Journal
ARCHIVES OF TOXICOLOGY
Volume 87, Issue 1, Pages 19-48Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00204-012-0918-z
Keywords
Heat shock proteins; Heat shock factor; Cancer; Carcinogenesis; Drug resistance; Apoptosis; Metastasis; Prognosis
Categories
Funding
- NIH [RO-1CA047407, R0-1CA119045, RO-1CA094397]
- DRC: Agencia Nacional de Promocion Cientifica y Tecnologica [PICT 1047]
- CONICET [PIP 2428]
- Argentina Foundation for Cancer Research
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Heat shock proteins (HSP) are a subset of the molecular chaperones, best known for their rapid and abundant induction by stress. HSP genes are activated at the transcriptional level by heat shock transcription factor 1 (HSF1). During the progression of many types of cancer, this heat shock transcriptional regulon becomes co-opted by mechanisms that are currently unclear, although evidently triggered in the emerging tumor cell. Concerted activation of HSF1 and the accumulation of HSPs then participate in many of the traits that permit the malignant phenotype. Thus, cancers of many histologies exhibit activated HSF1 and increased HSP levels that may help to deter tumor suppression and evade therapy in the clinic. We review here the extensive work that has been carried out and is still in progress aimed at (1) understanding the oncogenic mechanisms by which HSP genes are switched on, (2) determining the roles of HSF1/HSP in malignant transformation and (3) discovering approaches to therapy based on disrupting the influence of the HSF1-controlled transcriptome in cancer.
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