ReviewPharmaceuticals (Basel, Switzerland)2011
Mechanisms of Resistance to Hsp90 Inhibitor Drugs: A Complex Mosaic Emerges.
Review in Pharmaceuticals (Basel, Switzerland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 52 citations in OpenAlex.
- Targeting heat shock protein 90 with usnic acid relieves immune suppression via aryl hydrocarbon receptor-mediated mechanisms in lung cancer.Molecular biomedicine · 2025Article
- Assessment of Hsp90β-selective inhibitor safety and on-target effects.Scientific reports · 2025Article
- Is theMicroorganisms · 2023Article
- Disruption of Proteostasis by Natural Products and Synthetic Compounds That Induce Pervasive Unfolding of Proteins: Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2023Article
- HSP90 inhibitors and cancer: Prospects for use in targeted therapies (Review).Oncology reports · 2023Review
- Preferential radiosensitization to glioblastoma cancer stem cell-like cells by a Hsp90 inhibitor, N-vinylpyrrolidone-AUY922.Oncology letters · 2022Article
- A novel C-terminal heat shock protein 90 inhibitor that overcomes STAT3-Wnt-β-catenin signaling-mediated drug resistance and adverse effects.Theranostics · 2022Article
- Virtual screening based identification of miltefosine and octenidine as inhibitors of heat shock protein 90.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Article
- Evodiamine inhibits both stem cell and non-stem-cell populations in human cancer cells by targeting heat shock protein 70.Theranostics · 2021Article
- Article
- A Brain-Penetrating Hsp90 Inhibitor NXD30001 Inhibits Glioblastoma as a Monotherapy or in Combination With Radiation.Frontiers in pharmacology · 2020Article
- Interplay between HSF1 and p53 signaling pathways in cancer initiation and progression: non-oncogene and oncogene addiction.Cellular oncology (Dordrecht, Netherlands) · 2019Review
- Novel Heat Shock Protein 90 Inhibitors Suppress P-Glycoprotein Activity and Overcome Multidrug Resistance in Cancer Cells.International journal of molecular sciences · 2019Article
- Nonsteroidal Anti-inflammatory Drugs Sensitize CD44-Overexpressing Cancer Cells to Hsp90 Inhibitor Through Autophagy Activation.Oncology research · 2019Article
- Design, Synthesis and Pharmacological Evaluation of Novel Hsp90N-terminal Inhibitors Without Induction of Heat Shock Response.ChemistryOpen · 2019Article
- Therapies targeting the signal pathways of pheochromocytoma and paraganglioma.OncoTargets and therapy · 2019Article
- Evaluation of [Theranostics · 2019Article
- HSP90 inhibition alters the chemotherapy-driven rearrangement of the oncogenic secretome.Oncogene · 2018Article
- Sensitization of multidrug-resistant cancer cells to Hsp90 inhibitors by NSAIDs-induced apoptotic and autophagic cell death.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular chaperone Hsp90 holds great promise as a cancer drug target, despite some of the initial clinical trials of Hsp90 inhibitor drugs having not lived up to expectation. Effective use of these drugs will benefit greatly from a much more detailed understanding of the factors that contribute to resistance, whether intrinsic or acquired. We review how cell culture studies have revealed a number of different mechanisms whereby cells can be rendered less susceptible to the effects of Hsp90 inhibitor treatment. A major influence is Hsp90 inhibition causing strong induction of the heat shock response, a stress response that increases cellular levels of prosurvival chaperones such as Hsp27 and Hsp70. Another problem seems to be that these inhibitors do not always access the Hsp90 proteins of the mitochondrion, forms of Hsp90 that-in cancer cells-are operating to suppress apoptosis. It should be possible to overcome these drawbacks through the appropriate drug redesign or with the combinatorial use of an Hsp90 inhibitor with a drug that targets either heat shock factor or the chaperone Hsp70. Still though, cells will often differ in the key antiapoptotic versus proapoptotic activities that are dependent on Hsp90, in the key steps in their apoptotic pathways responsive to Hsp90 inhibition or Hsp70 level, as well as the extents to which their survival is dependent on oncogenic tyrosine kinases that are clients of Hsp90. A systems approach will therefore often be required in order to establish the most prominent effects of Hsp90 inhibition in each type of cancer cell.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.