To dampen proteotoxic stresses and maintain protein homeostasis, organisms possess a stress-responsive molecular machinery that detects and neutralizes protein damage. A prominent feature of stressed cells is the increased synthesis of heat shock proteins (Hsps) that aid in the refolding of misfolded peptides and restrain protein aggregation. Transcriptional activation of the heat shock response is orchestrated by heat shock factor 1 (HSF1), which rapidly translocates to hsp genes and induces their expression. Although the role of HSF1 in protecting cells and organisms against severe stress insults is well established, many aspects of how HSF1 senses qualitatively and quantitatively different forms of stresses have remained poorly understood. Moreover, recent discoveries that HSF1 controls life span have prompted new ways of thinking about an old transcription factor. Here, we review the established role of HSF1 in counteracting cell stress and prospect the role of HSF1 as a regulator of disease states and aging.

Regulation of HSF1 Function in the Heat Stress Response: Implications in Aging and Disease

HSF1 Drives a Transcriptional Program Distinct from Heat Shock to Support Highly Malignant Human Cancers

Stress, inflammation, and defense of homeostasis.

Invited review: genes involved in the bovine heat stress response.

The Warburg effect describes the increased utilization of glycolysis rather than oxidative phosphorylation by tumour cells for their energy requirements under physiological oxygen conditions. This effect has been the basis for much speculation on the survival advantage of tumour cells, tumourigenesis and the microenvironment of tumours. More recently, studies have begun to reveal how the Warburg effect could influence drug efficacy and how our understanding of tumour energetics could be exploited to improve drug development. In particular, evidence is emerging demonstrating how better modelling of the tumour metabolic microenvironment could lead to a better prediction of drug efficacy and the identification of new combination strategies. This review will provide details of the current understanding of the complex interplay between glucose metabolism and pharmacology and discuss opportunities for utilizing the Warburg effect in future drug development.

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/bph.13422

The Warburg effect and drug resistance

Although HSF1 plays an important role in the cellular response to proteotoxic stressors, little is known about the structure and function of the human HSF1 signaling network under both stressed and unstressed conditions. In this study, we used a combination of chromatin immunoprecipitation microarray analysis and time course gene expression microarray analysis with and without siRNA-mediated inhibition of HSF1 to comprehensively identify genes regulated directly and indirectly by HSF1. The correlation between promoter binding and gene expression was not significant for all genes bound by HSF1, suggesting that HSF1 binding per se is not sufficient for expression. However, the correlation with promoter binding was significant for genes identified as HSF1-regulated following siRNA knockdown. Among promoters bound by HSF1 following heat shock, a gene ontology analysis showed significant enrichment only in categories related to protein folding. In contrast, analysis of the extended HSF1 signaling network following siRNA knockdown showed enrichment in a variety of categories related to protein folding, anti-apoptosis, RNA splicing, ubiquitinylation and others, highlighting a complex transcriptional program regulated directly and indirectly by HSF1.

Genome-wide analysis of human HSF1 signaling reveals a transcriptional program linked to cellular adaptation and survival

A Comparison of Transcriptomic and Metabonomic Technologies for Identifying Biomarkers Predictive of Two-Year Rodent Cancer Bioassays

The nasal epithelium is an important target site for chemically induced toxicity and carcinogenicity. Experimental studies show that site-specific lesions can arise within the nasal respiratory or olfactory epithelium following the inhalation of certain chemicals. Moreover, gender differences in epithelial response are also reported. To better understand and predict gender differences in response of the nasal epithelium to inhaled xenobiotics, gene expression profiles from naive male and female Sprague-Dawley rats were constructed. Epithelial cells were manually collected from the nasal septum, naso- and maxillo-turbinates, and ethmoid turbinates of nine male and nine female rats. Gene expression analysis was performed using the Affymetrix Rat Genome 430 2.0 microarray. Surprisingly, there were few gender differences in gene expression. Gene ontology enrichment analysis identified several functional categories, including xenobiotic metabolism, cell cycle, apoptosis, and ion channel/transport, with significantly different expression between tissue types. These baseline data will contribute to our understanding of the normal physiology and selectivity of the nasal epithelial cells’ response to inhaled environmental toxicants.

Basal Gene Expression in Male and Female Sprague-Dawley Rat Nasal Respiratory and Olfactory Epithelium

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Genome-wide analysis of human HSF1 signaling reveals a transcriptional program linked to cellular adaptation and survival

A Comparison of Transcriptomic and Metabonomic Technologies for Identifying Biomarkers Predictive of Two-Year Rodent Cancer Bioassays

Basal Gene Expression in Male and Female Sprague-Dawley Rat Nasal Respiratory and Olfactory Epithelium