Effect of p53 tumor suppressor on nucleotide excision repair in human colon carcinoma cells treated with 4-nitroquinoline 1-oxide

Young R. Seo, Sang H. Lee, Sung Sik Han, Jae Chun Ryu

Research output: Contribution to journalArticle

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Abstract

In probing the mechanism of nucleotide excision repair (NER) in response to 4-nitroquinoline 1-oxide (4NQO)-induced DNA damage, the effect of p53 tumor suppressor was investigated. The effect of p53 protein on the repair of damaged DNA was examined by comet assay. Expression of p53 and p21(Wafl/Cipl) proteins was measured by the Enzyme-linked immunosorbent assay (ELISA) and immunocytochemistry, respectively. Compared to RKO cells having the wild-type p53 gene, increased cytotoxicity by 4NQO was observed in RKOmp53 cells with a mutation in p53 protein. DNA single strand breaks (SSB), indicative of the DNA repair, were considerably increased in 4NQO-treated RKO cells. Also, the expression of p53 and p21 proteins was significantly increased in 4NQO- treated RKO cells. In RKOmp53 cells, no effect of 4NQO on p21 expression was observed. Our findings suggest that 4NQO-induced NER is p53-dependent and involves up-regulation of its downstream regulator, p21(Wafl/Cipl) proteins.

Original languageEnglish
Pages (from-to)157-164
Number of pages8
JournalResearch Communications in Molecular Pathology and Pharmacology
Volume104
Issue number2
Publication statusPublished - 1999 Dec 1

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4-Nitroquinoline-1-oxide
DNA Repair
Colon
Carcinoma
Neoplasms
Proteins
Single-Stranded DNA Breaks
Comet Assay
p53 Genes
DNA Damage
Up-Regulation
Enzyme-Linked Immunosorbent Assay
Immunohistochemistry
Mutation

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Effect of p53 tumor suppressor on nucleotide excision repair in human colon carcinoma cells treated with 4-nitroquinoline 1-oxide. / Seo, Young R.; Lee, Sang H.; Han, Sung Sik; Ryu, Jae Chun.

In: Research Communications in Molecular Pathology and Pharmacology, Vol. 104, No. 2, 01.12.1999, p. 157-164.

Research output: Contribution to journalArticle

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