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A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling

Breast cancer remains a major health problem worldwide. While chemotherapy represents an important therapeutic modality against breast cancer, limitations in the clinical use of chemotherapy remain formidable because of chemoresistance. The HER2/PI-3K/Akt pathway has been demonstrated to play a caus...

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Autores principales: Zhu, Xun, He, Zhenjian, Wu, Jueheng, Yuan, Jie, Wen, Weitao, Hu, Yiwen, Jiang, Yi, Lin, Cuiji, Zhang, Qianhui, Lin, Min, Zhang, Henan, Yang, Wan, Chen, Hong, Zhong, Lili, She, Zhigang, Chen, Shengping, Lin, Yongcheng, Li, Mengfeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366670/
https://www.ncbi.nlm.nih.gov/pubmed/22690138
http://dx.doi.org/10.3390/md10040694
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author Zhu, Xun
He, Zhenjian
Wu, Jueheng
Yuan, Jie
Wen, Weitao
Hu, Yiwen
Jiang, Yi
Lin, Cuiji
Zhang, Qianhui
Lin, Min
Zhang, Henan
Yang, Wan
Chen, Hong
Zhong, Lili
She, Zhigang
Chen, Shengping
Lin, Yongcheng
Li, Mengfeng
author_facet Zhu, Xun
He, Zhenjian
Wu, Jueheng
Yuan, Jie
Wen, Weitao
Hu, Yiwen
Jiang, Yi
Lin, Cuiji
Zhang, Qianhui
Lin, Min
Zhang, Henan
Yang, Wan
Chen, Hong
Zhong, Lili
She, Zhigang
Chen, Shengping
Lin, Yongcheng
Li, Mengfeng
author_sort Zhu, Xun
collection PubMed
description Breast cancer remains a major health problem worldwide. While chemotherapy represents an important therapeutic modality against breast cancer, limitations in the clinical use of chemotherapy remain formidable because of chemoresistance. The HER2/PI-3K/Akt pathway has been demonstrated to play a causal role in conferring a broad chemoresistance in breast cancer cells and thus justified to be a target for enhancing the effects of anti-breast cancer chemotherapies, such as adriamycin (ADR). Agents that can either enhance the effects of chemotherapeutics or overcome chemoresistance are urgently needed for the treatment of breast cancer. In this context, SZ-685C, an agent that has been previously shown, as such, to suppress Akt signaling, is expected to increase the efficacy of chemotherapy. Our current study investigated whether SZ-685C can override chemoresistance through inhibiting Akt signaling in human breast cancer cells. ADR-resistant cells derived from human breast cancer cell lines MCF-7, MCF-7/ADR and MCF-7/Akt, were used as models to test the effects of SZ-685C. We found that SZ-685C suppressed the Akt pathway and induced apoptosis in MCF-7/ADR and MCF-7/Akt cells that are resistant to ADR treatment, leading to antitumor effects both in vitro and in vivo. Our data suggest that use of SZ-685C might represent a potentially promising approach to the treatment of ADR-resistant breast cancer.
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spelling pubmed-33666702012-06-11 A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling Zhu, Xun He, Zhenjian Wu, Jueheng Yuan, Jie Wen, Weitao Hu, Yiwen Jiang, Yi Lin, Cuiji Zhang, Qianhui Lin, Min Zhang, Henan Yang, Wan Chen, Hong Zhong, Lili She, Zhigang Chen, Shengping Lin, Yongcheng Li, Mengfeng Mar Drugs Article Breast cancer remains a major health problem worldwide. While chemotherapy represents an important therapeutic modality against breast cancer, limitations in the clinical use of chemotherapy remain formidable because of chemoresistance. The HER2/PI-3K/Akt pathway has been demonstrated to play a causal role in conferring a broad chemoresistance in breast cancer cells and thus justified to be a target for enhancing the effects of anti-breast cancer chemotherapies, such as adriamycin (ADR). Agents that can either enhance the effects of chemotherapeutics or overcome chemoresistance are urgently needed for the treatment of breast cancer. In this context, SZ-685C, an agent that has been previously shown, as such, to suppress Akt signaling, is expected to increase the efficacy of chemotherapy. Our current study investigated whether SZ-685C can override chemoresistance through inhibiting Akt signaling in human breast cancer cells. ADR-resistant cells derived from human breast cancer cell lines MCF-7, MCF-7/ADR and MCF-7/Akt, were used as models to test the effects of SZ-685C. We found that SZ-685C suppressed the Akt pathway and induced apoptosis in MCF-7/ADR and MCF-7/Akt cells that are resistant to ADR treatment, leading to antitumor effects both in vitro and in vivo. Our data suggest that use of SZ-685C might represent a potentially promising approach to the treatment of ADR-resistant breast cancer. MDPI 2012-03-23 /pmc/articles/PMC3366670/ /pubmed/22690138 http://dx.doi.org/10.3390/md10040694 Text en © 2012 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Article
Zhu, Xun
He, Zhenjian
Wu, Jueheng
Yuan, Jie
Wen, Weitao
Hu, Yiwen
Jiang, Yi
Lin, Cuiji
Zhang, Qianhui
Lin, Min
Zhang, Henan
Yang, Wan
Chen, Hong
Zhong, Lili
She, Zhigang
Chen, Shengping
Lin, Yongcheng
Li, Mengfeng
A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling
title A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling
title_full A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling
title_fullStr A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling
title_full_unstemmed A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling
title_short A Marine Anthraquinone SZ-685C Overrides Adriamycin-Resistance in Breast Cancer Cells through Suppressing Akt Signaling
title_sort marine anthraquinone sz-685c overrides adriamycin-resistance in breast cancer cells through suppressing akt signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3366670/
https://www.ncbi.nlm.nih.gov/pubmed/22690138
http://dx.doi.org/10.3390/md10040694
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