Date Published: November 6th 2018.
Author: Onkologi Sverige (the Oncology Society of Sweden)
Summary of Article’s Focus:
For a long time, it was believed that a cell’s identity, which is created during embryonic development, is a permanent feature. Thus, once a cell has been instructed to become, for example, a muscle cell, a nerve cell or a skin cell, it will remain this type of cell, no matter what.
Today, however, we know that a cell’s identity is not as solid and can change under pathological conditions such as cancer. Cancer cells mostly originate from a cell type called epithelial cells that form the skin, the inner surfaces of our tubular organs, and glands, for example in the breast. Recent studies show that breast cancer cells may lose their epithelial identity and acquire invasive and metastatic properties through a process termed epithelial-mesenchymal transition (EMT).
Relevance to Your Original Work:
For my expertise in the Akt signaling, I was asked to collaborate with a researcher from Karolinska Institutet to investigate the interplay between Akt and CAR membrane protein. We have found that the CAR trans-membrane protein is an important anchoring point for breast cancer cells, preventing them from losing their epithelial cell identity and becoming invasive. We found that CAR regulates the stability and function of the phosphatases and AKT inhibitors PTEN and PHLPP2.
The published paper the article refers to:
Nilchian A, Johansson J, Ghalali A, Asanin ST, Santiago A, Rosencrantz O, Sollerbrant K, Vincent CT, Sund M, Stenius U, Fuxe J. CXADR-Mediated Formation of an AKT Inhibitory Signalosome at Tight Junctions Controls Epithelial-Mesenchymal Plasticity in Breast Cancer. Cancer Res. 2019 Jan 1;79(1):47-60.