RT Journal Article
SR Electronic
T1 Acyclic Retinoid Combined With Tenascin-C-derived Peptide Reduces the Malignant Phenotype of Neuroblastoma Cells Through N-Myc Degradation
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3487
OP 3492
DO 10.21873/anticanres.13494
VO 39
IS 7
A1 OTSUKA, KAZUKI
A1 SASADA, MANABU
A1 HIRANO, YU
A1 NOHARA, YUSUKE
A1 IYODA, TAKUYA
A1 HIGAMI, YOSHIKAZU
A1 KODAMA, HIROAKI
A1 FUKAI, FUMIO
YR 2019
UL http://ar.iiarjournals.org/content/39/7/3487.abstract
AB Background/Aim: Despite intensive chemotherapy, the survival rates for high-risk neuroblastoma, most of which have MYCN amplification, remain low. Overexpression of N-myc oncoprotein promotes expression of cancer-associated properties. We recently found that combination of all-trans retinoic acid (ATRA) with the β1-integrin-activating peptide TNIIIA2 attenuated cancer-associated properties of neuroblastoma cells through N-Myc degradation. However, ATRA has serious side-effects and there are concerns about late adverse effects. The aim of this study was to examine the effects of the combination of acyclic retinoid (ACR) with TNIIIA2 on neuroblastoma. Materials and Methods: The effects of ACR and TNIIIA2 were examined by neuroblastoma cell proliferation and survival assays as well as by using a neuroblastoma xenograft model. The levels of N-Myc and cancer-associated malignant properties were assayed by western blot and colony formation assay, respectively. Results: Combining ACR, which is clinically safe, with TNIIIA2 induced proteasomal degradation of N-Myc and reduction of neuroblastoma cell malignant properties. An in vivo experiment showed therapeutic potential. Conclusion: ACR-TNIIIA2 combination treatment may be efficacious and clinical safe chemotherapy for high-risk neuroblastoma.