ArticleCell stress & chaperones2015
Effects of temozolomide (TMZ) on the expression and interaction of heat shock proteins (HSPs) and DNA repair proteins in human malignant glioma cells.
Article in Cell stress & chaperones, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- Synthesis and characterization of chitosan-functionalized nanostructured lipid carriers with temozolomide: cytotoxic effects and chromosomal instability in human glioblastoma cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Therapeutic Potential ofInternational journal of general medicine · 2026Article
- Defining treatment-resistant brain cancer: Genetic screening to identify oncogene-driven immunomodulation and therapy resistance.Cancer gene therapy · 2026Review
- Evaluation of (Z)-endoxifen as a potential therapy for glioblastoma multiforme through computational and experimental analyses.Scientific reports · 2025Article
- Chrysin sensitizes glioblastoma cells and spheroids to temozolomide treatment by reducing EMT and stemness phenotypes, as well as targeting multidrug resistance proteins.Frontiers in pharmacology · 2025Article
- Review
- Targeting Retinaldehyde Dehydrogenases to Enhance Temozolomide Therapy in Glioblastoma.International journal of molecular sciences · 2024Article
- Temozolomide promotes matrix metalloproteinase 9 expression through p38 MAPK and JNK pathways in glioblastoma cells.Scientific reports · 2024Article
- The antagonistic effects of temozolomide and trichostatin a combination on MGMT and DNA mismatch repair pathways in Glioblastoma.Medical oncology (Northwood, London, England) · 2023Article
- A Novel and Highly Selective Epidermal Growth Factor Receptor Inhibitor, SMUZ106, for the Treatment of Glioblastoma.Pharmaceutics · 2023Article
- Targeting Heat Shock Proteins in Malignant Brain Tumors: From Basic Research to Clinical Trials.Cancers · 2022Review
- Temozolomide increases heat shock proteins in extracellular vesicles released from glioblastoma cells.Molecular biology reports · 2022Article
- The Risk of Heart Disease-Related Death Among Anaplastic Astrocytoma Patients After Chemotherapy: A SEER Population-Based Analysis.Frontiers in oncology · 2022Article
- Forkhead box O1 targeting replication factor C subunit 2 expression promotes glioma temozolomide resistance and survival.Annals of translational medicine · 2021Article
- Tumor treating fields (TTFields) impairs aberrant glycolysis in glioblastoma as evaluated by [Neoplasia (New York, N.Y.) · 2021Article
- Inhibition of the de novo pyrimidine biosynthesis pathway limits ribosomal RNA transcription causing nucleolar stress in glioblastoma cells.PLoS genetics · 2020Article
- Combination therapy of cold atmospheric plasma (CAP) with temozolomide in the treatment of U87MG glioblastoma cells.Scientific reports · 2020Article
- Heat-shock proteins: chaperoning DNA repair.Oncogene · 2020Review
- PAXX Participates in Base Excision Repair via Interacting with Pol β and Contributes to TMZ Resistance in Glioma Cells.Journal of molecular neuroscience : MN · 2018Article
- Phosphorylated Hsp27 is mutually exclusive with ATRX loss and the IDH1Journal of clinical pathology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported the association of HSPA1A and HSPB1 with high-grade astrocytomas, suggesting that these proteins might be involved in disease outcome and response to treatment. With the aim to better understand the resistance/susceptibility processes associated to temozolomide (TMZ) treatment, the current study was performed in three human malignant glioma cell lines by focusing on several levels: (a) apoptotic index and senescence, (b) DNA damage, and (c) interaction of HSPB1 with players of the DNA damage response. Three human glioma cell lines, Gli36, U87, and DBTRG, were treated with TMZ evaluating cell viability and survival, apoptosis, senescence, and comets (comet assay). The expression of HSPA (HSPA1A and HSPA8), HSPB1, O6-methylguanine-DNA methyltransferase (MGMT), MLH1, and MSH2 was determined by immunocytochemistry, immunofluorescence, and Western blot. Immunoprecipitation was used to analyze protein interaction. The cell lines exhibited differences in viability, apoptosis, and senescence after TMZ administration. We then focused on Gli36 cells (relatively unstudied) which showed very low recovery capacity following TMZ treatment, and this was related to high DNA damage levels; however, the cells maintained their viability. In these cells, MGMT, MSH2, HSPA, and HSPB1 levels increased significantly after TMZ administration. In addition, MSH2 and HSPB1 proteins appeared co-localized by confocal microscopy. This co-localization increased after TMZ treatment, and in immunoprecipitation analysis, MSH2 and HSPB1 appeared interacting. In contrast, HSPB1 did not interact with MGMT. We show in glioma cells the biological effects of TMZ and how this drug affects the expression levels of heat shock proteins (HSPs), MGMT, MSH2, and MLH1. In Gli36 cells, the results suggest that interactions between HSPB1 and MSH2, including co-nuclear localization, may be important in determining cell sensitivity to TMZ.
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