Effects of far-infrared rays on prostate cancer cells and normal prostate epithelial cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE15266 | GEO | 2012/12/19
SECONDARY ACCESSION(S): PRJNA116493
REPOSITORIES: GEO
Similar Datasets
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: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: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: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: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 Two-condition experiment,RB-treated vs.non-RB-treated cells.: 2 reference control without RB, independently grown and harvested. One replicate per array.
2013-03-14 | E-GEOD-16077 | biostudies-arrayexpress
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:Far-infrared radiation (FIR) exerts numerous beneficial effects on health and cell physiology. Recent studies revealed that the biological effects of FIR are independent of thermal effects. There is no proper method for measuring the parameters of the non-thermal biological effects of FIR, which limits its biomedical application. In this study, we established a cell detection platform using epithelial cell migration to measure the limits of the biological effects of FIR. FIR promoted the migration of rat renal tubular epithelial cells as revealed by our standardized detection method. We defined the ratio of the FIR-promoted migration area to the migration area of the control group as the FIR biological index (FBI). An increase of the FBI was highly associated with FIR-promoted mitochondrial function. Through FBI detection, we revealed the limits of the biological effects of FIR, including effective irradiation time, wavelengths, and temperature. FBI detection can be used to clarify important parameters of the biological effects of FIR in biomedical studies and health industry applications.
| S-EPMC6690987 | biostudies-literature
Project description:Epigenetic changes, including aberrant DNA methylation, result in altered gene expression and play an important role in carcinogenesis. Phytochemicals such as sulforaphane (SFN) and 3,3'-diindolylmethane (DIM) are promising chemopreventive agents for the treatment of prostate cancer. Both have been shown to induce re-expression of genes, including tumor suppressor genes silenced in cancer cells, via modulation of epigenetic marks including DNA methylation. However, it remained unclear the effects SFN and DIM on DNA methylation at a genomic scale. The goal of this study was to determine the genome-wide effects of SFN and DIM on promoter methylation in normal prostate epithelial cells and prostate cancer cells. Both SFN and DIM treatment decreased DNA methyltransferase expression in normal prostate epithelial cells (PrEC), and androgen-dependent (LnCAP) and androgen-independent (PC3) prostate cancer cells. The effects of SFN and DIM on promoter methylation profiles in normal PrEC, LnCAP and PC3 prostate cancer cells were determined using methyl-DNA immunoprecipitation followed by genome-wide DNA methylation array. We showed widespread changes in promoter methylation patterns, including both increased and decreased methylation, in all three prostate cell lines in response to SFN or DIM treatments. In particular, SFN and DIM altered promoter methylation in distinct sets of genes in PrEC, LnCAP, and PC3 cells, but shared similar gene targets within a single cell line. We further showed that SFN and DIM reversed many of the cancer-associated methylation alterations, including aberrantly methylated genes that are dysregulated or are highly involved in cancer progression. Overall, our data suggested that both SFN and DIM are epigenetic modulators that have broad and complex effects on DNA methylation profiles in both normal and cancerous prostate epithelial cells. Results from our study may provide new insights into the epigenetic mechanisms by which SFN and DIM exert their cancer chemopreventive effects.
| S-EPMC3899342 | biostudies-literature
Project description:Rex1 (zfp42) was identified by our laboratory because of its reduced expression in F9 teratocarcinoma stem cells after retinoic acid (RA) treatment. The Rex1 (Zfp42) gene is currently widely used as a marker of embryonic stem cells. We compared the transcriptional regulation of the human Rex1 gene in NTera-2 (NT-2) human teratocarcinoma, normal human prostate epithelial cells (PrEC), and prostate cancer cells (PC-3) by promoter/luciferase analyses. Oct4, Sox2, Nanog, and Dax1 transcripts are expressed at higher levels in NT-2 and PrEC cells than in PC-3 cells. Co-transfection analyses showed that YY1 and Rex1 are positive regulators of hRex1 transcription in NT-2 and PrEC cells, whereas Nanog is not. Serial deletion constructs of the hRex1 promoter were created and analyzed, by which we identified a potential negative regulatory site that is located between -1 and -0.4 kb of the hRex1 promoter. We also delineated regions of the hRex1 promoter between -0.4 kb and the TSS that, when mutated, reduced transcriptional activation; these are putative Rex1 binding sites. Mutation of a putative Rex1 binding site in electrophoretic mobility shift assays (EMSA) resulted in reduced protein binding. Taken together, our results indicate that hRex1 binds to the hRex1 promoter region at -298 bp and positively regulates hRex1 transcription, but that this regulation is lost in PC-3 human prostate cancer cells. This lack of positive transcriptional regulation by the hRex1 protein may be responsible for the lack of Rex1 expression in PC-3 prostate cancer cells.
| S-EPMC3306262 | biostudies-literature
Project description:Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p < 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (??m) increased 1.5- and 3.4-fold (p < 0.05 and p < 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ??m of the GLUT3 siRNA-treated cells increased 3.0-fold (p < 0.001), whereas that of the control group increased 4.6-fold (p < 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.
| S-EPMC7893496 | biostudies-literature