ZR-75-1 human breast cancer cells: expression of inducible nitric oxide synthase and effect of tamoxifen and phorbol ester on nitric oxide production

Alalami, O; Martin, Noreen

doi:10.1016/s0304-3835(97)00404-7

Cited by 18 publications

(9 citation statements)

References 20 publications

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“…exert a direct effect on NO production. An identical nding was reported in ZR-75-1 human breast cancer cells; moreover, tamoxifen signi cantly downregulated phorbol ester-increased NO production in this cell line (1). Although the precise molecular mechanism of the action of steroid hormones remains to be worked out, our experiments provide strong evidence that these hormones stimulate the production of NO, an effect that is inhibited by tamoxifen in T47D cells.…”

Section: Discussionsupporting

confidence: 87%

The Effect of N G -monomethyl-L-arginine and Tamoxifen on Nitric Oxide Production in Breast Cancer Cells Stimulated by Oestrogen and Progesterone

Thamrongwittawatpong

Sirivatanauksorn²,

Batten³

et al. 2001

The European Journal of Surgery

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Section: Discussionsupporting

confidence: 87%

The Effect of N G -monomethyl-L-arginine and Tamoxifen on Nitric Oxide Production in Breast Cancer Cells Stimulated by Oestrogen and Progesterone

Thamrongwittawatpong

Sirivatanauksorn²,

Batten³

et al. 2001

The European Journal of Surgery

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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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“…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: 86%

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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ZR-75-1 human breast cancer cells: expression of inducible nitric oxide synthase and effect of tamoxifen and phorbol ester on nitric oxide production

Cited by 18 publications

References 20 publications

The Effect of N G -monomethyl-L-arginine and Tamoxifen on Nitric Oxide Production in Breast Cancer Cells Stimulated by Oestrogen and Progesterone

The Effect of N G -monomethyl-L-arginine and Tamoxifen on Nitric Oxide Production in Breast Cancer Cells Stimulated by Oestrogen and Progesterone

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

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