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Dual programmed cell death pathways induced by p53 transactivation overcome resistance to oncolytic adenovirus in

Joe Hasei1, Tsuyoshi Sasaki, Hiroshi Tazawa

  • 1Department of Orthopaedic Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.

Molecular Cancer Therapeutics
|January 15, 2013
PubMed

Insights

A novel p53-expressing oncolytic adenovirus, OBP-702, effectively targets resistant osteosarcoma cells. OBP-702 induces apoptosis and autophagy, offering a promising strategy for enhanced cancer therapy.

Area of Science:

  • Oncolytic virotherapy
  • Molecular biology
  • Cancer research

Background:

  • Tumor suppressor p53 regulates cell fate, including apoptosis and autophagy.
  • Oncolytic adenoviruses show antitumor activity, but resistance occurs.
  • The mechanism of p53's enhancement of oncolytic adenovirus activity is unclear.

Purpose of the Study:

  • Investigate the antitumor activity of p53-expressing oncolytic adenovirus OBP-702.
  • Elucidate the p53-mediated cell death pathway in resistant osteosarcoma cells.
  • Evaluate OBP-702's efficacy in a preclinical osteosarcoma model.

Main Methods:

  • Assessed cytopathic activity of OBP-702 in sensitive and resistant osteosarcoma cell lines.
  • Investigated apoptosis and autophagy induction by OBP-702.
  • Utilized an orthotopic osteosarcoma xenograft model to assess antitumor effects.

Main Results:

  • OBP-702 demonstrated superior viability suppression in osteosarcoma cells compared to OBP-301 or Ad-p53.
  • OBP-702 induced significantly greater apoptosis and autophagy.
  • OBP-702 suppressed tumor growth in vivo.

Conclusions:

  • OBP-702 effectively targets resistant osteosarcoma cells by inducing dual apoptotic and autophagic cell death.
  • p53 transactivation via OBP-702 regulates miRNA and DRAM, mediating cell death.
  • OBP-702 represents a promising antitumor strategy for osteosarcoma.

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