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E1B-deleted adenovirus replicates in p53-deficient lung cancer cells due to the absence of apoptosis

Naoki Harada1, Yoshimasa Maniwa, Masahiro Yoshimura

  • 1Department of Cardiovascular, Thoracic and Pediatric Surgery, Kobe University Graduate School of Medicine, 7-5-2 Kusuniki-cho, Chuo-ku, Kobe 650-0017, Japan.

Oncology Reports
|October 8, 2005
PubMed

Insights

E1B55K-deleted adenovirus selectively targets and kills p53-mutant lung cancer cells, demonstrating potential for gene therapy. Wild-type p53 lung cancer cells resist infection and promote apoptosis, preventing viral replication.

Area of Science:

  • Oncolytic virotherapy
  • Molecular oncology
  • Gene therapy

Background:

  • Adenovirus protein E1B55K inactivates host cell p53, promoting viral replication and cancer cell proliferation.
  • Understanding the role of p53 in adenovirus infection is crucial for developing targeted cancer therapies.

Purpose of the Study:

  • To investigate the cytopathic effects of E1B55K-deleted adenovirus (AxE1AdB) in primary lung cancer cells.
  • To evaluate the potential of AxE1AdB as a gene therapy agent for lung cancer, particularly in relation to p53 status.

Main Methods:

  • Infection of p53 wild-type (SBC3) and p53 mutant (SBC5, PC3, EBC1) lung cancer cell lines with AxE1AdB.
  • Assessment of viral cytotoxicity and induction of apoptosis.
  • cDNA array analysis to study mRNA expression in virus-infected cells.

Main Results:

  • AxE1AdB showed no cytopathic effect on p53 wild-type SBC3 cells, which continued to replicate.
  • AxE1AdB efficiently killed p53 mutant lung cancer cell lines (SBC5, PC3, EBC1).
  • Apoptosis was observed in SBC3 cells, while restricted in p53-mutant lines; Bax mRNA increased in SBC3 and decreased in SBC5.

Conclusions:

  • AxE1AdB selectively replicates in and exhibits strong cytotoxicity against p53-mutant lung cancer cells.
  • p53-intact cells induce apoptosis via Bax expression, preventing virus replication and infection spread.
  • E1B55K-deleted adenovirus holds promise for targeted gene therapy in p53-mutant lung cancers.

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