cancer cells make excess cholesterol, deposit it in mitochondria membrane to prevent release of pro-apoptotic molecules (statins inhibit cholesterol synthesis)
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From: Steve on 14 Jul 2008 16:32 According to the link below, in liver cancer cells (and possibly other types of cancer cells - they mention colorectal and melanoma), excess cholesterol is made which is deposited in the membranes of mitochondria which decreases the membranes' flexibility and thus their permeability and prevents pro-apoptotic molecules (such as bax and bak) from being released from the mitochondria. When these pro-apoptotic molecules are released from the mitochondria, they initiate apoptosis (cell suicide) by activating the caspase enzymes (though the release of these pro-apoptotic molecules does not guarantee apoptosis since the cancer cells will try to prevent the caspase enzymes from working). One more reason why statins are strong anti-cancer agents. Their most prominent anti-cancer action is they prevent the ras protein from getting anchored to the cell membrane and thus the ras protein cannot get activated - the cancer cell relies on an activated ras protein. Statins do this by preventing the synthesis of a molecule (by inhibiting the enzyme that makes cholesterol) that is the cell membrane anchor for the ras protein. http://www.idibaps.ub.edu/homex.php?idi=eng&progx=http://www.idibaps.ub.edu/ eng/detallenot.php?it=1648&idi=eng&tdet=3
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