Voltage-gated sodium channels potentiate the invasive capacities of human non-small-cell lung cancer cell lines

P2X7 receptor activation enhances SK3 channels- and cystein cathepsin-dependent cancer cells invasiveness

“…Although these cancer cells mainly expressed P2X 7 R, low levels of mRNA for P2X 4 , P2X 5 and P2X 6 receptors were also detected ( Figure 1c). As in cancer cells mRNA expression does not always correlate to the translation in functional proteins (Roger et al, 2007), we performed patch clamp experiments to assess the functionality of such receptors. We conducted experiments using 10 mM ATP, which is supposed to activate all P2X receptors except P2X 7 R, but did not record any ATP-evoked current from cancer cells.…”

NaV1.5 enhances breast cancer cell invasiveness by increasing NHE1-dependent H+ efflux in caveolae

“…One key step is the acquisition by cancer cells of an invasive potency, mainly relying on the capacity to degrade basement membranes and extracellular matrices (Gupta and Massague, 2006) by various proteases such as matrix metalloproteinases (Egeblad and Werb, 2002) or cysteine cathepsines (Mohamed and Sloane, 2006). We and others have shown that voltage-gated sodium channels (Na V ) are abnormally expressed in cancer cells of epithelial origin and associated with cancer progression (Laniado et al, 1997;Roger et al, 2003Roger et al, , 2006Roger et al, , 2007Fraser et al, 2005;Diaz et al, 2007). In the highly invasive MDA-MB-231 breast cancer cell line, Na V 1.5 activity enhances extracellular matrix invasion by increasing the activity of acidic cysteine cathepsins B and S through an acidification of the pericellular microenvironment (Gillet et al, 2009).…”

The Human Papilloma Virus – Ion Channel Link in Cancer: An Alternative Opportunity for Diagnosis and Therapy

“…Metastasis is a process where cells escape from a primary tumor, enter circulation (blood or lymph), migrate and invade other tissues, proliferate and form secondary tumors. In in vitro experiments, it has been shown that VGSCs are associated to proliferation, motility, and invasion of breast, lung, ovary and prostate cancer (Roger et al, 2003;Gao et al, 2010;Diss et al 2005;Chioni et al, 2010;Roger et al, 2007;House, et al, 2010;Bennett et al, 2004). In prostate cancer cells, the main VGSC overexpressed is the Na V 1.7 subunit, while in breast, colon and ovary the Na V 1.5 subunit is the predominant subunit overexpressed.…”

“…Expression of Na V 1.4, Na V 1.6 and Na V 1.7 channels has been detected in biopsies from cervical cancer (Díaz et al, 2007). Whether the activity of the sodium channel participates in the invasiveness of cervical cancer cells remains to be determined, but the pharmacological blockade of VGSCs commonly results in the reduced migration of highly metastatic cell lines, whereas the facilitation of channel opening by agonists enhances migration without impairing cell proliferation or viability (Roger et al, 2007). The abnormal expression of these VGSCs might be used as a tumor marker and a potential therapeutic target for cervical carcinoma.…”