Brain type of creatine kinase induces doxorubicin resistance via TGF-β signaling in MDA-MB-231 breast cancer cells

Bibliographic Details
Title: Brain type of creatine kinase induces doxorubicin resistance via TGF-β signaling in MDA-MB-231 breast cancer cells
Authors: Seogho Son, Seung-ah Yoo, KeeSoo Nam, Sunhwa Oh, Kyung-min Lee, Jae Youn Yi, Incheol Shin
Source: Animal Cells and Systems, Vol 26, Iss 5, Pp 203-213 (2022)
Publisher Information: Taylor & Francis Group, 2022.
Publication Year: 2022
Collection: LCC:Medicine (General)
LCC:Biology (General)
Subject Terms: Apoptosis, brain type of creatine kinase (CKB), doxorubicin, MDA-MB-231, transforming growth factor-β (TGF-β), Medicine (General), R5-920, Biology (General), QH301-705.5
More Details: Brain type of creatine kinase (CKB) regulates energy homeostasis by reversibly transferring phosphate groups between phosphocreatine and ATP at sites of high energy demand. Several types of cancer cells exhibit upregulated CKB expression, but the function of CKB in cancer cells remains unclear. In this study, we investigated the function of CKB in breast cancer by overexpressing CKB in MDA-MB-231 cells. The overexpression of CKB did not affect cell growth rate, cell cycle distribution, ATP level or key mediators of aerobic glycolysis and lactate dehydrogenase isoform levels. Meanwhile, CKB overexpression did increase resistance to doxorubicin. TGF-β-induced Smad phosphorylation and Smad-dependent transcriptional activity were significantly up-regulated by CKB expression without changes in inhibitory Smad protein levels. Moreover, treatment with TGF-β considerably enhanced cell viability during doxorubicin treatment and decreased doxorubicin-induced apoptosis in CKB-expressing MDA-MB-231 cells compared to control cells. These results suggest that CKB attenuates doxorubicin-induced apoptosis and potentiates resistance to doxorubicin by enhancing TGF-β signaling in MDA-MB-231 cells.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 19768354
2151-2485
1976-8354
Relation: https://doaj.org/toc/1976-8354; https://doaj.org/toc/2151-2485
DOI: 10.1080/19768354.2022.2107070
Access URL: https://doaj.org/article/12819d0484a149a6ac75fd6c9a9818cd
Accession Number: edsdoj.12819d0484a149a6ac75fd6c9a9818cd
Database: Directory of Open Access Journals
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More Details
ISSN:19768354
21512485
DOI:10.1080/19768354.2022.2107070
Published in:Animal Cells and Systems
Language:English