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Ineffectiveness of the presence of H-ras/p53 combination of mutations in squamous cell carcinoma cells to induce a conversion of a nontumorigenic to a tumorigenic phenotype

  • Hakjoo Lee
    ,
  • D. Li
    ,
  • T. Prior
    ,
  • B. C. Casto
    ,
  • C. M. Weghorst
    ,
  • C. F. Shuler
*Corresponding author for this work
  • Ohio State University
    ,
  • University of Southern California
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Sustainable Development Goals

  • SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well

Abstract

Human tumor cells have properties in vitro or in surrogate hosts that are distinct from those of normal cells, such as immortality, anchorage independence, and tumor formation in nude mice. However, different cells from individual tumors may exhibit some, but not all of these features. In previous years, human tumor cell lines derived from different tumor and tissue types have been studied to determine those molecular changes that are associated with the in vitro properties listed above and with tumorigenicity in nude mice. In the present study, seven cell lines derived from human tumors were characterized for p53 and ras mutations that may occur in SCC tumor phenotypes and for tumor formation in nude mice. This investigation was designed to examine whether co-occurrence of mutated ras and p53 lead to a malignant stage in the progression process. None of the seven cell lines contained mutations in the recognized 'hot spots' of the p53 tumor suppressor gene, but four had a nonsense/splice mutation in codon 126 and a mutation in codon 12 of the H-ras gene. The remaining three cell lines had p53 mutations in intron 5, in codon 193, and a missense mutation in codon 126, respectively. Four of seven cell lines were nontumorigenic; two of these cell lines contained a nonsense p53-126 mutation and mutated ras; one had a missense mutation at codon 126 but no mutated ras; the the fourth had only a p53 mutation at codon 193. Two of the nontumorigenic cell lines were converted to tumorigenicity after treatment with methyl methanesulfonate or N-methyl-N'-nitro-N-nitrosoguanidine with no apparent additional mutations in either gene. Our analysis revealed that there was a high frequency of genetic diversity and mutations in both p53 and H-ras. There was also a lack of a causal relationship in the presence of mutations in p53 and the cells' ability to exhibit a malignant potential in nude mice.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 419-434 (16 pages)

Journal (Volume, Issue Number)

Cell Biology and Toxicology (Volume 13, Issue 6)

Publication milestones

  • Published - 1997

Publication status

Published - 1997

ISSN

0742-2091

Publication IDs

  • Scopus: 0030766184
  • PubMed: 9352120

Publication metrics

Metrics

SciVal
citations
12
Fractional count
1
Fractional count
0.14
Fractional count
6
Fractional count
0.86
Fractional count
1
Fractional count
1
Scopus
citations
SciVal
FWCI
0.68
SciVal
Author count
7
SciVal
Paper percentile
63

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Citation count
12
Captures
7

Funding Details

This research was supported in part by NIH-NCI-CA-25907 (G.E.M., C.F.S.).