A Novel Association between the Human Heat Shock Transcription Factor 1 (HSF1) and Prostate Adenocarcinoma

Hoang, Arthur T.; Huang, Jiapeng; Rudra-Ganguly, Nandini; Zheng, Jianping; Powell, William C.; Rabindran, Sridhar K.; Wu, Carl; Roy-Burman, Pradip

doi:10.1016/s0002-9440(10)64954-1

Cited by 140 publications

(113 citation statements)

References 34 publications

(35 reference statements)

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“…The heat shock element was present in the promoter region of many genes such as HSP90, HSP27, HSP70 and drug resistant gene MDR1 [21] . Hoang [22] recently reported HSF1 expression was increased in a prostate cancer cell line. Our study not only provided the first evidence to demonstrate the association of HSF1 gene expression and CRC, but also suggested that the induction of HSF1 gene expression might be associated with a broad range of cancer.…”

Section: Discussionmentioning

confidence: 99%

Induction of HSF1 expression is associated with sporadic colorectal cancer

Cen

Zheng²,

Fang³

et al. 2004

WJG

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AIM:To explore the activation of signal transduction pathways related with the carcinogenesis of sporadic colon cancers. METHODS:A gene array monitoring the activation of 8 signal transduction pathways (PathwayFinder GEArray) was used to screen the differentially expressed genes between colorectal cancer and normal colon tissues. The differentially expressed genes were further analyzed by RT-PCR, using RNA derived from colorectal cancer and normal colon tissue of 35 patients. RESULTS:The expression of HSF1, HSF27, HSP90 and iNOS was increased in colon cancer tissues compared to normal colon tissue using PathwayFinder GEArray. The RT-PCR results showed that the expression of HSF1 was increased in 86% (30/35) patients and the expression of iNOS was increased in 63% (22/35) patients. CONCLUSION:The induction of HSF1 gene expression is associated with sporadic colon cancer. HSF1 induces heat shock stress signaling pathway, which might play a role in the carcinogenesis of sporadic colorectal cancer.Cen H, Zheng S, Fang YM, Tang XP, Dong Q. Induction of HSF1 expression is associated with sporadic colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Induction of HSF1 expression is associated with sporadic colorectal cancer

Cen

Zheng²,

Fang³

et al. 2004

WJG

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“…Heat shock factor 1 is overexpressed in human prostate cancer cells. 61 Although there is no previous information on the expression of HSF-2 in the bladder, a recent report indicates that urothelial cells can respond to urine of IC patients with a modest alteration in a 72-kd stress protein. 36 It has been shown that heat shock proteins and stress can reduce the inflammatory response.…”

Section: Heat Shock Transcription Factormentioning

confidence: 99%

Gene Expression Profiling of Mouse Bladder Inflammatory Responses to LPS, Substance P, and Antigen-Stimulation

Saban

Nguyen

Hammond

et al. 2002

The American Journal of Pathology

110

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Inflammatory bladder disorders such as interstitial cystitis (IC) deserve attention since a major problem of the disease is diagnosis. IC affects millions of women and isClinical and animal models of acute and chronic urinary bladder inflammation have provided several lines of evidence suggesting a central role of mast cells, sensory nerves, and neurokinin (NK)-1 receptors. Fundamental work regarding the participation of sensory nerves and mast cells in cystitis provides indirect evidence, such as increased numbers of mast cells in the detrusor and submucosa, and morphological evidence of mast cell activation and degranulation. [1][2][3][4] In addition, the extensive tissue remodeling seen in some clinical forms of bladder inflammation such as interstitial cystitis, 4 along with increased urinary levels of histamine and tryptase 5 suggest a role for mast cells. Because both mast cells 6 -8 and NK-1 receptors are increased in bladder biopsies of interstitial cystitis (IC) patients, 9,10 it is tempting to propose a role for sensory peptides-mast cell communication in the pathogenesis of this disorder.Experimentally, we have used classical morphometric analysis and microarray technology to determine the role of mast cells, NK-1 receptors, and bacterial toxins in animal models of cystitis. Time-course experiments indicated early and late genes involved in bladder inflammatory responses. 11 The availability of mice genetically deficient in neurokinin-1 receptor (NK-1R Ϫ/Ϫ ) allowed us to propose a mandatory role of SP receptors in cystitis. 12 We also determined genes that depend on the presence of tissue mast cells for their expression by comparing inflammatory responses in mast cell-deficient (Kit W /

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“…Homology between the amino-acid sequences of human HSFs is only 30-40%, and evidence for specific functions of HSFs beyond heat-shock response is speculative. Many types of tumors contain high concentrations of HSPs of the HSP27, HSP70 and HSP90 families (Hoang et al, 2000;Cen et al, 2004). The roles of HSPs in tumor development may also be related to their functions in the development of tolerance to applied stress (Li and Werb, 1982).…”

Section: Introductionmentioning

confidence: 99%

A novel function for HSF1-induced mitotic exit failure and genomic instability through direct interaction between HSF1 and Cdc20

Lee

et al. 2007

Oncogene

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Although heat-shock factor (HSF) 1 is a known transcriptional factor of heat-shock proteins, other pathways like production of aneuploidy and increased protein stability of cyclin B1 have been proposed. In the present study, the regulatory domain of HSF1 (amino-acid sequence 212-380) was found to interact directly with the amino-acid sequence 106-171 of Cdc20. The association between HSF1 and Cdc20 inhibited the interaction between Cdc27 and Cdc20, the phosphorylation of Cdc27 and the ubiquitination activity of anaphase-promoting complex (APC). The overexpression of HSF1 inhibited mitotic exit and the degradations of cyclin B1 and securin, which resulted in production of aneuploidy and multinucleated cells, but regulatory domain-deficient HSF1 did not. Moreover, HSF1-overexpressing cells showed elevated levels of micronuclei and genomic alteration. The depletion of HSF1 from cells highly expressing HSF1 reduced nocodazole-mediated aneuploidy in cells. These findings suggest a novel function of HSF1 frequently overexpressed in cancer cells, to inhibit APC/C activity by interacting with Cdc20, and to result in aneuploidy development and genomic instability.

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A Novel Association between the Human Heat Shock Transcription Factor 1 (HSF1) and Prostate Adenocarcinoma

Cited by 140 publications

References 34 publications

Induction of HSF1 expression is associated with sporadic colorectal cancer

Induction of HSF1 expression is associated with sporadic colorectal cancer

Gene Expression Profiling of Mouse Bladder Inflammatory Responses to LPS, Substance P, and Antigen-Stimulation

A novel function for HSF1-induced mitotic exit failure and genomic instability through direct interaction between HSF1 and Cdc20

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