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Author Notes:

Correspondence: E-mail: jing937@hotmail.com

Conceived and designed the experiments: SL JH.

Performed the experiments: SL GC JH.

Analyzed the data: HCJ ST.

Contributed reagents/materials/analysis tools: HCJ QT.

Wrote the paper: SL.

We thank Qinglan Ruan, Hong Mei, Ying Yang for experimental discussion and assistance.

The authors have declared that no competing interests exist.

The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.


Research Funding:

Grant support: the National Natural Science Foundation of China (NSFC) grants 81070429 (Jing He), 30600278 and 30772359 (Qiangsong Tong).


  • Science & Technology
  • Multidisciplinary Sciences
  • Science & Technology - Other Topics
  • GENE
  • IAPS
  • Apoptosis
  • Small interfering RNAs
  • Neuroblastoma cells
  • DNA fragmentation
  • Immunoblotting
  • Cancer treatment
  • Tubulins
  • Protein expression

Noscapine Induced Apoptosis via Downregulation of Survivin in Human Neuroblastoma Cells Having Wild Type or Null p53


Journal Title:



Volume 7, Number 7


, Pages e40076-e40076

Type of Work:

Article | Final Publisher PDF


Neuroblastoma is the most common extracranial solid tumor of childhood. It accounts for 15% of pediatric cancer deaths. Chemotherapy is the mainstay of treatment in children with advanced neuroblastoma. Noscapine, a nontoxic natural compound, can trigger apoptosis in many cancer types. We now show that p53 is dispensable for Noscapine-induced cell death in neuroblastoma cell lines, proapoptotic response to this promising chemopreventive agent is mediated by suppression of survivin protein expression. The Noscapine treatment increased levels of total and Ser 15 -phosphorylated p53 protein in SK-SY5Y cells, but the proapoptotic response to this agent was maintained even after knockdown of the p53 protein level. Exposure of SK-SY5Y and LA1-5S cells to Noscapine resulted in a marked decrease in protein and mRNA level of survivin as early as 12 hours after treatment. Ectopic expression of survivin conferred statistically significant protection against Noscapine-mediated cytoplasmic histone-associated apoptotic DNA fragmentation. Also, the Noscapine-induced apoptosis was modestly but statistically significantly augmented by RNA interference of survivin in both cell lines. Furthermore, Noscapine-induced apoptotic cell death was associated with activation of caspase-3 and cleavage of PARP. In conclusion, the present study provides novel insight into the molecular circuitry of Noscapine-induced apoptosis to indicate suppression of survivin expression as a critical mediator of this process.

Copyright information:

© 2012 Li et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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