A magnesium deficient diet inhibits tumor cell proliferation by altering the activity of cell cycle regulatory proteins.

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Magnesium is a vital mineral involved with many cellular and metabolic functions. As the most abundant cation in the human body, magnesium is essential to cell proliferation, protein synthesis and energy production (Wolf, et al 2007). Among its many functions, magnesium plays a central role in the regulation of cell growth (Ruben, 1975). As such, the relationship between magnesium and the proliferation and growth of tumor cells has been the subject of numerous studies.
Cellular growth, cell cycle proteins and the role of magnesium.
Harry Rubin, who conducted many studies on the role of magnesium, found that the rate of protein synthesis is highly sensitive to availability of intracellular magnesium (Ruben, 2007). His 2007 study found that increased or decreased levels of Mg2+ altered the rates of cellular proliferation for several hours (Ruben, 2007).
There are four phases in the cycle of cellular division including the M phase (mitosis and cell division), G1 phase, S phase (DNA replication) and G2 phase (Tsihlias, et al 1999). Progression through these phases is regulated by a family of proteins called cyclin-dependent kinases (CDKs) (Tsihlias, et al 1999). Activation or inactivation of cyclin-CDK complexes regulates movement through the cell cycle (Sgamboto et al, 1999 and Sherr and Roberts 1995).
Cell cycle progression is promoted by two families of enzymes, D cyclins (D1-3) and cyclin E (Wolf and Trapani, 2008 and Nabel, 2002). These enzymes are activated in the G1 phase and promote cell progression through S phase.(Wolf and Trapani, 2008 and Nabel, 2002).
Negative regulator proteins include those in the CIP/KIP family specifically p21cip1 and p27kip1 which prevent progression from G1 to S phase (Wolf and Trapani,...

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