Cytochrome P450 CYP1A1: wider roles in cancer progression and prevention

Androutsopoulos, Vasilis P.; Tsatsakis, Aristidis; Spandidos, Demetrios Α.

doi:10.1186/1471-2407-9-187

Cited by 372 publications

(252 citation statements)

References 118 publications

(149 reference statements)

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“…The increase in CYP1A1 activity leads to H 2 O 2 production. An increase in cellular levels of H 2 O 2 has been linked to several key alternations in cells leading to cancer including DNA alternation, cell proliferation, apoptosis resistance, metastasis, angiogenesis and hypoxia-inducible factor 1 (Androutsopoulos et al, 2009;Wincent et al, 2012). In current study statistically significant downregulation of GSTP1 was observed in brain tumor samples compared to control samples.…”

Section: Discussionsupporting

confidence: 48%

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Wahid¹,

Mahjabeen²,

Baig³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Most of the exogenous and endogenous chemical compounds are metabolized by enzymes of xenobiotic processing pathways, including the phase I cytochrome p450 species. Carcinogens and their metabolites are generally detoxified by phase II enzymes like glutathione-S-transferases (GST). The balance of enzymes determines whether metabolic activation of pro-carcinogens or inactivation of carcinogens occurs. Under certain conditions, deregulated expression of xenobiotic enzymes may also convert endogenous substrates to metabolites that can facilitate DNA adduct formation and ultimately lead to cancer development. In this study, we aimed to test the association between deregulation of metabolizing genes and brain tumorigenesis. The expression profile of metabolizing genes CYP1A1 and GSTP1 was therefore studied in a cohort of 36 brain tumor patients and controls using Western blotting. In a second part of the study we analyzed protein expression of GSTs in the same study cohort by ELISA. CYP1A1 expression was found to be significantly high (p<0.001) in brain tumor as compared to the normal tissues, with ~4 fold (OR=4, 95%CI=0.43-37) increase in some cases. In contrast, the expression of GSTP1 was found to be significantly low in brain tumor tissues as compared to the controls (p<0.02). This down regulation was significantly higher (OR=0.05, 95%CI=0.006-0.51; p<0.007) in certain grades of lesions. Furthermore, GSTs levels were significantly down-regulated (p<0.014) in brain tumor patients compared to controls. Statistically significant decrease in GST levels was observed in the more advanced lesions (III-IV, p<0.005) as compared to the early tissue grades (I-II). Thus, altered expression of these xenobiotic metabolizing genes may be involved in brain tumor development in Pakistani population. Investigation of expression of these genes may provide information not only for the prediction of individual cancer risk but also for the prevention of cancer.

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Section: Discussionsupporting

confidence: 48%

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Wahid¹,

Mahjabeen²,

Baig³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…Cytochrome P450 1A1 (CYP1A1) is a member of the CYP1 family and participates in the metabolism of a vast number of xenobiotics, as well as endogenous substrates [1]. The metabolism of xenobiotics may well lead to their activation, and in the case of CYP1A1, the activation of benzo[a]pyrene represents a well-studied reaction [1,2].…”

Section: Introductionmentioning

confidence: 99%

“…Cytochrome P450s are enzymes that catalyze Phase-I metabolism reactions, such as C-, N-and S-oxidation and dealkylation [1]. Cytochrome P450 1A1 (CYP1A1) is a member of the CYP1 family and participates in the metabolism of a vast number of xenobiotics, as well as endogenous substrates [1].…”

Section: Introductionmentioning

confidence: 99%

Four polymorphisms in cytochrome P450 1A1 (CYP1A1) gene and breast cancer risk: a meta-analysis

Sergentanis

Economopoulos

2009

Breast Cancer Res Treat

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Cytochrome P450s are enzymes which catalyze Phase-I metabolism reactions; cytochrome P450 1A1 (CYP1A1) is a member of the CYP1 family and participates in the metabolism of a vast number of xenobiotics, as well as endogenous substrates. Four single nucleotide polymorphisms in CYP1A1 have been studied concerning their potential implication in terms of breast cancer risk: T3801C, T3205C, A2455G (Ile462Val), and C2453A (Thr461Asp); controversy exists regarding their role. This meta-analysis aims to examine whether the four aforementioned polymorphisms are associated with breast cancer risk. Separate analyses were performed on Caucasian, Chinese, and African populations, as well as on premenopausal and postmenopausal women. Eligible articles were identified by a search of MEDLINE bibliographical database for the period up to October 2009. Concerning T3801C, 32 studies were eligible (11,909 cases and 16,179 controls), 29 studies (12,257 cases and 20,379 controls) were eligible for A2455G, 11 studies (7,189 cases and 8,491 controls) were eligible for C2453A, and eight studies were eligible for T3205C (1,378 cases and 1,642 controls). Pooled odds ratios (OR) were appropriately derived from fixed-or random-effect models. Sensitivity analysis excluding studies whose genotype frequencies in controls significantly deviated from Hardy-Weinberg equilibrium was performed. Homozygous subjects of Caucasian origin carrying the A2455G G allele exhibited elevated breast cancer risk (pooled OR = 2.185, 95% CI 1.253-3.808, fixed effects), whereas heterozygous carriers did not (pooled OR = 1.062, 95% CI 0.852-1.323, random effects). A2455G polymorphism status was not associated with breast cancer risk in Chinese subjects or specifically in premenopausal/postmenopausal women. T3801C, T3205C, and C2453A status were not associated with breast cancer risk at any analysis. In conclusion, this meta-analysis points to the A2455G G allele as a risk factor for breast cancer among Caucasian subjects. On the contrary, T3801C, T3205C, and C2453A status does not seem capable of modifying breast cancer risk.

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“…CYP1A1 has been studied as the hallmark of AHR-mediated gene induction. CYP1A1 metabolically activates a variety of environmental carcinogens, and furthermore, its overexpression can lead to carcinogenesis (6). Understanding the regulation of CYP1A1 will therefore contribute not only to an understanding of the dysregulation of AHR target genes but also the resulting toxicity of this dysregulation.…”

Section: Discussionmentioning

confidence: 99%

SIN3A, Generally Regarded as a Transcriptional Repressor, Is Required for Induction of Gene Transcription by the Aryl Hydrocarbon Receptor

Solaimani¹,

Wang

Hankinson³

2014

Journal of Biological Chemistry

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Background: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) activates transcription of CYP1A1. Results: Ectopic expression of SIN3A reverses the inhibitory effect of SIN3A siRNAs on CYP1A1 induction. TCDD stimulates SIN3A binding to the CYP1A1 enhancer and promoter. Conclusion: SIN3A coactivates TCDD induction of CYP1A1 transcription. Significance: The anomalous stimulatory effect of SIN3A on transcription is extended to a gene that is rapidly and dramatically induced.

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Cytochrome P450 CYP1A1: wider roles in cancer progression and prevention

Cited by 372 publications

References 118 publications

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Four polymorphisms in cytochrome P450 1A1 (CYP1A1) gene and breast cancer risk: a meta-analysis

SIN3A, Generally Regarded as a Transcriptional Repressor, Is Required for Induction of Gene Transcription by the Aryl Hydrocarbon Receptor

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