,Shuzhong |
author_facet |
Wang,Shuzhong Wang,Yanmei Wang,Chuanyun |
author_role |
author |
author2 |
Wang,Yanmei Wang,Chuanyun |
author2_role |
author author |
dc.contributor.author.fl_str_mv |
Wang,Shuzhong Wang,Yanmei Wang,Chuanyun |
dc.subject.por.fl_str_mv |
ARHGEF39 ccRCC migration viability AKT/ERK signaling |
topic |
ARHGEF39 ccRCC migration viability AKT/ERK signaling |
description |
Abstract We attempted to explore the effect of Rho guanine nucleotide exchange factor 39 (ARHGEF39) on the phenotypes of clear cell renal cell carcinoma (ccRCC) cells and the underlying mechanism. Analyses of the data from The Cancer Genome Atlas (TCGA) illustrated that ARHGEF39 expression was upregulated in ccRCC and high ARHGEF39 expression was correlated with a worse prognosis. The mRNA and protein expression of ARHGEF39 in ccRCC and nontumorigenic cells was measured by qRT-PCR and western blotting, respectively. The results showed that ARHGEF39 expression was upregulated in ccRCC cells compared with nontumorigenic cells. CCK8 and clonogenic assays were used to measure the viability of ccRCC cells after knockdown or overexpression of ARHGEF39. Transwell assays were used to examine the changes in cell motility after alterations in ARHGEF39 expression and treatment with LY294002 (an AKT inhibitor) or PD98059 (an ERK inhibitor). ARHGEF39-mediated changes in the phosphorylation of AKT and ERK were measured by western blotting. The results indicated that ARHGEF39 promoted the viability, migration and invasion of ccRCC cells by regulating the activation of the AKT/ERK signaling pathway. Overall, our research suggested that ARHGEF39 was upregulated in ccRCC and possibly facilitated the malignant development of ccRCC by modulating the AKT/ERK signaling pathway. |
publishDate |
2020 |
dc.date.none.fl_str_mv |
2020-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000600702 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572020000600702 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/1678-4685-gmb-2019-0383 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Sociedade Brasileira de Genética |
publisher.none.fl_str_mv |
Sociedade Brasileira de Genética |
dc.source.none.fl_str_mv |
Genetics and Molecular Biology v.43 n.4 2020 reponame:Genetics and Molecular Biology instname:Sociedade Brasileira de Genética (SBG) instacron:SBG |
instname_str |
Sociedade Brasileira de Genética (SBG) |
instacron_str |
SBG |
institution |
SBG |
reponame_str |
Genetics and Molecular Biology |
collection |
Genetics and Molecular Biology |
repository.name.fl_str_mv |
Genetics and Molecular Biology - Sociedade Brasileira de Genética (SBG) |
repository.mail.fl_str_mv |
||editor@gmb.org.br |
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1752122390166372352 |