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Apoptosis induced by the potential chemotherapeutic drug N1, N11-Diethylnorspermine in a neuroblastoma cell line.

  • Erika Söderstjerna
  • Martina Holst
  • Kersti Alm
  • Stina Oredsson
Publishing year: 2010
Language: English
Pages: 917-926
Publication/Series: Anti-Cancer Drugs
Volume: 21
Issue: 10
Document type: Journal article
Publisher: Rapid Communications
Additional info: The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Functional Zoology (432112239), Neuronal Survival (013212041), Molecular Cell Biology (432112241), Animal Physiology (Closed 2011) (011011000), Department of Biology (000016100)

Abstract english

Neuroblastoma is a highly malignant neoplasm found in young children. Although children with high-risk neuroblastoma respond to chemotherapy, relapses are common. On account of poor treatment outcome, new treatment strategies are constantly sought for neuroblastoma. Polyamine analogues are potentially novel substances for treatment of neuroblastoma. In this study, we have treated two neuroblastoma cell lines, SH-SY5Y and LA-N-1, with the spermine analogue N, N-Diethylnorspermine (DENSPM). SH-SY5Y was the most sensitive cell line, in which DENSPM treatment resulted in an inhibition of cell proliferation and an induction of cell death. The cell death induced by DENSPM treatment was apoptotic, as evidenced by cleavage of procaspase 3 and induction of caspase-3 activity. In contrast, DENSPM treatment only resulted in a slight inhibition of cell proliferation in LA-N-1 cells. There were several possible causes for the lower sensitivity to DENSPM treatment in the latter cell line when compared with SH-SY5Y cells. DENSPM-induced polyamine depletion was more extensive in SH-SY5Y cells than in LA-N-1 cells. This was partly because of a higher induction of the polyamine catabolic enzyme spermidine/spermine N-acetyltransferase in the cell line SH-SY5Y. The DENSPM-induced polyamine depletion was also caused by the inhibition of ornithine decarboxylase. LA-N-1 cells contained a higher level of the prosurvival protein survivin, which was further increased after DENSPM treatment. In contrast, DENSPM treatment resulted in a decreased survivin level in SH-SY5Y cells.


  • Neurosciences


  • ISSN: 0959-4973
Stina Oredsson
E-mail: stina [dot] oredsson [at] biol [dot] lu [dot] se


Functional zoology

+46 46 222 94 97



Principal investigator

LUCC - Lund University Cancer Centre

Research group

Animal Physiology


Cell proliferation

Doctoral students and postdocs

PhD Students, main supervisor

Wendy Soria Sotillo

PhD Students, assistant supervisor

Atena Malakpour Permlid