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Fig. S1. Morphological changes and relative telomerase activity in IMR90, IMR90 WThTERT and LOX melanoma cancer cells.

Fig. S2. IMR90 WThTERT cells infected with MT-hTer-47A and -AU5 showing colocalization of TRF2 with γ-H2AX foci.

Fig. S3. IMR90 WThTERT cells infected with MT-hTer-47A and -AU5 exhibiting colocalization of TRF2 with 53BP1 foci.

Fig. S4. Quantitation of mean total number of TRF2 foci showing no difference in both IMR90 and IMR90 WThTERT cells transduced with either empty lentiviral vector, WThTER, MT-hTer-47A or -AU5.

Fig. S5. Western blot quantification of TRF2, phospho-ATM S1981 and phospho-p53 Ser15 before day 15 post-infection.

Fig. S6. MT-hTers activate ATM and phosphorylate at S1981 in hTERT-overexpressed IMR90 cells.

Fig. S7. Western blot quantification showing MT-hTers phosphorylate ATM at S1981 and p53 at Ser15 via repression of TRF2 in hTERT-overexpressed IMR90 cells.

Fig. S8. Western blot quantification showing the overexpression of TRF2 prevents the activation of ATM and p53.

Fig. S9. MT-hTers induce apoptosis via up-regulation of phospho-p53 and cleaved caspase 3 in IMR90 WThTERT cells transduced with MT-hTer-47A and -AU5.

Fig. S10. MT-hTer-treated IMR90 WThTERT cells showing up-regulation of GADD45γ and 14-3-3σ and down-regulation of NFκB.

Table S1. Differential gene expression changes in MT-hTer-47A and -AU5 treated IMR90 WThTERT cells compared to MT-hTer-47A and -AU5 infected IMR90 cells.

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