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Int. J. Mol. Sci. 2017, 18(2), 468; doi:10.3390/ijms18020468

Heat Shock Factor 1 Depletion Sensitizes A172 Glioblastoma Cells to Temozolomide via Suppression of Cancer Stem Cell-Like Properties

1,2,3,* , 1,2
and
1,2,3,*
1
Department of Biochemistry, The Catholic University of Korea, Seoul 06591, Korea
2
Institute for Aging and Metabolic Diseases, The Catholic University of Korea, Seoul 06591, Korea
3
Cancer Evolution Research Center, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
*
Authors to whom correspondence should be addressed.
Academic Editors: Hiroyuki Tomita, Masahito Shimizu and Takuji Tanaka
Received: 24 December 2016 / Revised: 15 February 2017 / Accepted: 17 February 2017 / Published: 22 February 2017
(This article belongs to the Special Issue Cancer Stem Cells)
View Full-Text   |   Download PDF [3970 KB, uploaded 22 February 2017]   |  

Abstract

Heat shock factor 1 (HSF1), a transcription factor activated by various stressors, regulates proliferation and apoptosis by inducing expression of target genes, such as heat shock proteins and Bcl-2 (B-cell lymphoma 2) interacting cell death suppressor (BIS). HSF1 also directly interacts with BIS, although it is still unclear whether this interaction is critical in the regulation of glioblastoma stem cells (GSCs). In this study, we examined whether small interfering RNA-mediated BIS knockdown decreased protein levels of HSF1 and subsequent nuclear localization under GSC-like sphere (SP)-forming conditions. Consistent with BIS depletion, HSF1 knockdown also reduced sex determining region Y (SRY)-box 2 (SOX2) expression, a marker of stemness, accompanying the decrease in SP-forming ability and matrix metalloprotease 2 (MMP2) activity. When HSF1 or BIS knockdown was combined with temozolomide (TMZ) treatment, a standard drug used in glioblastoma therapy, apoptosis increased, as measured by an increase in poly (ADP-ribose) polymerase (PARP) cleavage, whereas cancer stem-like properties, such as colony-forming activity and SOX2 protein expression, decreased. Taken together, our findings suggest that targeting BIS or HSF1 could be a viable therapeutic strategy for GSCs resistant to conventional TMZ treatment. View Full-Text
Keywords: BIS; HSF1; glioblastoma; temozolomide; apoptosis BIS; HSF1; glioblastoma; temozolomide; apoptosis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Im, C.-N.; Yun, H.H.; Lee, J.-H. Heat Shock Factor 1 Depletion Sensitizes A172 Glioblastoma Cells to Temozolomide via Suppression of Cancer Stem Cell-Like Properties. Int. J. Mol. Sci. 2017, 18, 468.

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