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

Detalhes bibliográficos
Autor(a) principal: Wang,Shuzhong
Data de Publicação: 2020
Outros Autores: Wang,Yanmei, Wang,Chuanyun
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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spelling 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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