Cell Cycle Arrest Induced by Hydrogen Peroxide Is Associated with Modulation of Oxidative Stress Related Genes in Breast Cancer Cells

Chua, Pei‐Jou; Yip, George; Bay, Boon‐Huat

doi:10.3181/0903-rm-98

Cited by 67 publications

(41 citation statements)

References 43 publications

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“…As cancer cells are exposed to oxidative stress (75,76), it is possible that CYGB may func-tion as a ROS scavenger in a developing tumour, and loss or decreased CYGB expression may contribute to tumourigenesis. Recently, it was shown that ROS exposure of the MCF-7 breast cancer cell line resulted in the induction of CYGB expression as well as cell cycle arrest and apoptosis (77). It is also interesting to note that in our previous chromosome 17 transcriptome analyses, a number of genes reported to be hypoxia-related were underexpressed in EOC tumours relative to NOSE samples (34).…”

Section: Discussionmentioning

confidence: 91%

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

et al. 2012

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Abstract. It has been proposed that the frequent loss of heterozygosity (LOH) of an entire chromosome 17 contig in epithelial ovarian cancers (EOC) is the consequence of the inactivation of multiple tumour suppressor genes on this chromosome. We report the characterization of a 453 Kb 17q25 locus shown previously to exhibit a high frequency of LOH in EOC samples. LOH analysis further defined the minimal region of deletion to a 65 Kb interval flanked by D17S2239 and D17S2244, which contains RHBDF2, CYGB and PRCD as tumour suppressor gene candidates. Tissue specific expression excluded PRCD as a candidate. RHBDF2 was expressed at low levels in the majority of benign and low malignant potential (LMP) tumours, and in a subset of malignant ovarian tumour samples, as compared with primary cultures of normal ovarian surface epithelial cell (NOSE) samples. CYGB was expressed at low levels in the majority of LMP and malignant samples compared with benign and NOSE samples. In contrast to CYGB expression, RHBDF2 was expressed at low or undetectable levels in EOC cell lines exhibiting tumourigenic characteristics and up-regulated in a genetically modified EOC cell line rendered non-tumourigenic. DNA sequence analysis identified variants but no apparent deleterious mutations in either gene. Methylation-specific PCR analysis suggested that promoter methylation of CYGB but not RHBDF2 occurred in 6 of 31 malignant samples. The results combined suggest that RHBDF2 and CYGB may play distinctive roles in ovarian cancer and could be added to the growing roster of chromosome 17 genes implicated in this disease.

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Section: Discussionmentioning

confidence: 91%

Chromosome 17q25 genes, RHBDF2 and CYGB, in ovarian cancer

et al. 2012

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“…In HepG2 cells, which, compared with BR293 and MCF-7 cells, are relatively resistant to peroxide (34,35), IL-6-induced SIE reporter expression was reduced by peroxide in a dosedependent manner. The effective peroxide concentration was cell number dependent, and statistical reproducibility required accurate plating of cells and close adherence to a time schedule.…”

Section: Redox Control Of Stat3 Reporter Gene Expression and Promotermentioning

confidence: 96%

Modulation of Gene Expression and Tumor Cell Growth by Redox Modification of STAT3

et al. 2010

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Reactive oxygen species (ROS) promote tumor cell proliferation and survival by directly modulating growthregulatory molecules and key transcription factors. The signal transducer and activator of transcription 3 (STAT3) is constitutively active in a variety of tumor cell types, where the effect of ROS on the Janus kinase/ STAT pathway has been examined. We report here that STAT3 is directly sensitive to intracellular oxidants. Oxidation of conserved cysteines by peroxide decreased STAT3 binding to consensus serum-inducible elements (SIE) in vitro and in vivo and diminished interleukin (IL)-6-mediated reporter expression. Inhibitory effects produced by cysteine oxidation in STAT3 were negated in redox-insensitive STAT3 mutants. In contrast, ROS had no effect on IL-6-induced STAT3 recruitment to the c-myc P2 promoter. Expression of a redoxinsensitive STAT3 in breast carcinoma cells accelerated their proliferation while reducing resistance to oxidative stress. Our results implicate STAT3 in coupling intracellular redox homeostasis to cell proliferation and survival. Cancer Res; 70(20); 8222-32. ©2010 AACR.

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“…Total RNA was extracted from the homogenates of liver tissues using the RNeasy Mini Kit (Qiagen, Valencia, CA). cDNA was synthesized using 1 g of total RNA, ReverTra Ace (Toyobo, Osaka), and oligo (dT) [12][13][14][15][16][17][18] primers, according to the manufacturer's instructions. Thirty-five PCR cycles (30 seconds at 94°C, 30 seconds at 68°C, and 1 minute at 72°C) were run using the following mouse Cygb primers: forward, 5=-GCGACATGGAGATAGAGCGT-3=; and reverse, 5=-CTG-TACCCAGCCCACTTCCT-3=.…”

Section: Genotyping Of Micementioning

confidence: 99%