Supplementary Figure 16 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 16 shows that CP-d/n-ATF5 inhibits growth of BE(2)-C tumors and increases apoptosis</p

Supplementary Figure 5 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 5 shows that overexpression of ATF5 promotes anoikis resistance of CHLA-255 in vitro</p

Supplementary Figure 15 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 15 shows that CP-d/n-ATF5 treatment does not induce BMF under adherent conditions</p

Supplementary Figure 9 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 9 shows that BMF knockdown rescues ATF5 loss-induced reduction of anchorage-independent cell viability</p

Supplementary Figure 17 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 17 shows that CP-dn-ATF5 reduces tumor growth and metastasis of SK-N-DZ in vivo</p

FIGURE 3 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Depletion of ATF5 induces anoikis and decreases metastasis of neuroblastoma cells. A and B, Viability of BE(2)-C and SK-N-DZ suspension cells in poly-HEMA–coated plates, expressing Dox-inducible shATF5-1 or shATF5-2 at different timepoints after Dox treatment. Mean ± SD. C and D, Quantification of anoikis of BE(2)-C and SK-N-DZ suspension cells cultured as in A and B at different timepoints after Dox addition. Mean ± SD. E, Quantification of whole-body bioluminescence flux (photons/second) in mice 24 hours after intracardiac injection of BE(2)-C-shATF5-2 cells, + Dox (n = 9); −Dox, (n = 9). Mice were maintained on drinking water containing Dox (2 mg/mL) from 3 days before injection to the time of euthanasia. F, Bioluminescent images at 24 hours after intracardiac injection under conditions described in E. G, Quantification of bioluminescence of blood from mice collected 12 and 24 hours after intracardiac injection under conditions described in E. H, Quantification of apoptosis of BE(2)-C-shATF5-2 CTCs isolated from mice 12 hours after intracardiac injection and treatment ± Dox (see E and Materials and Methods), + Dox (n = 5), −Dox, (n = 5). I, RT-PCR analyses of ATF5 and ACTB in circulating BE(2)-C-shATF5-2 cells isolated after 12 hours. J, Time course of whole-body bioluminescence flux in mice treated as in E. + Dox (n = 8); −Dox, (n = 9). The mice were monitored for metastatic spread by bioluminescence and euthanized at day 31. K, Quantification of total flux (photons/second) by ex vivo liver bioluminescence at the time of euthanasia (day 31). L, Quantification of bioluminescence in bone marrow homogenates at the time of euthanasia (day 31). *, P P P P < 0.0001.</p

Supplementary Figure 2 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 2 shows that ATF5 knockdown decreases neuroblastoma cell viability and promotes apoptosis under adherent conditions</p

Supplementary Figure 12 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 12 shows that CP-d/n-ATF5 inhibits the growth of MYCN-amplified and MYCN-non-amplified cell lines in a dose-dependent manner</p

Supplementary Figure 7 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Figure 7 shows that ATF5 knockdown decreases SK-N-DZ CTC survival</p

Supplementary Table 1 from Activating Transcription Factor 5 Promotes Neuroblastoma Metastasis by Inducing Anoikis Resistance

Supplementary Table 1. List of antibodies used in this study</p