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GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()

GALNT14 is a member of N-acetylgalactosaminyltransferase enzyme family and mediates breast cancer cell development. Here, we find that GALNT14 regulates multidrug resistance (MDR) in breast cancer. The expression of GALNT14 is associated with MDR in breast cancer. Higher level of GALNT14 facilitates...

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Detalles Bibliográficos
Autores principales: Shan, Jinshuai, Liu, Yang, Wang, Yukun, Li, Yimiao, Yu, Xiaochun, Wu, Chen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Neoplasia Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058006/
https://www.ncbi.nlm.nih.gov/pubmed/29702465
http://dx.doi.org/10.1016/j.tranon.2018.04.003
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author Shan, Jinshuai
Liu, Yang
Wang, Yukun
Li, Yimiao
Yu, Xiaochun
Wu, Chen
author_facet Shan, Jinshuai
Liu, Yang
Wang, Yukun
Li, Yimiao
Yu, Xiaochun
Wu, Chen
author_sort Shan, Jinshuai
collection PubMed
description GALNT14 is a member of N-acetylgalactosaminyltransferase enzyme family and mediates breast cancer cell development. Here, we find that GALNT14 regulates multidrug resistance (MDR) in breast cancer. The expression of GALNT14 is associated with MDR in breast cancer. Higher level of GALNT14 facilitates MCF-7 cells to resist Adriamycin, whereas knockdown of GALNT14 sensitizes cells to Adriamycin. Moreover, the expression of GALNT14 associates with the expression of P-gp, the efflux pump localized on the cell membrane, which could be the underlying mechanism of how GALNT14 induces MDR. In-depth analysis shows that GALNT14 regulates the stability of P-gp. Finally, GALNT14 associates with higher level of P-gp in chemotherapy-resistant human breast cancer tissues. Taken together, our studies reveal a molecular mechanism in breast cancer MDR.
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spelling pubmed-60580062018-07-26 GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()() Shan, Jinshuai Liu, Yang Wang, Yukun Li, Yimiao Yu, Xiaochun Wu, Chen Transl Oncol Original article GALNT14 is a member of N-acetylgalactosaminyltransferase enzyme family and mediates breast cancer cell development. Here, we find that GALNT14 regulates multidrug resistance (MDR) in breast cancer. The expression of GALNT14 is associated with MDR in breast cancer. Higher level of GALNT14 facilitates MCF-7 cells to resist Adriamycin, whereas knockdown of GALNT14 sensitizes cells to Adriamycin. Moreover, the expression of GALNT14 associates with the expression of P-gp, the efflux pump localized on the cell membrane, which could be the underlying mechanism of how GALNT14 induces MDR. In-depth analysis shows that GALNT14 regulates the stability of P-gp. Finally, GALNT14 associates with higher level of P-gp in chemotherapy-resistant human breast cancer tissues. Taken together, our studies reveal a molecular mechanism in breast cancer MDR. Neoplasia Press 2018-04-24 /pmc/articles/PMC6058006/ /pubmed/29702465 http://dx.doi.org/10.1016/j.tranon.2018.04.003 Text en © 2018 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original article
Shan, Jinshuai
Liu, Yang
Wang, Yukun
Li, Yimiao
Yu, Xiaochun
Wu, Chen
GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()
title GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()
title_full GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()
title_fullStr GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()
title_full_unstemmed GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()
title_short GALNT14 Involves the Regulation of Multidrug Resistance in Breast Cancer Cells()()
title_sort galnt14 involves the regulation of multidrug resistance in breast cancer cells()()
topic Original article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6058006/
https://www.ncbi.nlm.nih.gov/pubmed/29702465
http://dx.doi.org/10.1016/j.tranon.2018.04.003
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