Regulation of URG4/URGCP and PPARα gene expressions after retinoic acid treatment in neuroblastoma cells

Tumour Biol. 2013 Dec;34(6):3853-7. doi: 10.1007/s13277-013-0970-1. Epub 2013 Jul 3.

Abstract

Neuroblastoma (NB), originating from neural crest cells, is the most common extracranial tumor of childhood. Retinoic acid (RA) which is the biological active form of vitamin A regulates differentiation of NB cells, and RA derivatives have been used for NB treatment. PPARα (peroxisome proliferator-activated receptor) plays an important role in the oxidation of fatty acids, carcinogenesis, and differentiation. URG4/URGCP gene is a proto-oncogene and that overexpression of URG4/URGCP is associated with metastasis and tumor recurrence in osteosarcoma. It has been known that URG4/URGCP gene is an overexpressed gene in hepatocellular carcinoma and gastric cancers. This study aims to detect gene expression patterns of PPARα and URG4/URGCP genes in SH-SY5Y NB cell line after RA treatment. Expressions levels of PPARα and URG4/URGCP genes were analyzed after RA treatment for reducing differentiation in SH-SY5Y NB cell line. To induce differentiation, the cells were treated with 10 μM RA in the dark for 3-10 days. Gene expression of URG4/URGCP and PPARα genes were presented as the yield of polymerase chain reaction (PCR) products from target genes compared with the yield of PCR products from the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene. SH-SY5Y cells possess small processes in an undifferentiated state, and after treatment with RA, the cells developed long neurites, resembling a neuronal phenotype. PPARα gene expression increased in RA-treated groups; URG4/URGCP gene expression decreased in SH-SY5Y cells after RA treatment compared with that in the control cells. NB cell differentiation might associate with PPARα and URG4/URGCP gene expression profile after RA treatment.

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Cell Differentiation / drug effects
  • Cell Differentiation / genetics
  • Cell Line, Tumor
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Neoplasm Proteins / genetics*
  • Neuroblastoma / genetics
  • Neuroblastoma / pathology
  • PPAR alpha / genetics*
  • Proto-Oncogene Mas
  • Reverse Transcriptase Polymerase Chain Reaction
  • Time Factors
  • Tretinoin / pharmacology*

Substances

  • Antineoplastic Agents
  • MAS1 protein, human
  • Neoplasm Proteins
  • PPAR alpha
  • Proto-Oncogene Mas
  • URGCP protein, human
  • Tretinoin