HSF1: Primary Factor in Molecular Chaperone Expression and a Major Contributor to Cancer Morbidity

Heat shock factor 1 (HSF1) is the primary component for initiation of the powerful heat shock response (HSR) in eukaryotes. The HSR is an evolutionarily conserved mechanism for responding to proteotoxic stress and involves the rapid expression of heat shock protein (HSP) molecular chaperones that pr...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2020-04, Vol.9 (4), p.1046
Main Authors: Prince, Thomas L, Lang, Benjamin J, Guerrero-Gimenez, Martin E, Fernandez-Muñoz, Juan Manuel, Ackerman, Andrew, Calderwood, Stuart K
Format: Article
Language:English
Subjects:
Animals
Binding sites
Breast cancer
Cancer
Cell cycle
Cell Transformation, Neoplastic - metabolism
Cell Transformation, Neoplastic - pathology
Cell viability
Chaperones
Deoxyribonucleic acid
DNA
Gene expression
Gene regulation
heat shock factor 1
Heat shock factors
Heat shock proteins
Heat Shock Transcription Factors - genetics
Heat Shock Transcription Factors - metabolism
HSF1
HSF1 protein
HSPs
Humans
Metastases
Metastasis
molecular chaperones
Molecular Chaperones - genetics
Molecular Chaperones - metabolism
Molecular Targeted Therapy
Morbidity
Neoplasms - epidemiology
Neoplasms - genetics
Neoplasms - metabolism
Proteins
Review
Roles
Therapeutic applications
Tumorigenesis
Tumors
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Summary:Heat shock factor 1 (HSF1) is the primary component for initiation of the powerful heat shock response (HSR) in eukaryotes. The HSR is an evolutionarily conserved mechanism for responding to proteotoxic stress and involves the rapid expression of heat shock protein (HSP) molecular chaperones that promote cell viability by facilitating proteostasis. HSF1 activity is amplified in many tumor contexts in a manner that resembles a chronic state of stress, characterized by high levels of gene expression as well as HSF1-mediated non- gene regulation. HSF1 and its gene targets are essential for tumorigenesis across several experimental tumor models, and facilitate metastatic and resistant properties within cancer cells. Recent studies have suggested the significant potential of HSF1 as a therapeutic target and have motivated research efforts to understand the mechanisms of HSF1 regulation and develop methods for pharmacological intervention. We review what is currently known regarding the contribution of HSF1 activity to cancer pathology, its regulation and expression across human cancers, and strategies to target HSF1 for cancer therapy.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells9041046