Title:Cross Talks Between Oncoprotein Signaling Networks and Tumor Suppressor p53 in Breast Cancer
Volume: 11
Issue: 1
Author(s): Nabilah Ibnat and Ezharul Hoque Chowdhury
Affiliation:
Keywords:
Anti-sense oligonucleotide, Bcl-2, breast cancer, epithelial to messenchymal transition
(EMT), FAK, HER-2/neu, MDM2 and cullin 7, NF-κB, oncogene, p21, p53, reactive oxygen species
(ROS), siRNA, survivin, TGF-β, tumor suppressor, VEGF.
Abstract: Oncogenic transformation of growth factors, growth factor receptors, transcription factors as well
as important cellular proteins and their association with the principal tumor suppressor p53 may provide essential
insights toward integrated therapy in breast cancer. In this review we discuss growth factor HER-2/neu
receptor tyrosine kinase; FAK, non-receptor tyrosine kinase; TGF-β, and their roles in tumorigenesis in breast
cell with respect to p53. VEGF is a powerful angiogenic factor and its expression is also regulated by p53. E3
ligases like MDM2 and cullin 7 are considered as oncoproteins and they interact differently with p53 in breast
cells. Aberrant expression of these ligases is associated with tumorigenesis. The transcription factor cyclin E
is involved in cell cycle progression while its activity is subjected to p53 regulation through p21. The necrosis
factor NF-κB regulates p53 expression by binding to its promoter and modulates expression of anti-apoptotic
protein survivin in breast cancer cell. Apoptosis by Bcl-2 family of protein is largely dependent upon the balance
of pro-apoptotic and anti-apoptotic protein expression regulated by p53. In essence, the complexities of
p53 interactions with various types of oncogene products require close exploration towards an integrated therapy
against breast cancer.
