Common gene expression patterns responsive to mild temperature hyperthermia in normal human fibroblastic cells

Tabuchi, Yoshiaki; Furusawa, Yukihiro; Kariya, Ayako; Wada, Shigehito; Ohtsuka, Kenzo; Kondo, Takashi

doi:10.3109/02656736.2012.753163

Cited by 12 publications

(15 citation statements)

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“…By contrast, several genes that were upregulated or downregulated by ≥1.5-fold were identified in both cancer cell lines following exposure to MHT. These results were comparable to those from previous studies on MHT conditions using cancer or normal cell lines (17,(23)(24)(25)(26)(27). Previous studies have indicated that heat induces a significant decrease in mRNA and protein synthesis in order to increase the transcription of heat-responsive genes, such as HSPs, and that this overall reprogramming of gene expression permits the selective synthesis of HSPs (31,32).…”

Section: Discussionsupporting

confidence: 89%

“…That is, cancer cells exposed to temperatures >42.5˚C undergo cell death; however, the exposure of cells to a temperature of up to 42.5˚C induces little or no cytotoxicity (2). In the present study, the exposure of HeLa and HSC-3 human SCC cells to MHT at 41˚C, below the inflection point, did not affect cell viability or the cell cycle, as has also been shown in our previous studies (24)(25)(26)(27). By contrast, several genes that were upregulated or downregulated by ≥1.5-fold were identified in both cancer cell lines following exposure to MHT.…”

Section: Discussionsupporting

confidence: 86%

“…Gene network A included several HSPs, as well as BAG3, and was specifically associated with the biological functions of cellular function and maintenance. Several microarray studies have demonstrated that the induction of HSPs is a common response to heat stress with or without cell death (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27). HSPs protect cells both by limiting the effects of protein-damaging agents through protein chaperoning and refolding and by directly blocking the pathway of cell death, such as apoptosis or necrosis (12).…”

Section: Discussionmentioning

confidence: 99%

“…To this end, a number of studies have found that the most effective approach for investigating heat responses is to use global-scale microarrays and bioinformatics tools. Several genes and biological functions in a wide variety of cell types affected by heat stress have thus been reported (15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25)(26)(27).…”

Section: Introductionmentioning

confidence: 99%

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Identification of common gene networks responsive to mild hyperthermia in human cancer cells

Kariya

Tabuchi

Yunoki

et al. 2013

International Journal of Molecular Medicine

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Hyperthermia (HT) has been used as a possible treatment modality for various types of malignant tumors. Due to its pleiotropic effects, its combined use with radiotherapy and/or chemotherapy has proven to be beneficial. However, the molecular mechanisms underling the cellular responses to heat stress remain unclear. Therefore, the aim of this study was to identify common gene expression patterns responsive to mild HT (MHT) in human cancer cells. HeLa human cervical squamous cell carcinoma (SCC) and HSC-3 human oral SCC cells were exposed to MHT at 41˚C for 30 min, followed by culture at 37˚C for 0-24 h. MHT did not affect cell viability or the cell cycle. GeneChip microarray analysis clearly revealed that many probe sets were differentially expressed by a factor of ≥1.5 in both cell lines following exposure to MHT. Of the many differentially expressed probe sets, 114 genes were found to be commonly upregulated in both HeLa and HSC‑3 cells, and two significant gene networks were obtained from the commonly upregulated genes. Gene network A included several heat shock proteins, as well as BCL2-associated athanogene 3 (BAG3), and was found to be mainly associated with the biological functions of cellular function and maintenance. Gene network B included several anti-cell death genes, such as early growth response 1 (EGR1) and endothelin 1 (EDN1) and was found to be associated with the biological functions of cell death and survival. Real‑time quantitative polymerase chain reaction demonstrated that the gene expression patterns of the 12 genes selected were consistent with the microarray data in four cancer cell lines. These findings may provide further insight into the detailed molecular mechanisms of the MHT response in cancer cells.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Identification of common gene networks responsive to mild hyperthermia in human cancer cells

