Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence
Autor(a) principal: | |
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Data de Publicação: | 2023 |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | Brazilian Journal of Pharmaceutical Sciences |
Texto Completo: | https://www.revistas.usp.br/bjps/article/view/220152 |
Resumo: | Paclitaxel (PTX) is one of the most effective drugs used in the treatment of breast cancer. Nonetheless, the appearance of MDR1 (multidrug resistance 1) in tumor cells has become a significant hindrance for efficacious chemotherapy. In this study, we show that the expression level of Egr-1 (early growth response gene-1) in cancer tissues (from paclitaxel chemotherapy failure patients) and MCF-7/PTX cells (the breast cancer cell line that was resistant to paclitaxel) was increased. Cell proliferation assay and apoptosis assay revealed that Egr-1 could promote cell growth and inhibit apoptosis in MCF-7/PTX. Mechanistic studies indicated that Egr-1 could bind to the proximal MDR1 promoter and enhance MDR1 transcription. These findings indicate that paclitaxel induced Egr-1 accumulation and upregulated the expression of MDR1, thereby inducing the drug resistance in MCF-7/PTX. Our results suggest a novel pathway by which paclitaxel induces MDR1 expression, possibly illuminating a potential target pathway for the prevention of MDR1-mediated drug resistance. |
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Brazilian Journal of Pharmaceutical Sciences |
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Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 DependenceEgr-1;Breast cancer;MDR1;Drug resistance.Paclitaxel (PTX) is one of the most effective drugs used in the treatment of breast cancer. Nonetheless, the appearance of MDR1 (multidrug resistance 1) in tumor cells has become a significant hindrance for efficacious chemotherapy. In this study, we show that the expression level of Egr-1 (early growth response gene-1) in cancer tissues (from paclitaxel chemotherapy failure patients) and MCF-7/PTX cells (the breast cancer cell line that was resistant to paclitaxel) was increased. Cell proliferation assay and apoptosis assay revealed that Egr-1 could promote cell growth and inhibit apoptosis in MCF-7/PTX. Mechanistic studies indicated that Egr-1 could bind to the proximal MDR1 promoter and enhance MDR1 transcription. These findings indicate that paclitaxel induced Egr-1 accumulation and upregulated the expression of MDR1, thereby inducing the drug resistance in MCF-7/PTX. Our results suggest a novel pathway by which paclitaxel induces MDR1 expression, possibly illuminating a potential target pathway for the prevention of MDR1-mediated drug resistance.Universidade de São Paulo. Faculdade de Ciências Farmacêuticas2023-08-28info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://www.revistas.usp.br/bjps/article/view/220152Brazilian Journal of Pharmaceutical Sciences; Vol. 59 (2023); 10Brazilian Journal of Pharmaceutical Sciences; v. 59 (2023); 10Brazilian Journal of Pharmaceutical Sciences; Vol. 59 (2023); 102175-97901984-8250reponame:Brazilian Journal of Pharmaceutical Sciencesinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/bjps/article/view/220152/200959https://creativecommons.org/licenses/by/4.0/info:eu-repo/semantics/openAccessGong, Pei-yao 2023-12-12T15:48:39Zoai:revistas.usp.br:article/220152Revistahttps://www.revistas.usp.br/bjps/indexPUBhttps://old.scielo.br/oai/scielo-oai.phpbjps@usp.br||elizabeth.igne@gmail.com2175-97901984-8250opendoar:2023-12-12T15:48:39Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP)false |
dc.title.none.fl_str_mv |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
title |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
spellingShingle |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence Gong, Pei-yao Egr-1; Breast cancer; MDR1; Drug resistance. |
title_short |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
title_full |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
title_fullStr |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
title_full_unstemmed |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
title_sort |
Egr-1 Enhances Drug Resistance of Breast Cancer Cells by MDR1 Dependence |
author |
Gong, Pei-yao |
author_facet |
Gong, Pei-yao |
author_role |
author |
dc.contributor.author.fl_str_mv |
Gong, Pei-yao |
dc.subject.por.fl_str_mv |
Egr-1; Breast cancer; MDR1; Drug resistance. |
topic |
Egr-1; Breast cancer; MDR1; Drug resistance. |
description |
Paclitaxel (PTX) is one of the most effective drugs used in the treatment of breast cancer. Nonetheless, the appearance of MDR1 (multidrug resistance 1) in tumor cells has become a significant hindrance for efficacious chemotherapy. In this study, we show that the expression level of Egr-1 (early growth response gene-1) in cancer tissues (from paclitaxel chemotherapy failure patients) and MCF-7/PTX cells (the breast cancer cell line that was resistant to paclitaxel) was increased. Cell proliferation assay and apoptosis assay revealed that Egr-1 could promote cell growth and inhibit apoptosis in MCF-7/PTX. Mechanistic studies indicated that Egr-1 could bind to the proximal MDR1 promoter and enhance MDR1 transcription. These findings indicate that paclitaxel induced Egr-1 accumulation and upregulated the expression of MDR1, thereby inducing the drug resistance in MCF-7/PTX. Our results suggest a novel pathway by which paclitaxel induces MDR1 expression, possibly illuminating a potential target pathway for the prevention of MDR1-mediated drug resistance. |
publishDate |
2023 |
dc.date.none.fl_str_mv |
2023-08-28 |
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/bjps/article/view/220152 |
url |
https://www.revistas.usp.br/bjps/article/view/220152 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
https://www.revistas.usp.br/bjps/article/view/220152/200959 |
dc.rights.driver.fl_str_mv |
https://creativecommons.org/licenses/by/4.0/ info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/4.0/ |
eu_rights_str_mv |
openAccess |
dc.publisher.none.fl_str_mv |
Universidade de São Paulo. Faculdade de Ciências Farmacêuticas |
publisher.none.fl_str_mv |
Universidade de São Paulo. Faculdade de Ciências Farmacêuticas |
dc.source.none.fl_str_mv |
Brazilian Journal of Pharmaceutical Sciences; Vol. 59 (2023); 10 Brazilian Journal of Pharmaceutical Sciences; v. 59 (2023); 10 Brazilian Journal of Pharmaceutical Sciences; Vol. 59 (2023); 10 2175-9790 1984-8250 reponame:Brazilian Journal of Pharmaceutical Sciences instname:Universidade de São Paulo (USP) instacron:USP |
instname_str |
Universidade de São Paulo (USP) |
instacron_str |
USP |
institution |
USP |
reponame_str |
Brazilian Journal of Pharmaceutical Sciences |
collection |
Brazilian Journal of Pharmaceutical Sciences |
repository.name.fl_str_mv |
Brazilian Journal of Pharmaceutical Sciences - Universidade de São Paulo (USP) |
repository.mail.fl_str_mv |
bjps@usp.br||elizabeth.igne@gmail.com |
_version_ |
1800222918317178880 |