Korean J Urol.  1997 Mar;38(3):229-234.

Effect of Retinoic Acid on Growth and Transduced Tumor Necrosis Factor-alpha Gene Expression of Human Bladder Tumor Cell Lines

Affiliations
  • 1Seoul National University College of Medicine, Seoul, Korea.

Abstract

INTRODUCTION AND OBJECTIVES: Retinoic acid (RA) is known as a potent chemopreventive agent in bladder tumor. Recently, RA has gained attention for up-regulation of transduced gene expression via long terminal repeat (LTR) transcriptional promotion. In this study, we investigated the possible dual effect of RA, growth inhibition and up-regulation of transduced gene expression which contains LTR promoter in human bladder carcinoma cell lines.
MATERIALS AND METHODS
Human bladder carcinoma cell lines CY-24, J-82, HT-1197, ATCC) were transduced with Moloney murine leukemia virus containing cDNA of TNF-alpha. The growth of transduced and parent cell line was measured by tetrazolium based colorimetric assay (MTF). Transduced TNF-alpha gene expression was determined by ELISA method.
RESULTS
TNF-alpha production was increased approximately twofold after treatment with RA (10 uM) in all three cell lines. This increase was dependent on RA concentration. RA treatment of transduced and parent cell line resulted in dose dependent inhibition of cell proliferation(up to 80% inhibitionwith 10 uM RA) in all parental and transduced cell lines.
CONCLUSIONS
These results indicate that RA shows dual effect in cytokine gene transduced bladder carcinoma cells with retroviral vector containing LTR promoter and could be a supplement to the gene therapy of bladder cancer.

Keyword

gene therapy; tumor necrosis factor-alpha (TNF-alpha)

MeSH Terms

Cell Line*
DNA, Complementary
Enzyme-Linked Immunosorbent Assay
Gene Expression*
Genetic Therapy
Humans*
Moloney murine leukemia virus
Parents
Terminal Repeat Sequences
Tretinoin*
Tumor Necrosis Factor-alpha*
Up-Regulation
Urinary Bladder Neoplasms*
Urinary Bladder*
Zidovudine
DNA, Complementary
Tretinoin
Tumor Necrosis Factor-alpha
Zidovudine
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