[DOWNLOAD] "Cross-Talk Between IGF/IGFR and Psoriasin (S100A7) Enhancing Growth and Metastasis of Breast Cancer" by Ghassan Ab Ahmed Tranesh # Book PDF Kindle ePub Free

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eBook details

• Title: Cross-Talk Between IGF/IGFR and Psoriasin (S100A7) Enhancing Growth and Metastasis of Breast Cancer
• Author : Ghassan Ab Ahmed Tranesh
• Release Date : January 18, 2013
• Genre: Science & Nature,Books,Professional & Technical,Medical,
• Pages : * pages
• Size : 5121 KB

Description

Breast cancer is the most common type of malignant tumors and the second most common cause of cancer-related deaths in women worldwide. Breast cancer metastasis is the main cause of death from this disease. Psoriasin (S100A7), a member of the S100 family proteins, is characterized by having calcium-binding domains and is involved in multiple physiopathological processes in the cell such as cell cycle progression and cellular differentiation. Overexpression of S100A7 is a well known factor for inducing progression of the preinvasive to invasive form of breast cancer and its presence is correlated with poor prognosis. Insulin-like Growth Factor (IGF), especially types 1 and 2, has also been shown to play an important role in cellular growth and proliferation of breast and other types ofcancer. The purpose of this study was to investigate the cross-talk between S100A7 and IGF-induced signaling mechanism on breast cancer progression and metastasis. We have shown that overexpression of S100A7 in ERα- breast cancer cell lines MDA-MB-231 and SCP6 enhances IGF-induced growth, wound healing, chemotaxis and chemoinvasion. MDA-MB-231 overexpressing S100A7 cell lines showed enhanced metastasis compared to vector control cells. Furthermore, delineation of signaling mechanisms revealed that S100A7 overexpression also enhanced IGF-induced IGFR phosphorylation and activation/phosphorylation of downstream signaling molecules Akt and ERK. These studies suggest that S100A7 may modulate breast cancer progression and metastasis through enhancing IGF-induced signaling and activation of cell survival molecules Akt and ERK, which have been shown to enhance proliferation. In summary, our studies indicate that crosstalk between S100A7 and IGF/IGFR-induced signaling enhances metastatic potential and proliferation of breastcancers.

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