A Mechanism That Sends Cells On The Road To Cancer
Using a common virus as a tool for investigating abnormal cell proliferation, a team led by scientists at Cold Spring Harbor Laboratory has succeeded in clarifying an intricate series of biochemical steps that shed light on a way that cancer can begin.
The research involves adenovirus, a type of virus that causes the common cold in people, but whose genome contains known oncogenes — genes whose expression can promote cancer under certain conditions. The focus is on an adenoviral oncogene called E1A, and a protein that it codes for with the same name.
Viruses can’t reproduce on their own. A DNA virus like adenovirus is little more than a tiny, double-stranded segment of DNA enclosed within a protein shell. It must find a way to enter the nucleus of a living cell and hijack the cell’s reproductive machinery in order to reproduce itself.
Because a tumor virus needs to commandeer the reproductive machinery of a living cell to survive, it must force the host cell to enter the reproductive, or S-phase, of its cycle. Past research has demonstrated that a protein called E2F is central in the process by which S-phase is activated. When the cell is not reproducing, E2F is known to be inhibited by its binding to another protein, called Rb, or retinoblastoma protein.
The E1A protein, after binding Rb, is capable of physically pulling it off the E2F molecule. This unleashes the cell to replicate its DNA. And this, in turn, can promote transformations associated with cancer. Recently, it’s been shown that E1A’s cancer-promoting activity is more extensive, also involving a gene-regulating protein called p400. More…
Source: Eureka, 22 April 2008
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