Heat shock transcription factors and sensory placode development

Nakai, Asami

doi:10.5483/bmbrep.2009.42.10.631

Cited by 18 publications

(17 citation statements)

References 58 publications

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“…In contrast, HSF1 also induces cell death by upregulating proapoptotic genes in response to stress [22][23][24]. Furthermore, HSFs play critical roles in developmental processes such as gametogenesis and neurogenesis, in the maintenance of sensory organs and ciliated tissues, and in immune responses [25,26]. It has long been established that Hsp levels increase in a wide range of tumor types [27][28][29].…”

Section: Introductionmentioning

confidence: 90%

Silencing HSF1 by short hairpin RNA decreases cell proliferation and enhances sensitivity to hyperthermia in human melanoma cell lines

Nakamura

Fujimoto

Hayashida

et al. 2010

Journal of Dermatological Science

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Section: Introductionmentioning

confidence: 90%

Silencing HSF1 by short hairpin RNA decreases cell proliferation and enhances sensitivity to hyperthermia in human melanoma cell lines

Nakamura

Fujimoto

Hayashida

et al. 2010

Journal of Dermatological Science

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“…Mainly expressed in the human heart, brain, skeletal muscle, and pancreas [56], HSF4 has been shown to be required for the development and maintenance of sensory organs [5,57,58]. During this process, HSF4 either cooperates or competes with HSF1 for common target genes, including members of the Fibroblast Growth Factor (FGF) family, in a cell-specific manner in lens and olfactory epithelium [45,59].…”

Section: Hsf Structure Expression and Functionmentioning

confidence: 99%

Implication of Heat Shock Factors in Tumorigenesis: Therapeutical Potential

Thonel

Mezger

Garrido

2011

Cancers

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Heat Shock Factors (HSF) form a family of transcription factors (four in mammals) which were named according to the discovery of their activation by a heat shock. HSFs trigger the expression of genes encoding Heat Shock Proteins (HSPs) that function as molecular chaperones, contributing to establish a cytoprotective state to various proteotoxic stresses and in pathological conditions. Increasing evidence indicates that this ancient transcriptional protective program acts genome-widely and performs unexpected functions in the absence of experimentally defined stress. Indeed, HSFs are able to re-shape cellular pathways controlling longevity, growth, metabolism and development. The most well studied HSF, HSF1, has been found at elevated levels in tumors with high metastatic potential and is associated with poor prognosis. This is partly explained by the above-mentioned cytoprotective (HSP-dependent) function that may enable cancer cells to adapt to the initial oncogenic stress and to support malignant transformation. Nevertheless, HSF1 operates as major multifaceted enhancers of tumorigenesis through, not only the induction of classical heat shock genes, but also of “non-classical” targets. Indeed, in cancer cells, HSF1 regulates genes involved in core cellular functions including proliferation, survival, migration, protein synthesis, signal transduction, and glucose metabolism, making HSF1 a very attractive target in cancer therapy. In this review, we describe the different physiological roles of HSFs as well as the recent discoveries in term of non-cogenic potential of these HSFs, more specifically associated to the activation of “non-classical” HSF target genes. We also present an update on the compounds with potent HSF1-modulating activity of potential interest as anti-cancer therapeutic agents.

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“…7,19 Subsequently, disruption of the HSF1 gene was shown to result in altered expression of HSP and non-HSP genes in the tissues and to be required for development and maintenance, 20,21 suggesting that HSF1 regulates gene expression in unstressed cells. We found that HSF1 binds to the promoter of the NFATc2 gene in unstressed MEF cells and its expression is markedly reduced in HSF1-null cells.…”

Section: Non-hsp Proteostasis Pathwaysmentioning

confidence: 99%