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A naturally occurring p73 mutation in a p73-p53 double-mutant lung cancer cell line encodes p73 alpha protein with a

Huqun1, Yoshiyuki Endo, Hong Xin

  • 1Department of Respiratory Oncology and Molecular Medicine, Institute of Development, Aging and Cancer, Tohoku University, Aoba-ku, Sendai 980-8575, Japan.

Cancer Science
|August 7, 2003
PubMed

Insights

The p73 tumor suppressor

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The tumor suppressor p73, a homolog of p53, plays a role in cell growth and apoptosis, but its function in cancer is debated.
  • Multiple p73 isotypes exist, with Delta N isotypes potentially inhibiting TA isotypes, complicating its role.
  • The rarity of p73 mutations and lack of tumors in knockout mice add to the controversy surrounding its cancer relevance.

Purpose of the Study:

  • To investigate the functional impact of naturally occurring p73 mutants found in lung cancer cell lines.
  • To analyze the effects of specific p73 mutations on transactivation activity and colony formation suppression.
  • To understand the combined effect of p73 and p53 mutations in lung cancer progression.

Main Methods:

  • Analysis of three naturally occurring p73 mutants from lung cancer cell lines (NCI-H1155, DMS 92, A427).
  • Characterization of p73 alpha(G264W) mutant in NCI-H1155 cells, assessing its transactivation activity and dominant-negative potential.
  • Evaluation of p73(Del418) and p73(Del603) mutants in DMS 92 and A427 cells for transactivation and colony formation suppression.

Main Results:

  • The p73 alpha(G264W) mutant in NCI-H1155 cells demonstrated loss of transactivation and dominant-negative inhibition of wild-type p73 alpha.
  • p73 alpha(G264W) failed to suppress colony formation, indicating a loss of tumor suppressor function.
  • Mutations p73(Del418) and p73(Del603) retained wild-type levels of transactivation and colony formation suppression, with unclear biological significance.
  • NCI-H1155 cells harbor both p73 and p53 mutations, suggesting an additive growth advantage.

Conclusions:

  • The p73 alpha(G264W) mutation acts as a dominant-negative mutant, impairing wild-type p73 alpha function and contributing to cancer cell growth.
  • The biological significance of p73(Del418) and p73(Del603) mutations requires further investigation.
  • Co-occurring p73 and p53 mutations in lung cancer may confer an additive growth advantage, highlighting the complex interplay of tumor suppressors in cancer development.

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