Therapeutic inhibitors of MIR17HG exert potent antitumor activity in vitro and in vivo in animal models of human MM. (A) Subcutaneous in vivo tumor growth of AMO1 cells in NOD SCID mice, 21 days after treatment with G2-15b∗-TO (G; n = 5), B9-19-TO (B; n = 5), or vehicle (NC; n = 5). (B-C) qRT-PCR analysis of lnc-17-92 (C) and lnc-17-92 targets (D) in AMO1 xenografts, retrieved from animals treated with G2-15b∗-TO (G; n = 1), B9-19-TO (B; n = 1), or vehicle (NC; n = 1) as a control. Raw Ct values were normalized to ACTB mRNA and expressed as ΔΔCt values calculated using the comparative cross threshold method. Expression levels in NC were set as an internal reference. (D) Bioluminescent imaging–based (BLI-based) measurement of in vivo tumor growth of MOLP8-luc⁺ in NSG mice, after treatment with G2-15b∗-TO (G; n = 8), B9-19-TO (B; n = 6), or vehicle (NC; n = 11). On the top, a scatter plot shows the analysis of bioluminescence intensity. Red bars indicate median value. Bioluminescence was measured at the end of the treatment cycle (day 15). Image acquisition (below). Mice removed from the study owing to failed IV injection of tumor cells are covered by a black rectangle. (E) Survival analysis from experiment in panel E. (F) Human κ light chain enzyme-linked immunosorbent assay–based measurement of in vivo tumor growth of MM patient cells in NSG mice (PDX-NSG), after treatment with G2-15b∗-TO (G; n = 2), bortezomib (BTZ; n = 2), or vehicle (NC; n = 3). Black arrows indicate treatments. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. Max, maximum; Min, minimum; ns, not significant.