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N-Myc knockdown and apigenin treatment controlled growth of malignant neuroblastoma cells having N-Myc amplification.

Abstract
Malignant neuroblastomas mostly occur in children and are frequently associated with N-Myc amplification. Oncogene amplification, which is selective increase in copy number of the oncogene, provides survival advantages in solid tumors including malignant neuroblastoma. We have decreased expression of N-Myc oncogene using short hairpin RNA (shRNA) plasmid to increase anti-tumor efficacy of the isoflavonoid apigenin (APG) in human malignant neuroblastoma SK-N-DZ and SK-N-BE2 cell lines that harbor N-Myc amplification. N-Myc knockdown induced morphological and biochemical features of neuronal differentiation. Combination of N-Myc knockdown and APG most effectively induced morphological and biochemical features of apoptotic death. This combination therapy also prevented cell migration and decreased N-Myc driven survival, angiogenic, and invasive factors. Collectively, N-Myc knockdown and APG treatment is a promising strategy for controlling the growth of human malignant neuroblastoma cell lines that harbor N-Myc amplification.
AuthorsMd Motarab Hossain, Naren L Banik, Swapan K Ray
JournalGene (Gene) Vol. 529 Issue 1 Pg. 27-36 (Oct 15 2013) ISSN: 1879-0038 [Electronic] Netherlands
PMID23941992 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Copyright© 2013 Elsevier B.V. All rights reserved.
Chemical References
  • Antineoplastic Agents
  • Proto-Oncogene Proteins c-myc
  • RNA, Messenger
  • RNA, Small Interfering
  • Apigenin
  • CASP3 protein, human
  • CASP8 protein, human
  • Caspase 3
  • Caspase 8
Topics
  • Antineoplastic Agents (pharmacology)
  • Apigenin (pharmacology)
  • Apoptosis (drug effects)
  • Caspase 3 (genetics, metabolism)
  • Caspase 8 (genetics, metabolism)
  • Cell Differentiation (drug effects)
  • Cell Line, Tumor
  • Cell Movement (drug effects)
  • Gene Knockdown Techniques
  • Humans
  • Neuroblastoma (genetics, pathology)
  • Proto-Oncogene Proteins c-myc (genetics, metabolism)
  • RNA, Messenger (genetics, metabolism)
  • RNA, Small Interfering (genetics, metabolism)
  • Transfection

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