Tumor promotion by hydrogen peroxide in rat liver epithelial cells

Huang, Ruo‐Pan; Ao, Ping; Hossain, Mohammad Zakir; Fan, Yi; Jagdale, Ajit B.; Boynton, Alton L.

doi:10.1093/carcin/20.3.485

Cited by 62 publications

(54 citation statements)

References 64 publications

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“…As reported by others (Chen et al, 1995;Huang et al, 1998;Ko er et al, 2000), the FACS analyses showed that the percentage of G1-phase cells in all the ®ve Cx43-transfected clones was signi®cantly higher than that in the parental or vectortransfected cells; accordingly, the cell populations in the S and G2/M phases clearly decreased (Figure 2b). On the other hand, little di erence of cell death was observed among the parental, vector-, and Cx43-transfected clones; moreover, the cell death rate was less than 5% (Figure 2c).…”

Section: Negative Proliferation Control Of U2os Cells By Cx43 Via Slosupporting

confidence: 78%

“…As reported (Huang et al, 1998;Krutovskikh et al, 2000), the ability of U2OS cells to form colonies in soft agar (Figure 1e) and tumors in nude mice ( Figure 1f) signi®cantly decreased in Cx43-transfected cells compared with the parental and vector-transfected cells. These data suggest that expression of Cx43 inhibited the tumorigenicity of U2OS cells.…”

Section: Restoration Of Gjic and Inhibition Of Tumorigenicity Of U2ossupporting

confidence: 76%

“…It has shown wide inhibitory e ects on tumor growth of various cell lines (Zhu et al, 1992;Chen et al, 1995;Mesnil et al, 1995;Proulx et al, 1997;Huang et al, 1998;Omori and Yamasaki, 1998;Krutovskikh et al, 2000). We ®rst illustrate that forced expression of Cx43 inhibited the proliferation of U2OS cells through a reduced rate of G1/S transition of the cell cycle.…”

Section: Introductionmentioning

confidence: 76%

“…Cx43 had a punctate distribution in the cell pool at regions of intercellular contact ( Figure 1b, the lowest panel), which is characteristic of GJ channels (Huang et al, 1998). In addition, nearly 100% cells in the cell pool exhibited membrane staining of Cx43.…”

Section: Restoration Of Gjic and Inhibition Of Tumorigenicity Of U2osmentioning

confidence: 98%

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Connexin43 suppresses proliferation of osteosarcoma U2OS cells through post-transcriptional regulation of p27

et al. 2001

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Many lines of evidence indicate that connexin genes expressing gap junction (GJ) proteins inhibit tumor cell proliferation. However, the precise molecular mechanisms remain unclear. In this study, we show that overexpression of connexin43 (Cx43) suppressed proliferation of human osteosarcoma U2OS cells through inhibition of the cell cycle transition from G1 to S phase. This inhibition was attributed to a signi®cant accumulation of the hypophosphorylated retinoblastoma (Rb) protein, which was causally related to decreases in the kinase activities of cyclin-dependent kinases (CDKs) 2 and 4. Enforced Cx43 expression markedly increased the level of the CDK inhibitor p27. This increase resulted from an increased synthesis and a reduced degradation of the p27 proteins, but not in¯uence of the p27 mRNA. Moreover, we show that the Cx43-modulated GJ function was the main contributor to the elevation in p27 levels, in which cAMP was involved. These data suggest that Cx43 appears to inhibit proliferation of U2OS cells by increasing the levels of p27 proteins via post-transcriptional regulatory mechanisms. Oncogene (2001) 20, 4138 ± 4149.

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Section: Negative Proliferation Control Of U2os Cells By Cx43 Via Slosupporting

confidence: 78%

Section: Restoration Of Gjic and Inhibition Of Tumorigenicity Of U2ossupporting

confidence: 76%

Section: Introductionmentioning

confidence: 76%

Section: Restoration Of Gjic and Inhibition Of Tumorigenicity Of U2osmentioning

confidence: 98%

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Connexin43 suppresses proliferation of osteosarcoma U2OS cells through post-transcriptional regulation of p27

et al. 2001

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“…The tumor-promoting effects of hydrogen peroxide are supported by the formation of colonies in soft agar, appearance of foci in monolayer cultures, and disruption of GJIC [36]. Peroxynitrite, a mediator of toxicity in inflammatory processes, also diminishes GJIC in rat liver epithelial cells [100].…”

Section: Oxidative Stress and Cancermentioning

confidence: 99%

The roles of polyphenols in cancer chemoprevention

2006

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Abstract.Oxidative stress imposed by reactive oxygen species (ROS) plays a crucial role in the pathophysiology associated with neoplasia, atherosclerosis, and neurodegenerative diseases. The ROS-induced development of cancer involves malignant transformation due to altered gene expression through epigenetic mechanisms as well as DNA mutations. Considerable attention has been focused on identifying naturally occurring antioxidative phenolic phytochemicals that are able to decrease ROS levels, but the efficacies of antioxidant therapies have been equivocal at best. Several studies have shown that some antioxidants exhibit prooxidant activity under certain conditions and potential carcinogenicity under others, and that dietary supplementation with large amounts of a single antioxidant may be deleterious to human health. This article reviews the intracellular signaling pathways that respond to oxidative stress and how they are modulated by naturally occurring polyphenols. The possible toxicity and carcinogenicity of polyphenols is also discussed.

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