Polymorphism in heme oxygenase-1 (HO-1) promoter is related to the risk of oral squamous cell carcinoma occurring on male areca chewers

Chang, Kuo Wei; Lee, T. C.; Yeh, Wen I.; Chung, Ming Yi; Liu, C. J.; Y., L.; Lin, Shu Chun

doi:10.1038/sj.bjc.6602186

Cited by 87 publications

(76 citation statements)

References 34 publications

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“…An association between long HO-1 alleles and breast cancer risk is a novel observation and consistent with previous findings showing the long HO-1 allele to be a risk factor for chronic pulmonary emphysema (63), lung adenocarcinoma (93), and oral squamous cell carcinoma (94). Induction of HO-1 is postulated to be cytoprotective due to decreased levels of pro-oxidant heme, increased levels of antioxidant bilirubin (52), and up-regulation of ferritin leading to rapid iron sequestration (95,96).…”

Section: Discussionsupporting

confidence: 75%

Genetic Variability in Iron-Related Oxidative Stress Pathways (Nrf2, NQ01, NOS3, andHO-1), Iron Intake, and Risk of Postmenopausal Breast Cancer

Hong

Ambrosone

Ahn

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Oxidative stress resulting from excess reactive oxygen species and/or deficiencies in antioxidant capabilities may play a role in breast cancer etiology. In a nested case-control study of postmenopausal women (505 cases and 502 controls) from the American Cancer Society Prevention II Nutrition Cohort, we examined relationships between breast cancer risk and genetic polymorphisms of enzymes involved in the generation and removal of iron-mediated reactive oxygen species. Using unconditional logistic regression, genetic variations in Nrf2 (11108C>T), NQO1 (609C>T), NOS3 (894G>T), and HO-1 [(GT) n dinucleotide length polymorphism] were not associated with breast cancer risk in a multivariate model. A significant dose trend (P trend = 0.04), however, was observed for total number of putative ''at-risk'' alleles (Nrf T, NQO1 T, NOS T, and HO-1 LL and LM genotypes), with those carrying three or more at-risk alleles having an odds ratio (OR) of 1.56 [95% confidence interval (95% CI), 0.97-2.51] compared with those having none. When examined in relation to iron, carriage of three or more high-risk alleles in the highest tertile of iron intake (OR, 2.27; 95% CI, 0.97-5.29; P trend = 0.02; P interaction = 0.30) or among users of supplemental iron (OR, 2.39; 95% CI, 1.09-5.26; P trend = 0.02; P interaction = 0.11) resulted in a greater than 2-fold increased risk compared with women with no high-risk alleles. Increased risk was also observed among supplement users with the HO-1 LL or LM genotypes (OR, 1.56; 95% CI, 1.01-2.41; P interaction = 0.32) compared with S allele carriers and MM genotypes combined. These results indicate that women with genotypes resulting in potentially higher levels of iron-generated oxidative stress may be at increased risk of breast cancer and that this association may be most relevant among women with high iron intake. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1784 -94)

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Section: Discussionsupporting

confidence: 75%

Genetic Variability in Iron-Related Oxidative Stress Pathways (Nrf2, NQ01, NOS3, andHO-1), Iron Intake, and Risk of Postmenopausal Breast Cancer

Hong

Ambrosone

Ahn

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…It was demonstrated that frequencies of cancers are lower in patients with a shorter sequence of (GT)n in the HO-1 promoter that are supposed to have a higher level of HO-1 induction in response to oxidative stress. 66,67 It seems that these benefits may result from antioxidative properties of HO-1, which contribute to protection of healthy cells against carcinogens. However, in already existing tumors, the increased level of HO-1 leads to better tumor cell survival and faster proliferation.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Heme Oxygenase-1 in Murine Melanoma

Waś

Cichoń²,

Smolarczyk³

et al. 2006

The American Journal of Pathology

174

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Heme oxygenases (HOs) catalyze the oxidation of heme to the biologically active products carbon monoxide (CO), biliverdin, and ferrous iron. Two distinct variants of HOs have been described in humans and rodents, each encoded by a different gene: HO-2, which is constitutively expressed, and HO-1, which is potently induced in many cell types by heme, inflammatory cytokines, and oxidative stress-related factors.

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“…2,30 Evidences indicated that ANE was a stress inducer. [7][8][9] A low concentration of ANE was used in this study to dissect the signaling responses relevant to the chronic oral exposure in target cells.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Areca chewing is epidemiologically linked to the high incidence of oral squamous cell carcinoma (OSCC) and other oral lesions in this population. 3,4 Areca nuts contain polyphenols, arecoline, arecaidine and other ingredients.…”

mentioning

confidence: 99%

Areca (betel) nut extract activates mitogen‐activated protein kinasesand NF‐κB in oral keratinocytes

Lin

Lee

et al. 2005

Intl Journal of Cancer

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Areca (betel) was recently proved a carcinogenic substance by the International Agency for Research on Cancer. However, the signaling impact of areca in oral keratinocyte is still obscure. Mitogen‐activated protein kinase superfamilies, including extracellular signal‐regulated kinase (ERK), c‐Jun N‐terminal kinases (JNK) and p38, together with transcription factor NF‐κB, are important signaling elements. We examined the activation of these signaling pathways in OECM‐1 and SAS oral keratinocytes, treated with ripe areca nut extract (ANE). In both cells, a rapid increase in JNK1 activity at 0.5 hr was noted following treatment of ANE. ERK was profoundly activated during 0.5–2 hr in OECM‐1 cells. Contrasting p38 activity was noted in these 2 cells. In both cells, ANE also activated NF‐κB pathway in a biphasic manner, particularly for SAS cells. NF‐κB was activated by ∼ 2‐ to 4‐fold at 0.5–1 hr and a plateau or slight decrease of activity existed between 1 and 6 hr. Later, another higher episode of NF‐κB activity was raised. This was accompanied with the rapid degradation in cytosolic IκBα as well as an increase of nuclear NF‐κB in both cells. ANE treatment did not activate epidermal growth factor receptor signaling system, but blockage of NF‐κB activation rendered the suppression of ANE‐modulated COX‐2 upregulation in OECM‐1. This study identified that ANE affected interactive signaling systems in oral keratonocytes that could be the pathogenetic basis for areca. © 2005 Wiley‐Liss, Inc.

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Polymorphism in heme oxygenase-1 (HO-1) promoter is related to the risk of oral squamous cell carcinoma occurring on male areca chewers

Abstract: Polymorphism in heme oxygenase-1 (HO-1) promoter is related to the risk of oral squamous cell carcinoma occurring on male areca chewers

Cited by 87 publications

References 34 publications

Genetic Variability in Iron-Related Oxidative Stress Pathways (Nrf2, NQ01, NOS3, andHO-1), Iron Intake, and Risk of Postmenopausal Breast Cancer

Genetic Variability in Iron-Related Oxidative Stress Pathways (Nrf2, NQ01, NOS3, andHO-1), Iron Intake, and Risk of Postmenopausal Breast Cancer

Overexpression of Heme Oxygenase-1 in Murine Melanoma

Areca (betel) nut extract activates mitogen‐activated protein kinasesand NF‐κB in oral keratinocytes

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