ArticleInternational journal of molecular sciences2017
Heat Shock Factor 1 Depletion Sensitizes A172 Glioblastoma Cells to Temozolomide via Suppression of Cancer Stem Cell-Like Properties.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Identification of a cancer stem cell-like subpopulation that promotes HCC metastasis.JHEP reports : innovation in hepatology · 2025Article
- MDK induces temozolomide resistance in glioblastoma by promoting cancer stem-like properties.American journal of cancer research · 2022Article
- Heat shock factor 1 in brain tumors: a link with transient receptor potential channels TRPV1 and TRPA1.Journal of molecular histology · 2021Article
- Mebendazole Mediates Proteasomal Degradation of GLI Transcription Factors in Acute Myeloid Leukemia.International journal of molecular sciences · 2021Article
- Inhibition of the Heat Shock Protein A (HSPA) Family Potentiates the Anticancer Effects of Manumycin A.Cells · 2021Article
- Review
- HSF1 as a Cancer Biomarker and Therapeutic Target.Current cancer drug targets · 2019Review
- PLK1 inhibitor facilitates the suppressing effect of temozolomide on human brain glioma stem cells.Journal of cellular and molecular medicine · 2018Article
- Effect of BIS depletion on HSF1-dependent transcriptional activation in A549 non-small cell lung cancer cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2018Article
- Silencing of BAG3 inhibits the epithelial-mesenchymal transition in human cervical cancer.Oncotarget · 2017Article
- Combination Treatment with PPARBioMed research international · 2017Article
- BAG3 regulates cilia homeostasis of glioblastoma via its WW domain.BioFactors (Oxford, England)Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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