Gene networks involved in apoptosis induced by hyperthermia in human lymphoma U937 cells

Furusawa, Yukihiro; Tabuchi, Yoshiaki; Takasaki, Ichiro; Wada, Shigehito; Ohtsuka, Kenzo; Kondo, Takashi

doi:10.1016/j.cellbi.2009.08.009

Cited by 24 publications

(21 citation statements)

References 44 publications

(68 reference statements)

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“…The PCR amplification was analyzed by real-time PCR. The detailed conditions of PCR were described in our previous study [31]. The annealing temperature of RANK, RANKL, and -actin was 60 °C.…”

Section: Expression Analyses Of Rank and Rankl Mrnas In Fugu Pth1 (1-mentioning

confidence: 99%

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Parathyroid hormone 1 (1–34) acts on the scales and involves calcium metabolism in goldfish

Suzuki

Danks

Maruyama

et al. 2011

Bone

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The effect of fugu parathyroid hormone 1 (fugu PTH1) on osteoblasts and osteoclasts in teleosts was examined with an assay system using teleost scale and the following markers: alkaline phosphatase (ALP) for osteoblasts and tartrate-resistant acid phosphatase (TRAP) for osteoclasts. Synthetic fugu PTH1 (1-34) (100 pg/ml to 10 ng/ml) significantly increased ALP activity at 6 h of incubation. High-dose (10 ng/ml) fugu PTH1 significantly increased ALP activity even after 18 h of incubation. In the case of TRAP activity, fugu PTH1 did not change at 6 h of incubation, but fugu PTH1 (100 pg/ml to 10 ng/ml) significantly increased TRAP activity at 18 h. Similar results were obtained for human PTH (1-34), but there was an even greater response with fugu PTH1 than with human PTH. In vitro, we demonstrated that both the receptor activator of the NF-B ligand in osteoblasts and the receptor activator NF-B mRNA expression in osteoclasts increased significantly by fugu PTH1 treatment. In an in vivo experiment, fugu PTH1 induced hypercalcemia resulted from the increase of both osteoblastic and osteoclastic activities in the scale as well as the decrease of scale calcium contents after fugu PTH1 injection. In addition, an in vitro experiment with intramuscular autotransplanted scale indicated that the ratio of multinucleated osteoclasts/mononucleated osteoclasts in PTH-treated scales was significantly higher than that in the control scales. Thus, we concluded that PTH acts on osteoblasts and osteoclasts in the scales and regulates calcium metabolism in goldfish.3

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Section: Expression Analyses Of Rank and Rankl Mrnas In Fugu Pth1 (1-mentioning

confidence: 99%

“…The annealing temperature of PTH1R and PTH2R was 60 °C. The detailed conditions of PCR were described in our previous study [31].…”

Section: Comparison Of Pth1r and Pth2r Mrna Expression In The Scalesmentioning

confidence: 99%

Parathyroid hormone 1 (1–34) acts on the scales and involves calcium metabolism in goldfish

Suzuki

Danks

Maruyama

et al. 2011

Bone

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“…Recent DNA microarray and computational microarray analyzing technologies have provided a view of the expression (9,(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). It is well known that cancer cells exposed to HT of more than 42.5˚C will undergo cell death, whereas exposure to MHT conditions, i.e., temperatures up to 42.5˚C, produces only slight or no cytotoxicity (26).…”

Section: Introductionmentioning

confidence: 99%

Gene networks related to the cell death elicited by hyperthermia in human oral squamous cell carcinoma HSC-3 cells

