Prostate cancer can now be treated more effectively with the discovery of a cellular protein, reveals a research conducted by the Hokkaido University.
The drug Gefitinib is used to treat breast, lung, and other cancers by inhibiting epidermal growth factor receptor (EGFR) signaling, but it has only a limited effect on prostate cancer.
EGFR, present on the cell membrane, is involved in cell proliferation and the development of dermis, lung, and digestive tissues. When a mutation causes its over-activation, it can lead to increased cell proliferation and tumor formation.
When EGFR is attached to a small protein called ubiquitin, it is given "the kiss of death" and tagged for degradation inside the cell. This tagging process is facilitated by a protein called c-CBL.
The degradation of EGFR leads to less signaling from the receptor and reduced cell proliferation.
Matsuda and his team found that signal-transducing adaptor protein-2 (STAP-2) stabilizes EGFR by inhibiting its c-CBL-mediated ubiquitination.
Furthermore, when the team suppressed STAP-2, the prostate cancer cells showed reduced proliferation and did not form a tumor when transplanted into mice.
"STAP-2 inhibitors could play a role in treating Gefitinib-resistant prostate cancers. Further studies on STAP-2 will provide new insights into cancer physiology and support the development of anticancer therapies," says Tadashi Matsuda.
The study was published in the Journal of Biological Chemistry.