Kariya

Tabuchi

Yunoki

et al. 2013

International Journal of Molecular Medicine

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“…In mammalian cells, heat activates the transcription of heat responsive genes, including HSPs, coincident with a bulk decrease in mRNA and protein syntheses, and this overall reprogramming of gene expression permits the selective synthesis of HSPs (40)(41)(42). In our previous studies using global-scale microarrays, we also detected a number of genes that were downregulated and participated in biological functions, including post-transcriptional modification and gene expression (43)(44)(45). This bulk decrease has been considered to represent a form of transcriptional suppression due to the binding of activated HSF1 to the promoter region of the gene (40).…”

Section: Function Of Hsf1mentioning

confidence: 99%

Targeting heat shock transcription factor 1 for novel hyperthermia therapy

Tabuchi

Kondo

2013

International Journal of Molecular Medicine

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Abstract. Hyperthermia (HT) has shown promising antitumor effects against various types of malignant tumors, and its pleiotropic effects support its combined use with radiotherapy and/or chemotherapy. However, HT is rendered less effective by the acquisition of thermoresistance in tumors, which arises through the elevation of heat shock proteins (HSPs) or other tumor responses. In mammals, the induction of HSPs is principally regulated at the transcriptional level by the activation of heat shock transcription factor 1 (HSF1). This transactivator has been shown to be abundantly expressed in a wide variety of tumors in humans. In addition, HSF1 participates in the initiation, proliferation and maintenance of tumors. Of note, HSF1 silencing has been shown to prevent the progression of tumors and to enhance their sensitivity to HT. Here, we review the physiological and pathological roles of HSF1 in cancer cells, and discuss its potential as a therapeutic target for HT therapy. Contents1. Introduction 2. Function of HSF1 3. HSF1 and cancer 4. HSF1 and hyperthermia 5. Discussion IntroductionHyperthermia (HT) is considered to have potential as a cancer treatment modality (1). HT in combination with radiotherapy and/or chemotherapy has been used for various types of cancer, and the anticancer effects of such combinations have been verified in many clinical trials (1-7). One of the problems with HT therapy is the acquisition of thermoresistance against heat stress (8-12). In general, cells have protective functions for various stressors that occur from outside of the cell. Heat shock proteins (HSPs), molecular chaperones with strong cytoprotective and antiapoptotic properties, are induced by a wide variety of stresses, particularly heat stress (13-16); they are also induced by treatment with HT, and, thus, it has been considered that HSPs play a role in the acquisition of thermoresistance in cells (10-12). In mammals, the expression of HSPs is mainly regulated by heat shock transcription factor 1 (HSF1) (17,18). Elevation of HSF1 has been observed in several types of human tumor tissues (19-26), and it has been shown to participate in the initiation, proliferation and maintenance of tumors (12,(25)(26)(27)(28)(29). Notably, both inhibition of the expression of HSF1 and the functional loss of HSF1 have been suggested to enhance the sensitivity to HT under basic experimental conditions (29)(30)(31)(32)(33)(34)(35)(36)(37)(38). In the present review, the physiological and pathological roles of HSF1 in cancer cells are summarized, and the potential of HSF1 as a therapeutic target for HT therapy is discussed. Function of HSF1The heat-shock response, which is a universal cellular response to heat, is a critical cellular event for cell adaptation. Heat stress elicits a wide spectrum of stress responses, including an induction of HSPs, protein aggregation, an imbalance of protein homeostasis, DNA and RNA damage, reactive oxygen species production, cell growth arrest and cell death in mammalian cells. HSPs are characterized as mo...

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Effect of heat stress on DNA damage: a systematic literature review

et al. 2022

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Common gene expression patterns responsive to mild temperature hyperthermia in normal human fibroblastic cells

Abstract: Common genes that were differentially expressed and/or acted within a gene network in response to MHT in NHF cells were identified. These findings provide the molecular basis for a further understanding of the mechanisms of the MHT response in NHF cells.

Cited by 12 publications

References 50 publications

Identification of common gene networks responsive to mild hyperthermia in human cancer cells

Identification of common gene networks responsive to mild hyperthermia in human cancer cells

Targeting heat shock transcription factor 1 for novel hyperthermia therapy

Effect of heat stress on DNA damage: a systematic literature review

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