HSF1 is an essential factor in the acute response to proteotoxic stress, in which it causes rapid
transcription of heat shock protein (HSP) genes in order to permit survival of cells and restoration of global
protein quality. In addition to this property however, HSF1 is chronically activated or overexpressed in a wide
range of cancers and is essential for multiple pathways of malignant transformation. Studies in recent years
indicate a remarkable pleiotropy in the properties of HSF1 in cancer. HSF1 functions as a transcription factor
for HSP genes, reminiscent of its role in the stress response, and the resultant elevation in HSP levels leads to
a reduction in programmed cell death and senescence and permits overexpression of mutated oncogenic
protein clients required to fuel tumor growth. In addition HSF1 plays a role as a signal modulator, stimulating
kinase activity, regulating energy metabolism and permitting the development of polyploidy in cancer cells.
HSF1 can also function as an inhibitor of transcription and in cooperation with NuRD family factors can repress
genes that oppose metastasis. Inhibitors of HSF1 are undergoing selection and future studies may see the
testing of HSF1 as a target in cancer therapy.
Keywords: Cancer growth metastasis, heat shock factor, stress, proteome, mutations, aggregation, conformations, central nervous system, protein folding, transcription factor, genes, RNA polymerase, translation elongation factor, posttranslational, chaperone
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