SRC-3 levels alleviated by aPKC in Breast Cancer Cells
by admin ~ July 15th, 2009.
As per a new research published by Cell Press in an issue of Molecular Cell, valuable insight has been obtained into a previously undescribed mechanism, which is expected to regulate prominent breast cancer-linked protein.
The research is expected to offer a new paradigm to improve the understanding of fundamental processes that contribute to breast cancer. It was remarked that steroid receptor coactivator-3 (SRC-3/AIB1), which plays an important role in cell growth is often left over expressed.
From News-Medical.Net:
The researchers found that aPKC stabilized cellular SRC-3 protein levels by inducing phosphorylation of a particular region of SRC-3. Specifically, phosphorylation of C-terminal residues induced a conformational change that made SRC-3 more resistant to degradation by the core proteasome. This effect of aPKC required estrogen and estrogen receptor and was not supported by other steroid receptors, suggesting that aPKC-mediated SRC-3 stabilization is a receptor-selective event. These results reveal a mechanism that links aPKC with estrogen-dependent growth and tumorigenesis and provide yet another layer of control for regulating levels of the SRC-3 oncogenic protein.
“Our data describe a new regulatory mechanism for SRC-3 protein turnover which may play an important role in regulating SRC-3 levels in normal and oncogenic cell growth,” offers Dr. O’Malley. “We propose that when aPKC is overexpressed in cancer cells, the consequence is increased SRC-3 function and powerful enhancement of estrogen-receptor target gene transcription and promotion of estrogen-dependent cell growth in cancer cells such as breast.”
According to Dr. Bert O’Malley from the Baylor College of Medicine, it was found that aPKC (atypical protein Kinase C) is chiefly responsible for alleviating the levels of cellular SRC-3 protein by inducing phosphorylation of a specific region of SRC-3.
Category: Anabolic Steroids | Tags: aPKC, atypical protein Kinase C, breast cancer, breast carcinoma, carcinoma cells, Kinase C, Steroid, steroid receptor coactivator-3