Dissertation > Medicine, health > Oncology > Genitourinary tumors > Male genitalia tumors > Prostate cancer

EGR-1 Promotes Cell Proliferation and Tumor Forming Through Up-regulation of IGF-1R In Prostate Cancer Cells

Author Ma
Tutor XiaoWeiHua
School University of Science and Technology of China
Course Cell and Molecular Biology
Keywords EGR-1 IGF-1R Prostate Cancer Tumor growth Tumor proliferation
CLC R737.25
Type PhD thesis
Year 2011
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Up-regulation of IGF-1R signaling, including IGF-1R and its principle ligandIGF-1, has been commonly found in a variety of primary human cancers such asprostate, colorectal, lung and breast cancers, and has been indicated in malignanttransformation, cancer growth and progress. Loss of tumor suppressor genes, such asp53, BRCA1 or WT1 has been considered as the result of IGF-1R overexpression. Butthe molecular mechanisms for loss the transcriptional control of IGF-1R and IGF-I arestill under investigation. In our effort in exploring EGR-1-driven genes in prostatecancer cells with microarray, it displayed that IGF-1R and IGF-II are the targets ofEGR-1. Further study shows that EGR-1 knockdown by a specific shRNA-EGR-1inhibits gene transcription of IGF-1R in human prostate cancer cells. By usingluciferase reporter assay and ChIPs assay, we found that EGR-1 directly binds toIGF-1R promoter and transcriptional regulates its expression. Consequently,knockdown of EGR-1 inhibited IGF-1R-mediated tumor colony formation andproliferation. In addition, expression of EGR-1 activates Erk and Akt throughinducing IGF-1R expression. The present study elucidated the molecular mechanismof EGR-1 on regulation of IGF-1R and underscored the important role of EGR-1 inprostate cancer.

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