Effects of far-infrared rays to human prostate cancer cell line PC-3
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Hiroki Shima
PROVIDER: E-GEOD-16077 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We introduce anticancer effect of the far-infrared rays. The growth of three human prostate cancer cells (DU145, PC-3 and LNCaP) was suppressed in vitro only by far-infrared rays. The far-infrared rays induced the gene activation involved in apoptosis that exert positive effects on cancer control. Shima, H. et al. Far-infrared rays control prostate cancer cells in vitro and in vivo. Nature Precedings, hdl:10101/npre.12008.11980.10101 (2008). Keywords: cancer control Twelve samples were analyzed. Each sample was cultured quadricate. One replicate per array. The DU145, PC-3 and LNCaP cell lines were obtained from American Type Culture Collection (Manassas, VA, USA). DU145 cells were maintained in minimum essential medium supplemented with 10% heat-inactivated fetal calf serum, 2 mM L-glutamine, 100 U/ml penicillin G and 0.1 mM non-essential amino acids in an atmosphere of 5% CO2 at 37°C. PC-3 and LNCaP cells were maintained in F-12K medium and RPMI medium with the same supplements, respectively. All three cancer cells were cultured for 21 and 28 days with or without exposure to far-infrared rays. The cells without exposure to far-infrared rays were used as the reference samples (Far-infrared rays-treated vs. non-treated cells). Natural or synthetic rubber/resin (RB) was obtained as far-infrared rays emitter from Yamamoto Corporation (Osaka, Japan). RB consisted of rubber, lime stone and titanium metal powder in a honeycomb structure comprised of micron-sized cells, and had the ability to radiate far-infrared rays (4â25 um). Experimental samples were sandwiched with RBs for 21 and 28 days. Channels 1 were exposed to RB.
2010-05-05 | E-GEOD-15260 | biostudies-arrayexpress
Project description:Far-infrared rays activated DNA repair genes in human prostate epithelial cells after 7 or 12 days' exposure to far-infrared rays. As far-infrared rays emitter, synthetic/natural rubber (RB) was used.
2017-03-14 | GSE15259 | GEO
Project description:Far-infrared rays activated DNA repair genes in human prostate cancer cells, PC-3, after 12days' exposure to far-infrared rays. As a far-infrared rays emitter, synthetic/natural rubber (RB) was used. Keywords: comparative genomic hybridization
2013-03-14 | GSE16077 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE15259: The effects of far-infrared rays on normal prostate epithelial cells (PrEC) GSE15260: Effects of far-infrared rays on 3 human prostate cancer cell lines GSE16077: Effects of far-infrared rays on human prostate cancer cell line PC-3 FIR stands for far-infrared rays that was reflected and radiated from RB. Refer to individual Series RNA was extracted with Isogen kit (NIPPON GENE CO., LTD. Osaka, Japan) from PrECs, and PC-3 with or without exposure to FIR on the 7th and 12th day of culture. Aliquots of 200 ng of total RNAs were labeled with Cy3- or Cy5- UTP using Agilent Quick Amp Labeling Kit (Agilent Technologies Inc, Tokyo, Japan) according to the manufacturer instructions. The Cy3-labeled probe using RNA from cells treated with DMSO and the Cy5-labeled probe using RNA from cells treated with DNCB for 4.5 hr were mixed, fragmented, and then suspended in GE hybridization buffer in the Gene Expression Hybridization Kit (Agilent Technologies Inc, Tokyo, Japan). The probes were applied to Whole Human Genome Oligo array (Agilent Technologies Inc, Tokyo, Japan), and hybridization, washing, and scanning by Agilent Microarray Scanner were performed according to the manufacturer $B!G (Bs recommended protocol. The images were processed using Feature Extraction Software (ver9.5.3.1, Agilent). For each hybridized spot, background intensity was subtracted and normalized by the global LOWESS normalization method. Dye-swap was performed. More than 2 fold and less than 0.5 fold changes are assigned positive on data analysis. RNA extracted from FIR-treated and non-FIR treated DU145, PC3, and LNCaP on the 21st and 28th day of culture were also treated in the same way except the use of commercially available IntelliGene HS Human Expression chip (TAKARA BIO, Otsu, Japan). Data analysis was performed using the microarray data analysis software, Expressionist (GeneData AG, Basel, Switzerland). Functional analyses were performed and the networks were generated using Ingenuity Pathways Analysis (Ingenuity Systems, CA, USA) cDNA microarray. BRCA1 and associated genes for DNA repair were significantly up-regulated in PrECs on the 7th day, and PC-3 on the 12th day when they were exposed to FIR (Fig. 2). These up-regulated genes were all normalized on the 12th day in PrECs, and there were no significant up-regulation of DNA repair pathway by FIR in DU145 and LNCaP on the 7th and 12th day.