Tabuchi

Wada

Furusawa³

et al. 2011

Int J Mol Med

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Abstract. Local hyperthermia (HT) for various types of malignant tumors has shown promising antitumor effects. To confirm the detailed molecular mechanism underlying cell death induced by HT, gene expression patterns and gene networks in human oral squamous cell carcinoma (OSCC) cells were examined using a combination of DNA microarray and bioinformatics tools. OSCC HSC-3 cells were treated with HT at 44˚C for 90 min or mild hyperthermia (MHT) at 42˚C for 90 min, followed by culturing at 37˚C for 0-24 h. Treatment of cells with HT prevented cell proliferation (62%) and induced cell death (17%), whereas these alterations were not observed in cells treated with MHT. Microarray analysis revealed substantial differences with respect to gene expression patterns and biological function for the two different hyperthermic treatments. Moreover, we identified the temperature-specific gene networks D and H that were obtained from significantly up-regulated genes in the HT and MHT conditions, respectively, using Ingenuity pathway analysis tools. Gene network D, which contains 14 genes such as ATF3, DUSP1 and JUN, was associated with relevant biological functions including cell death and cellular movement. Gene network H, which contains 13 genes such as BAG3, DNAJB1 and HSPA1B, was associated with cellular function and maintenance and cellular assembly and organization. These findings provide a basis for understanding the detailed molecular mechanisms of cell death elicited by HT in human OSCC cells. IntroductionIn the treatment of oral squamous cell carcinoma (OSCC), treatment outcomes have improved in the past two decades due to progress in reconstructive techniques, stereotactic radiotherapy, new anticancer drugs such as taxanes, and combinations of these therapeutic modalities (1). Nonetheless, it is well known that patients with advanced tumors or tumor recurrence have a poor prognosis with a median survival period less than one year (2). Local hyperthermia (HT) for various malignant tumors including OSCC has been recognized as an effective and attractive tool with the advantages of relatively few side effects and slight damage to normal tissue. Combinations of HT with chemotherapy, radiotherapy or both have been clinically used for patients with cancer in various organs, and their antitumor effects have been verified by many clinical trials (3-7).In general, HT elicits a wide spectrum of stress responses such as induction of heat shock proteins (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 (8,9). In particular, HSPs, which are induced by heat, behave as molecular chaperones and exert strong cytoprotective effects that prevent cell death. The treatment of cells with HT induces numerous signal transduction pathways which contribute variously to cell death and survival (10-12). Although many biological processes are affected by HT, the overall responses to HT in mammalian cells remain unknown.Re...

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“…It is well known that the mobility shift of HSF1 due to its phosphorylation indicates the activation of the molecule (31). In U937 cells, the elevated expression of HSPs such as Hsp70, Hsp40 and Hsp27 was observed following the activation of HSF1 under both non-apoptotic and apoptotic conditions (19,26). At 42˚C for 15 min, a transient mobility shift of HSF1 was observed at 0 and 0.5 h after the treatment.…”

Section: Resultsmentioning

confidence: 94%

“…Several investigators have indicated that heat stress affects the expression pattern of genes in many kinds of cell types with a cell death or no cell death condition (17-27). In addition, bioinformatics analysis have shown that differentially expressed genes influenced by heat could be sorted into several functional categories such as molecular chaperones, cell death, protein degradation, transcription, signal transduction and membrane transport (10,17,19,22,23,26). As described above, because heat stress induces complex cellular responses and changes in signal transduction, the mechanisms of heat response have not been elucidated in detail.…”

Section: Introductionmentioning

confidence: 99%

Identification of biological functions and gene networks regulated by heat stress in U937 human lymphoma cells

et al. 2011

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Abstract. although cancer cells exposed to temperatures >42.5˚C undergo cell death as the temperature rises, exposure of up to 42.5˚C induces slight or no cytotoxicity. The temperature of 42.5˚C is, therefore, well known to be the inflection point of hyperthermia. To better understand the molecular mechanisms underlying cellular responses to heat stress at temperatures higher and lower than the inflection point, we carried out global scale microarray and computational gene expression analyses. Human leukemia U937 cells were incubated at 42˚C or 44˚C for 15 min and cultured at 37˚C for 0-6 h. Apoptosis accompanied by the activation of caspase-3 and DNA fragmentation was only observed in cells treated with heat stress at 44˚C, but not at 42˚C. Although a large number of genes were differentially expressed by a factor of 2.0 or greater, we found substantial differences with respect to the biological functions and gene networks of the genes differentially expressed at the two temperatures examined. Interestingly, we identified temperature-specific gene networks that were considered to be mainly associated with cell death or cellular compromise and cellular function and maintenance at 44˚C or 42˚C, respectively, by using the Ingenuity pathway analysis tools. These findings provide the molecular basis for a further understanding of the mechanisms of the biological changes that are responsive to heat stress in human lymphoma cells.

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Gene networks involved in apoptosis induced by hyperthermia in human lymphoma U937 cells

Cited by 24 publications

References 44 publications

Parathyroid hormone 1 (1–34) acts on the scales and involves calcium metabolism in goldfish

Parathyroid hormone 1 (1–34) acts on the scales and involves calcium metabolism in goldfish

Gene networks related to the cell death elicited by hyperthermia in human oral squamous cell carcinoma HSC-3 cells

Identification of biological functions and gene networks regulated by heat stress in U937 human lymphoma cells

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