The "membrane magnesium mitosis" model attributes intracellular Mg²⁺ a central role in regulating the coordinate process in cell proliferation (Rubin, Arch Biochem Biophys. 2007). According to this model, stimulation of cells with growth factors promotes a long lasting elevation in free intracellular Mg²⁺ followed by an increase in protein and DNA synthesis, culminating in mitosis. The main direct target of Mg²⁺ is ATP. MgATP^2-, but not ATP, is necessary for phosphoryl transfer reactions required for protein synthesis. Consequently, proliferating cells have a higher demand for Mg²⁺ than non-proliferating cells. The transient receptor potential melastatin (TRPM) cation channel, TRPM7, is a transporter for Mg²⁺, is regulated by Mg²⁺ and contributes to cellular Mg²⁺ homeostasis (Kerschbaum et al., Biophys J. 2003; Touyz, Am J Physiol Heart Circ Physiol. 2008). Because Mg²⁺ is central in mitosis and is accumulated by some cancer cells, Mg²⁺ transporters may be relevant in regulation of mitosis in transformed cells. Interestingly, Cetuximab (antibody to EGF-receptor)-irinotecan treatment in advanced colorectal patients with hypomagnesaemia shows a better median time to progression and an overall survival compared to patients with less than 20% reduction of serum Mg²⁺ (Vincenzi et al., Clin Cancer Res 2008).

We evaluated whether B-lymphocytes from healthy donors as well as CD5+CD19+ B-lymphocytes from chronic lymphocytic leukemia (CLL) patients express TRPM7 using RT-PCR. B-lymphocytes from healthy donors revealed a signal for TRPM7 mRNA. Similarly, CD5+CD19+ B-lymphocytes from CLL patients contained TRPM7 mRNA. Activation of CLL cells using PMA and ionomycin revealed an increase in TRPM7 mRNA.