Cadmium (Cd) exposure is linked to breast cancer since Cd mimics the effects of estrogens in mammary epithelial cells (Johnson et al., 2003). However, Cd exposure leads to epithelial mammary cells transformation into a highly aggressive cancerous phenotype independently of hormonal receptors suggesting that Cd promotes cancer progression by different mechanisms (Benbrahim-Tallaa et al., 2009). Ion channels are involved in cancer progression by various mechanisms including membrane potential, volume and calcium signaling regulations. Among ion channels, the transient receptor potential melastatin related-7 (TRPM7) allows trace metals entry including Cd entry (Monteilh-Zoller et al., 2003). Importantly, TRPM7 overexpression predicts poor outcome in breast cancer patients (Middelbeek et al., 2012). Moreover, TRPM7 regulates breast cancer cell migration and invasion (Middelbeek et al., 2012; Guilbert et al., 2013), and metastasis formation in vivo (Middelbeek et al., 2012). The aim of this work is to assess the role of TRPM7 in transformed mammary epithelial cells induced by Cd exposure. MCF10A mammary epithelial cells were incubated with low Cd concentration (2.5 µM) during 40 weeks (Benbrahim-Tallaa et al., 2009). Invasive properties of transformed cells were studied by using Boyden chamber assays with and without Matrigel. Matrix Metalloprotease (MMP-2 and -9) secretion was assessed by gelatin zymography. Plasminogen activator secretion (tPA and uPA) was analyzed by gelatin-plasminogen zymography. Finally, activity of TRPM7 was studied by whole-cell patch-clamp. In MCF10A exposed to Cd, both cell migration and invasion were increased (+29.74 ± 3.22% for migration (N=4), and +33.24 ± 0.03% for invasion (N=3)) when compared to non-treated cells (p<0.001). Moreover, Cd exposure stimulated MMP-2 and MMP-9 as well as tPA and uPA secretions. TRPM7 current was also increased in MCF10A exposed to Cd (44.91 ± 3.89 pA.pF-1 at +100 mV; n=15) when compared to the non-treated cells (27.67 ± 2.17 pA.pF-1 at +100 mV; n=14 ; p<0.001). TRPM7 silencing decreased more migration in Cd-treated cells (-73.13 ± 1.64 %, N=4; p<0.001) than in non-treated cells (-52.36 ± 1.92 %, N=4; p<0.001). Similarly, TRPM7 silencing decreased cell invasion by 55.64 ± 2.95 %, in non-treated cells and in a larger manner in Cd-treated cells (-82.57 ± 1.04 %; N=3; p<0.001), and also inhibited proteases secretion. Collectively, our results clearly show that TRPM7 regulates invasiveness in Cd-transformed mammary epithelial cells.