KCNK9 mediates the inhibitory effects of genistein on hepatic metastasis from colon cancer
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Outros Autores: | , , , |
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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Clinics |
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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 |
_version_ |
1800222767127199744 |