Regulation of the gene encoding glutathione S-transferase M1 (GSTM1) by the Myb oncoprotein

Bartley, Paul C.; Keough, Rebecca A.; Lutwyche, Jodi K.; Gonda, Thomas J.

doi:10.1038/sj.onc.1207136

Cited by 11 publications

(8 citation statements)

References 31 publications

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“…Thus, the knockout of mGSTA4 and mGSTZ1 has led to over-expression of GSTs of the α, µ and π classes [2]. However, our understanding of the regulation mechanisms of expression of particular GST genes, such as GSTM1, is only very fragmentary at present [138].…”

Section: Discussionmentioning

confidence: 98%

Relevance of the Deletion Polymorphisms of the Glutathione S-Transferases GSTT1 and GSTM1 in Pharmacology and Toxicology

Bolt

Thier²

2006

CDM

258

181

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Although cytosolic glutathione S-transferase (GST) enzymes occupy a key position in biological detoxification processes, two of the most relevant human isoenzymes, GSTT1-1 and GSTM1-1, are genetically deleted (non-functional alleles GSTT1*0 and GSTM1*0) in a high percentage of the human population, with major ethnic differences. The structures of the GSTT and GSTM gene areas explain the underlying genetic processes. GSTT1-1 is highly conserved during evolution and plays a major role in phase-II biotransformation of a number of drugs and industrial chemicals, e.g. cytostatic drugs, hydrocarbons and halogenated hydrocarbons. GSTM1-1 is particularly relevant in the deactivation of carcinogenic intermediates of polycyclic aromatic hydrocarbons. Several lines of evidence suggest that hGSTT1-1 and/or hGSTM1-1 play a role in the deactivation of reactive oxygen species that are likely to be involved in cellular processes of inflammation, ageing and degenerative diseases. There is cumulating evidence that combinations of the GSTM1*0 state with other genetic traits affecting the metabolism of carcinogens (CYP1A1, GSTP1) may predispose the aero-digestive tract and lung, especially in smokers, to a higher risk of cancer. The GSTM1*0 status appears also associated with a modest increase in the risk of bladder cancer, consistent with a GSTM1 interaction with carcinogenic tobacco smoke constituents. Both human GST deletions, although largely counterbalanced by overlapping substrate affinities within the GST superfamily, have consequences when the organism comes into contact with distinct man-made chemicals. This appears relevant in industrial toxicology and in drug metabolism.

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Section: Discussionmentioning

confidence: 98%

Relevance of the Deletion Polymorphisms of the Glutathione S-Transferases GSTT1 and GSTM1 in Pharmacology and Toxicology

Bolt

Thier²

2006

CDM

258

181

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“…Both constitutive and inducible expression of GSTM1 has been shown to be controlled by the transcription factor Nrf2 [31]. Interestingly, GSTM1 was also shown to be transcriptionally upregulated by the Myb onco-protein [32]. In addition, GSTM1 has been shown to inhibit MEK kinase 1 (MEKK1) activity and suppress MEKK1-medaited apoptosis [33].…”

Section: Discussionmentioning

confidence: 99%

Identification of biomarkers associated with the development of hepatocellular carcinoma in CuZn superoxide dismutase deficient mice

et al. 2007

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To identify biomarkers associated with the development of hepatocellular carcinoma (HCC) in CuZn superoxide dismutase (CuZnSOD, Sod1) deficient mice, 2-DE followed by MS analysis was carried out with liver samples obtained from 18-month-old Sod1−/− and +/+ mice. The intra-cellular Ca binding protein, regucalcin (RGN), showed a divergent alteration in Sod1−/− samples. Whereas elevated RGN levels were observed in −/− samples with no obvious neoplastic changes, marked reduction in RGN was observed in −/− samples with fully developed HCC. GST mu1 (GSTM1), on the other hand, showed a significant increase only in the neoplastic regions obtained from Sod1−/− livers. No change in GSTM1 was observed in the surrounding normal tissues. Marked reduction was observed in two intracellular lipid transporters, fatty acid binding protein 1 (FABP1) and major urinary protein 11 and 8 (MUP 11&8), in Sod1−/− samples. Analysis of additional samples at 18−22 months of age showed a three-fold increase in enolase activities in Sod1−/− livers. Consistent with previous findings, carbonic anhydrase 3 (CAIII) levels were significantly reduced in Sod1−/− samples, and immunohistochemical analysis revealed that the reduction was not homogenous throughout the lobular structure in the liver.

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“…In silico prediction modeling indicated multiple putative binding sites of transcriptional factors, such as AP2, GATA1, PEA3, and RXR/RAR, in the promoter region of GSTM1 . Moreover, increased active transcriptional activity in the region from −600 to +34 of GSTM1 after response to the Myb gene has been reported 38. In this study, we sequenced the promoter of GSTM1 and found 14 genetic variants, including one insertion variant and 13 SNPs.…”

Section: Discussionmentioning

confidence: 78%

GSTM1 copy number and promoter haplotype as predictors for risk of recurrence and/or second primary tumor in patients with head and neck cancer

Zhang

Huang

Wu³

et al. 2013

PGPM

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The objective of this study was to determine copy number variant (CNV) and promoter genetic variants in glutathione S-transferase Mu class 1 (GSTM1) and the risk of recurrence (REC)/second primary tumor (SPT) in patients with previously diagnosed early stage head and neck cancer. Among 441 subjects, 133 experienced REC and/or an SPT, while 308 had single primary disease. TaqMan real-time polymerase chain reaction was used to measure the exact copy number of GSTM1 and direct sequencing was used to determine genetic variants in the GSTM1 promoter region. Multivariate Cox regression analysis was performed to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) associated with copy number and genetic variants. REC/SPT-free survival times were compared by constructing Kaplan–Meier curves and differences between curves were tested by logrank test. Results showed a significantly decreased REC/SPT (HR = 0.57; 95% CI = 0.35–0.95) and longer REC/SPT-free survival in subjects with at least two copies of GSTM1 compared with the GSTM1 homozygous deletion, but not in those with one copy of GSTM1. The −498G, −426G, and −339T alleles were significantly associated with REC/SPT, with HRs of 0.11 (0.02–0.85), 0.28 (0.11–0.74) and 2.02 (1.07–3.82), respectively. Kaplan–Meier survival analysis showed that the −498G, −426G, and −339C alleles were also significantly associated with increased REC/SPT-free survival. Further haplotype analysis showed the haplotype P−498G-−426G-−339C carriers had decreased REC/SPT with a HR of 0.09 (95% CI 0.01–0.71) and increased REC/SPT-free survival compared with those with haplotype P−498C-−426A-−339T. The P−498C-−426A-−339T-containing reporter construct had significantly increased luciferase expression. These results suggest that the GSTM1 CNV and promoter haplotype are better predictors of REC/SPTs of head and neck cancer than just measuring the presence/absence of GSTM1.

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Regulation of the gene encoding glutathione S-transferase M1 (GSTM1) by the Myb oncoprotein

Cited by 11 publications

References 31 publications

Relevance of the Deletion Polymorphisms of the Glutathione S-Transferases GSTT1 and GSTM1 in Pharmacology and Toxicology

Relevance of the Deletion Polymorphisms of the Glutathione S-Transferases GSTT1 and GSTM1 in Pharmacology and Toxicology

Identification of biomarkers associated with the development of hepatocellular carcinoma in CuZn superoxide dismutase deficient mice

GSTM1 copy number and promoter haplotype as predictors for risk of recurrence and/or second primary tumor in patients with head and neck cancer

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