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

Abstract

Oestrogen and progesterone have a role in stimulating NO production in T47D breast cancer cells. Inhibition of NO synthesis might be a novel therapeutic approach for reducing hormone-associated angiogenesis in breast cancer.

The link between the insecticide heptachlor epoxide, estradiol, and breast cancer

“…The idea that inflammation may contribute to breast cancer is supported by the observation that women with chronic mastitis have an approximate 2.5-fold increased risk of developing breast cancer [56]. Since NO synthase has been found in epithelial cells [57], endothelial cells, and macrophages of breast cancers [58,59] and since NO production in T47D breast cancer cells can be induced by 17b-E 2 [60], elevated levels of NO in breast tissue . HE-induced oxidants produced by human PMNs damages cell membranes of neighboring lymphocytes.…”

Possible role of nitric oxide in the biology of breast carcinoma: review of the available literature

“…10,14,18,19 Several human breast cancer cell lines express eNOS mRNA: this eNOS expression is closely correlated with the ER status of these lines. 20 Mapping of NOS expression within tumour tissue from breast and gastric cancers shows that iNOS is expressed predominantly in stromal (macrophage and endothelial) cells, although the level of NOS activity is at least 1,2 orders of magnitude lower than the enzyme activity associated with cytotoxicity and apoptosis. The correlation between NOS activity and grade for breast cancer suggests that NO may provide a positive growth signal within the tumour microenvironment: in vivo studies showing increased growth rate, vascular density and microinvasiveness of a human tumour cell line transfected for constitutive expression of iNOS support this observation.…”

Quantitative comparison of the inhibitory effects of GW5638 and tamoxifen on angiogenesis in the cornea pocket assay

“…The mechanisms of the antiangiogenic effects of tamoxifen have been investigated extensively in the literature [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23]. However, the mechanisms for GW5638 are still unknown.…”

“…It is well known that tamoxifen is a modulator of angiogenesis [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23] and can affect angiogenesis in an ER-independent manner [5][6][7][8][9][10][11][12][13]. Therefore, it is possible that GW5638 is an angiogenesis-modulator as well.…”