KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer

Detalhes bibliográficos
Autor(a) principal: Cheng, Yuan
Data de Publicação: 2023
Outros Autores: Tang, Yi, Tan, Yiming, Li, Juan, Zhang, Xuping
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/213708
Resumo: Objective: The tyrosine-protein kinase inhibitor, genistein, can inhibit cell malignant transformation and has an antitumor effect on various types of cancer. It has been shown that both genistein and KNCK9 can inhibit colon cancer. This research aimed to investigate the suppressive effects of genistein on colon cancer cells and the association between the application of genistein and KCNK9 expression level. Methods: The Cancer Genome Atlas (TCGA) database was used to study the correlation between the KCNK9 expression level and the prognosis of colon cancer patients. HT29 and SW480 colon cancer cell lines were cultured to examine the inhibitory effects of KCNK9 and genistein on colon cancer in vitro, and a mouse model of colon cancer with liver metastasis was established to verify the inhibitory effect of genistein in vivo. Results: KCNK9 was overexpressed in colon cancer cells and was associated with a shorter Overall Survival (OS), a shorter Disease-Specific Survival (DFS), and a shorter Progression-Free Interval (PFI) of colon cancer patients. In vitro experiments showed that downregulation of KCNK9 or genistein application could suppress cell proliferation, migration, and invasion abilities, induce cell cycle quiescence, promote cell apoptosis, and reduce epithelial-mesenchymal transition of the colon cancer cell line. In vivo experiments revealed that silencing of KCNK9 or application of genistein could inhibit hepatic metastasis from colon cancer. Additionally, genistein could inhibit KCNK9 expression, thereby attenuating Wnt/β-catenin signaling pathway. Conclusion: Genistein inhibited the occurrence and progression of colon cancer through Wnt/β-catenin signaling pathway that could be mediated by KCNK9.
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spelling KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancerKCNK9GenisteinColon cancerMetastasisObjective: The tyrosine-protein kinase inhibitor, genistein, can inhibit cell malignant transformation and has an antitumor effect on various types of cancer. It has been shown that both genistein and KNCK9 can inhibit colon cancer. This research aimed to investigate the suppressive effects of genistein on colon cancer cells and the association between the application of genistein and KCNK9 expression level. Methods: The Cancer Genome Atlas (TCGA) database was used to study the correlation between the KCNK9 expression level and the prognosis of colon cancer patients. HT29 and SW480 colon cancer cell lines were cultured to examine the inhibitory effects of KCNK9 and genistein on colon cancer in vitro, and a mouse model of colon cancer with liver metastasis was established to verify the inhibitory effect of genistein in vivo. Results: KCNK9 was overexpressed in colon cancer cells and was associated with a shorter Overall Survival (OS), a shorter Disease-Specific Survival (DFS), and a shorter Progression-Free Interval (PFI) of colon cancer patients. In vitro experiments showed that downregulation of KCNK9 or genistein application could suppress cell proliferation, migration, and invasion abilities, induce cell cycle quiescence, promote cell apoptosis, and reduce epithelial-mesenchymal transition of the colon cancer cell line. In vivo experiments revealed that silencing of KCNK9 or application of genistein could inhibit hepatic metastasis from colon cancer. Additionally, genistein could inhibit KCNK9 expression, thereby attenuating Wnt/β-catenin signaling pathway. Conclusion: Genistein inhibited the occurrence and progression of colon cancer through Wnt/β-catenin signaling pathway that could be mediated by KCNK9.Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2023-03-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/21370810.1016/j.clinsp.2022.100141Clinics; Vol. 78 (2023); 100141Clinics; v. 78 (2023); 100141Clinics; Vol. 78 (2023); 1001411980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/213708/195829Copyright (c) 2023 Clinicsinfo:eu-repo/semantics/openAccessCheng, YuanTang, YiTan, YimingLi, JuanZhang, Xuping2023-07-06T13:05:38Zoai:revistas.usp.br:article/213708Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2023-07-06T13:05:38Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
title KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
spellingShingle KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
Cheng, Yuan
KCNK9
Genistein
Colon cancer
Metastasis
title_short KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
title_full KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
title_fullStr KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
title_full_unstemmed KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
title_sort KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
author Cheng, Yuan
author_facet Cheng, Yuan
Tang, Yi
Tan, Yiming
Li, Juan
Zhang, Xuping
author_role author
author2 Tang, Yi
Tan, Yiming
Li, Juan
Zhang, Xuping
author2_role author
author
author
author
dc.contributor.author.fl_str_mv Cheng, Yuan
Tang, Yi
Tan, Yiming
Li, Juan
Zhang, Xuping
dc.subject.por.fl_str_mv KCNK9
Genistein
Colon cancer
Metastasis
topic KCNK9
Genistein
Colon cancer
Metastasis
description Objective: The tyrosine-protein kinase inhibitor, genistein, can inhibit cell malignant transformation and has an antitumor effect on various types of cancer. It has been shown that both genistein and KNCK9 can inhibit colon cancer. This research aimed to investigate the suppressive effects of genistein on colon cancer cells and the association between the application of genistein and KCNK9 expression level. Methods: The Cancer Genome Atlas (TCGA) database was used to study the correlation between the KCNK9 expression level and the prognosis of colon cancer patients. HT29 and SW480 colon cancer cell lines were cultured to examine the inhibitory effects of KCNK9 and genistein on colon cancer in vitro, and a mouse model of colon cancer with liver metastasis was established to verify the inhibitory effect of genistein in vivo. Results: KCNK9 was overexpressed in colon cancer cells and was associated with a shorter Overall Survival (OS), a shorter Disease-Specific Survival (DFS), and a shorter Progression-Free Interval (PFI) of colon cancer patients. In vitro experiments showed that downregulation of KCNK9 or genistein application could suppress cell proliferation, migration, and invasion abilities, induce cell cycle quiescence, promote cell apoptosis, and reduce epithelial-mesenchymal transition of the colon cancer cell line. In vivo experiments revealed that silencing of KCNK9 or application of genistein could inhibit hepatic metastasis from colon cancer. Additionally, genistein could inhibit KCNK9 expression, thereby attenuating Wnt/β-catenin signaling pathway. Conclusion: Genistein inhibited the occurrence and progression of colon cancer through Wnt/β-catenin signaling pathway that could be mediated by KCNK9.
publishDate 2023
dc.date.none.fl_str_mv 2023-03-09
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213708
10.1016/j.clinsp.2022.100141
url https://www.revistas.usp.br/clinics/article/view/213708
identifier_str_mv 10.1016/j.clinsp.2022.100141
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/213708/195829
dc.rights.driver.fl_str_mv Copyright (c) 2023 Clinics
info:eu-repo/semantics/openAccess
rights_invalid_str_mv Copyright (c) 2023 Clinics
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 78 (2023); 100141
Clinics; v. 78 (2023); 100141
Clinics; Vol. 78 (2023); 100141
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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