Publications by authors named "Alexandra A Mourad-Zeidan"
Article Synopsis
- Galectin-3 (Gal-3) is linked to the progression and spread of melanoma, as it accumulates during the disease's advancement from benign to metastatic forms.
- Silencing Gal-3 with small hairpin RNA significantly reduces the tumor growth and invasive abilities of melanoma cells, affecting their ability to form structures similar to blood vessels (vasculogenic mimicry).
- Gal-3 influences the expression of several genes associated with aggressive melanoma behavior, including vascular endothelial-cadherin and interleukin-8, and its silencing alters their promoter activities due to changes in transcription factor recruitment.
Purpose: Most studies accept a multistep pathogenic process in melanoma that may include the phases of benign nevi and dysplastic nevi, melanoma, and metastatic melanoma. Dysregulation of cellular proliferation and apoptosis is probably involved in melanoma progression and response to therapy. We have studied the expression of galectin-3, a beta-galactoside-binding protein involved in apoptosis, angiogenesis, and cell proliferation, in a large series of melanocytic lesions, and correlated the expression with clinical and histologic features.
View Article and Find Full Text PDFOverexpression of cAMP-response element (CRE)-binding protein (CREB) and activating transcription factor (ATF) 1 contributes to melanoma progression and metastasis at least in part by promoting tumor cell survival and stimulating matrix metalloproteinase (MMP) 2 expression. However, little is known about the regulation of CREB and ATF-1 activities and their phosphorylation within the tumor microenvironment. We analyzed the effect of platelet-activating factor (PAF), a potent phospholipid mediator of inflammation, for its ability to activate CREB and ATF-1 in eight cultured human melanoma cell lines, and we found that PAF receptor (PAFR) was expressed in all eight lines.
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