“I was so amazed by what I was seeing. We repeated and repeated our work to prove that the standard scientific dogma wasn’t the complete story.”
Recently, the University of Pittsburgh Cancer Institute (UPCI) researchers, technical and scientific discovery by an accidental combination, plus a hunch, reveals a previously unseen biological process, which may be associated with certain types of cancer rapid growth related.
Dr. Shuda and his colleagues found that when cells divide, a well-known cancer protein (called mTOR) – previously thought to be solely responsible for the control of cancer cells in the production of an important protein, called cap-dependent translation (cap -dependent translation) – You can create a different protein resale CDK1. They observed that the process also detects a key viral oncoproteins, make a common, usually harmless virus can convert healthy cells into cancer cells.
Merkel cell polyomavirus (MCV) was found in 2008 by the co-author of this article, Dr. Yuan Chang and Patrick S. Moore. The virus can cause a rare but deadly form of skin cancer, called Merkel cell carcinoma. And then they found a program called “small tumor protein (sT)” viral protein. It may lead to a series of reactions, tumor growth inhibition mTOR protein can resist anticancer drugs.
Dating back to the 1960s in the study, the scientists believe that during cell division, cap-dependent protein synthesis is turned off. New research shows that is not necessarily in the case, and CDK1 possible alternatives mTOR. mTOR and CDK1 works by inhibiting a gated protein (called 4E-BP1, can close the cap-dependent protein synthesis).
Even in very aggressive tumor, there are less than 1% of the cells in the active division cycle, called mitosis, which makes the study of mitotic cells become very difficult. Furthermore, traditionally drugs which used to arrest cell division, can inhibit protein production by CDK1. That may be why the study did not determine CDK1 seems to play an important role before.
Shuda uses a technique called flow cytometry to detect dividing cells. The use of special fluorescent label, he can see mitotic cells completely inactivated protein 4E-BP1 by CDK1. He also directly measured the mitotic process of manufacturing proteins.
Sure enough, even when mTOR is knockout, CDK1 persists, protein synthesis, cell division and make the necessary to proceed.
In this paper, the senior author, Dr. professor of molecular genetics and biochemistry, University of Pittsburgh Moore said: “Now, we can not say that this process involves CDK1 cause cancer – which is the next study we will deal with the problem, but it points to. Cell biology a basic control mechanisms, and brings an interesting possibility to create or combination of anticancer drugs, so that they inhibit the synthesis of mTOR and CDK1-related proteins, may be a useful therapy. “