Forced expression of RDH10 gene retards growth of HepG2 cells

Elena Rossi, Paola Picozzi, Beatrice Bodega, Cistiana Lavazza, Carmelo Carlo-Stella, Anna Marozzi, Enrico Ginelli

Research output: Contribution to journalArticlepeer-review

Abstract

The constitutive over-expression of the retinol dehydrogenase 10 (RDH10) gene, involved in retinoic acid (RA) biosynthesis, produced in HepG2 cells a significant antiproliferative response, but not signs of apoptosis. An indirect assay based on the Chloramphenicol AcetylTransferase (CAT) reporter gene driven by a retinoic acid responsive element (RARE) suggests in genetically modified HepG2 cells an increase of the endogenous RA concentration. Furthermore, the growth arrest of HepG2 cells over-expressing the RDH10 gene was associated with the upregulation and downregulation of, respectively, RARbβ/p21 Cip1 and CycE/CdK2 mRNAs. These results indicated that forced expression of RDH10 produces antiproliferative effects highly comparable to those achieved by retinoids treatment and thus the development of a gene therapy, finalized at the restoration of the enzymatic and receptorial machinery of the RA pathway, could be a possible curative strategy for hepatocellular carcinoma (HCC).

Original languageEnglish
Pages (from-to)238-245
Number of pages8
JournalCancer Biology and Therapy
Volume6
Issue number2
Publication statusPublished - Feb 2007

Keywords

  • Cell growth arrest
  • HCC
  • HepG2
  • p21
  • RARβ
  • RDH10 overexpression
  • Retinoic acid

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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