2010-06-05 | E-GEOD-15266 | biostudies-arrayexpress
Project description:We introduce anticancer effect of the far-infrared rays. The growth of three human prostate cancer cells (DU145, PC-3 and LNCaP) was suppressed in vitro only by far-infrared rays. The far-infrared rays induced the gene activation involved in apoptosis that exert positive effects on cancer control. Shima, H. et al. Far-infrared rays control prostate cancer cells in vitro and in vivo. Nature Precedings, hdl:10101/npre.12008.11980.10101 (2008). Keywords: cancer control
2010-03-15 | GSE15260 | GEO
Project description:We have previously reported that the deficiency of p53 alone or in combination with Rb (Rb-/- p53-/-) in adipose-derived MSCs (ASCs) promotes leiomyosarcoma-like tumors in vivo. Here, we hypothesized that the source of MSCs and/or the cell differentiation stage could determine the phenotype of sarcoma development. To investigate whether there is a link between the source of MSCs and sarcoma phenotype, we generated p53-/- and Rb-/-p53-/- MSCs from bone marrow (BM-MSCs). Both genotypes of BM-MSCs initiated leiomyosarcoma formation similar to p53-/- and Rb-/-p53-/- ASCs. In addition, gene expression profiling revealed a link between p53- or Rb-p53-deficient BM-MSCs and ASCs and muscle-associated sarcomagenesis. These data suggest that the tissue source of MSC does not seem a crucial factor in the development of a particular sarcoma phenotype. To analyze whether the differentiation stage defines the sarcoma phenotype, BM-MSCs and ASCs were induced to differentiate towards the osteogenic lineage, and both p53 and Rb were excised using Cre-expressing adenovectors at different stages along osteogenic differentiation. Regardless of the level of osteogenic commitment, the inactivation of Rb and p53 in BM-MSC-derived, but not in ASC-derived, osteogenic progenitors gave rise to osteosarcoma-like tumors which could be serially transplanted. This indicates that the osteogenic differentiation stage of BM-MSCs imposes the phenotype of in vivo sarcoma development, and that BM-MSC-derived osteogenic progenitors rather than undifferentiated BM-MSCs, undifferentiated ASCs or ASC-derived osteogenic progenitors, represent the cell of origin for osteosarcoma development. To analyse whether the BM-MSC and Fat-MSC (ASC) differentiation stage may define the sarcoma phenotype, RbloxP/loxPp53loxP/loxP BM-MSCs and ASCs were induced to differentiate towards the osteogenic lineage and both Rb and p53 were excised with adenoviral vectors expressing the Cre-recombinase gene (Ad-CMV-Cre) at different stages (day 0 and 10) along osteogenic differentiation. NSG mice were inoculated subcutaneously with 5M-CM-^W10^6 mutant cells. Animals were killed when tumors reached 1 cm3 or 150 days after infusion. Some of the obtained tumors were mechanically disaggregated to establish ex vivo MSC-transformed cell lines. Gene expression analysis was performed using: WT BM-MSCs and ASCs, Rb-/-p53-/- BM-MSCs and ASCs previously differentiated to the osteogenic lineage for 10 days and a tumor cell line derived from p53-/-Rb-/- BM-MSC differentiated to the osteogenic lineage for 10 days.
2013-01-28 | E-GEOD-43803 | biostudies-arrayexpress
Project description:We have previously reported that the deficiency of p53 alone or in combination with Rb (Rb-/- p53-/-) in adipose-derived MSCs (ASCs) promotes leiomyosarcoma-like tumors in vivo. Here, we hypothesized that the source of MSCs and/or the cell differentiation stage could determine the phenotype of sarcoma development. To investigate whether there is a link between the source of MSCs and sarcoma phenotype, we generated p53-/- and Rb-/-p53-/- MSCs from bone marrow (BM-MSCs). Both genotypes of BM-MSCs initiated leiomyosarcoma formation similar to p53-/- and Rb-/-p53-/- ASCs. In addition, gene expression profiling revealed a link between p53- or Rb-p53-deficient BM-MSCs and ASCs and muscle-associated sarcomagenesis. These data suggest that the tissue source of MSC does not seem a crucial factor in the development of a particular sarcoma phenotype. To analyze whether the differentiation stage defines the sarcoma phenotype, BM-MSCs and ASCs were induced to differentiate towards the osteogenic lineage, and both p53 and Rb were excised using Cre-expressing adenovectors at different stages along osteogenic differentiation. Regardless of the level of osteogenic commitment, the inactivation of Rb and p53 in BM-MSC-derived, but not in ASC-derived, osteogenic progenitors gave rise to osteosarcoma-like tumors which could be serially transplanted. This indicates that the osteogenic differentiation stage of BM-MSCs imposes the phenotype of in vivo sarcoma development, and that BM-MSC-derived osteogenic progenitors rather than undifferentiated BM-MSCs, undifferentiated ASCs or ASC-derived osteogenic progenitors, represent the cell of origin for osteosarcoma development. BM-MSC and ASC cultures were established from 3 mouse strains: (a) WT, (b) p53loxP/loxP and (c) p53loxP/loxP RbloxP/loxP. The corresponding mutant cells were generated by excision of the LoxP-flanked sequences by infection of all MSC cultures with adenoviral vectors expressing the Cre-recombinase gene (Ad-CMV-Cre). NSG mice were inoculated subcutaneously with 5×10^6 mutant cells. Animals were killed when tumors reached 1 cm3 or 150 days after infusion. Some of the obtained tumors were mechanically disaggregated to establish ex vivo MSC-transformed cell lines. Gene expression analysis was performed using BM-MSCs and ASCs from all genotypes, as well as tumor cell lines derived from p53-/- and p53-/-Rb-/- BM-MSC and ASC cultures.
2013-01-27 | E-GEOD-43781 | biostudies-arrayexpress
Project description:Effects of far-infrared rays on normal prostate epithelial cells (PrEC)
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| PRJNA123067 | ENA