Fig. 3
From: Therapeutic implications of cellular and molecular biology of cancer stem cells in melanoma
Molecular targeted therapy in melanoma CSCs. mAbs against FZD receptor, DLL4, Notch1, CD133, CD20 or ABCB5 attenuates the CSCs-dependent melanoma progression. Abrogation of Notch1, Hedgehog and Wnt siganling using DAPT, Andro, Honokiol, Cyclopamine or XAV939 depletes CSCs in melanoma. Anti-apoptotic small molecule inhibitors such as ABT-263 and a SIRT1 inhibitor, Tenovin-6 induce apoptosis and suppress CSC-mediated melanoma growth. Overexpression of ESAT-6gpi/IL-21 antigen sensitizes CSCs against NK cell-mediated apoptosis. MRP1-CD28 bivalent aptamers attenuate drug-resistance of CSCs in melanoma. CSCs: cancer stem cells; Hh: hedgehog; Fz: frizzled; DAPT: N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester, a γ-secretase inhibitor; SIRT1: sirtuin 1; ESAT-6gpi: 6 kDa early secreted antigenic target (ESAT-6) in the glycosylphosphatidylinositol (GPI)-anchored form; IL-21: interleukin-21; NK cells: natural killer cells; MRP1: multidrug resistant proteins 1; CTX: cyclophosphomide