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Poster Display & Cocktail

66P - Evaluation of Aurora: A targeting PROTACs efficacy in neuroblastoma cell lines

Date

03 Mar 2025

Session

Poster Display & Cocktail

Presenters

Georgiana Pamfil

Citation

Annals of Oncology (2025) 10 (suppl_2): 1-8. 10.1016/esmoop/esmoop104219

Authors

G. Pamfil1, E. Rubini2, D. Boi2, I.A. Asteriti2, B. Kennedy3, S. Rosignoli4, C. Lindon3, G. Guarguaglini2, A. Paiardini1

Author affiliations

  • 1 Department Of Biochemical Sciences, Sapienza University of Rome, 00185 - Rome/IT
  • 2 Institute Of Molecular Biology And Pathology, National Research Council, 00185 - Rome/IT
  • 3 Department Of Pharmacology, University of Cambridge, CB2 0QQ - Cambridge/GB
  • 4 Centre For Regenerative Medicine "stefano Ferrari", Department Of Life Sciences, University of Modena and Reggio Emilia, 41125 - Modena/IT

Resources

This content is available to ESMO members and event participants.

Abstract 66P

Background

Neuroblastoma is a pediatric tumor of the sympathetic nervous system. High levels of the N-Myc oncoprotein, due to MYCN oncogene amplification, are associated with high-risk neuroblastoma. Because of its disordered structure, no small molecules directly targeting N-Myc are available. The mitotic Aurora A kinase binds N-Myc and prevents its degradation, thus sustaining high levels of the oncoprotein and contributing to the development of MYCN-amplified (MNA) neuroblastoma. In the last few years, different Aurora A targeting PROTACs, i.e. molecules able to degrade a protein of interest, have been developed, but only one study focused its attention on the possibility to use them in MNA neuroblastoma. In the present study the effects of two available Aurora A PROTACs (JB300 and APEX-D) were investigated in a neuroblastoma context.

Methods

JB300 and APEX-D were tested at different concentrations in a panel of neuroblastoma cell lines (MNA and non-MNA) and in a non-cancerous cell line. Western blots were performed at 3 hours and 48 hours after treatment in order to assess Aurora A degradation and long term effects on N-Myc protein levels, respectively; MTT assays after 72 h enabled us to investigate the effects on cell viability.

Results

Obtained results indicate that both PROTACs are able to induce Aurora A degradation within a short time (3 hours) and low concentrations (50 nM, 150 nM, 300 nM). Analysis of cell viability in the non-cancerous cell line revealed a non-toxic effect. After 48 hours, it was possible to observe a decrease in N-Myc protein levels in MNA neuroblastoma cell lines, associated with PARP-1 cleavage which suggests the induction of cell death. Indeed, both PROTACs yielded a decrease in cell viability in MNA neuroblastoma cell lines, which was not observed in the non-MNA neuroblastoma cells.

Conclusions

JB300 and APEX-D, besides being non-toxic in a non-cancerous cell line, show a differential effect on cell viability between MNA and non-MNA neuroblastoma cell lines, associated with a decrease of N-Myc protein levels. Overall, Aurora A PROTACs may be considered as promising agents to be further investigated as a therapeutic strategy for MNA neuroblastoma.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

The main project is funded by the AIRC Foundation. Author fellowship is funded by the Eupaxx Biotech.

Disclosure

All authors have declared no conflicts of interest.

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