The Cav3 blocker drug mibefradil synergized with temozolomide (TMZ) and radiation to reduce in vivo tumor growth and prolong animal survival. Conclusions Together these data reveal a role for microenvironment Cav3 in promoting GBM tumor progression through regulating neuronal and glial processes particularly associated with the OPC-cell state. Targeting both intrinsic and microenvironment Cav3 with the inhibitor mibefradil significantly enhanced the anti-GBM effects of TMZ and radiation.
Blocking T-type Ca-channels using Mibefradil reduced cortical actin tension in these cells and enhanced their membrane vibrations and dissipation of intracellular mechanical work to the cell surroundings...Our results show that cell membrane vibrations and dissipation of mechanical work are higher in malignant cells relative to benign cells. Accordingly, these properties may be used to detect and monitor cellular and tissue malignancies.