Reduced expression of endothelial and inducible nitric oxide synthase in a human breast cancer cell line which has acquired estrogen independence

Martin, Noreen; Alalami, O; Berg, Hermann

doi:10.1016/s0304-3835(99)00198-6

Cited by 26 publications

(20 citation statements)

References 16 publications

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“…ZR-75 breast cancer cells, which express iNOS (15,16), were transiently transfected with T7-Author contributions: F.M. and R.K. designed research; S.K.R.…”

Section: Resultsmentioning

confidence: 99%

Dynamic interplay between nitration and phosphorylation of tubulin cofactor B in the control of microtubule dynamics

Rayala

Eisenacher²,

Sharina³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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Tubulin cofactor B (TCoB) plays an important role in microtubule dynamics by facilitating the dimerization of α- and β-tubulin. Recent evidence suggests that p21-activated kinase 1 (Pak1), a major signaling nodule in eukaryotic cells, phosphorylates TCoB on Ser-65 and Ser-128 and plays an essential role in microtubule regrowth. However, to date, no upstream signaling molecules have been identified to antagonize the functions of TCoB, which might help in maintaining the equilibrium of microtubules. Here, we discovered that TCoB is efficiently nitrated, mainly on Tyr-64 and Tyr-98, and nitrated-TCoB attenuates the synthesis of new microtubules. In addition, we found that nitration of TCoB antagonizes signaling-dependent phosphorylation of TCoB, whereas optimal nitration of TCoB requires the presence of functional Pak1 phosphorylation sites, thus providing a feedback mechanism to regulate phosphorylation-dependent MT regrowth. Together these findings identified TCoB as the third cytoskeleton protein to be nitrated and suggest a previously undescribed mechanism, whereby growth factor signaling may coordinately integrate nitric oxide signaling in the regulation of microtubule dynamics.

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“…ZR-75 breast cancer cells, which express iNOS (15,16), were transiently transfected with T7-Author contributions: F.M. and R.K. designed research; S.K.R.…”

Section: Resultsmentioning

confidence: 99%

Dynamic interplay between nitration and phosphorylation of tubulin cofactor B in the control of microtubule dynamics

Rayala

Eisenacher²,

Sharina³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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“…We have already established the importance of NO as a mediator of tumour cell cytotoxicity by human monocyte-derived macrophages [14]. We have also shown that normal human mammary epithelial cells express both eNOS and iNOS, with a much higher percentage positivity for iNOS in human mammary epithelial cells [15] compared to the ZR-75-1 human breast cancer cell line [9]. We have also shown reduced expression of eNOS and iNOS in a human breast cancer cell line which has acquired estrogen independence [15].…”

Section: Introductionmentioning

confidence: 73%

Endothelial Nitric Oxide Synthase: Correlation with Histologic Grade, Lymph Node Status and Estrogen Receptor Expression in Human Breast Cancer

Martin¹,

Begum²,

Alalami³

et al. 2000

Tumor Biol

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Nitric oxide is produced by several isoenzymes which are present in many different tissues. We have recently reported the presence of inducible nitric oxide synthase in a breast cancer cell line. The purpose of this study was to examine the distribution of endothelial nitric oxide synthase (eNOS) in a series of human breast tumours. Immunohistochemical investigations demonstrated immunolabelling of tumour cells with the primary antibody, bovine endothelial anti-nitric oxide synthase. Although there was no correlation between eNOS staining and tumour size, there was a significant (p < 0.005) negative correlation (ρ = –0.65) between the percentage of tumour cells staining positive for eNOS and the histologic grade of the tumour; there was also a significant (p < 0.05) negative correlation (ρ = –0.40) between the percentage of tumour cells staining positive for eNOS and the number of positive lymph nodes. A significant (p < 0.005) positive correlation (ρ = 0.63) between the percentage of tumour cells staining positive for eNOS and estrogen receptor (ER) expression by the tumour was also observed. In conclusion, our results demonstrate that eNOS is expressed by human breast tumours and that its presence negatively correlates with histologic grade and lymph node status and positively correlates with ER expression.

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“…NOS3 expression has been detected in breast tumors (44)(45)(46) and is positively associated with estrogen and progesterone receptor status (45,46) and negatively correlated with histologic grade and lymph node status (46). Loss of NOS3 expression has been associated with breast cancer progression in estrogen-independent cancers (47). A G894T polymorphism in exon 7 of NOS3 results in a Glu298Asp substitution (rs1799983; ref.…”

Section: Introductionmentioning

confidence: 99%

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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Reduced expression of endothelial and inducible nitric oxide synthase in a human breast cancer cell line which has acquired estrogen independence

Cited by 26 publications

References 16 publications

Dynamic interplay between nitration and phosphorylation of tubulin cofactor B in the control of microtubule dynamics

Dynamic interplay between nitration and phosphorylation of tubulin cofactor B in the control of microtubule dynamics

Endothelial Nitric Oxide Synthase: Correlation with Histologic Grade, Lymph Node Status and Estrogen Receptor Expression in Human Breast Cancer

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

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