A Retroviral Wild-type p53 Expression Vector Penetrates Human Lung Cancer Spheroids and Inhibits Growth by Inducing Apoptosis

Toshiyoshi Fujiwara, Elizabeth A. Grimm, Tapas Mukhopadhyay, Wei De Cai, Laurie B. Owen-Schaub, Jack A. Roth

Research output: Contribution to journalArticle

207 Citations (Scopus)

Abstract

Multicellular tumor spheroids approximate the three-dimensional configuration of primary and metastatic tumors. The effects of retrovirus-mediated transduction of wild-type p53 (wt-p53) were studied on multicellular tumor spheroids of human non-small cell lung cancer cell lines H322a, the p53 gene of which is homozygously mutated at codon 248, and WT226b, which has endogenous wt-p53. The growth of WT226b spheroids was not affected by exogenous wt-p53 transduction; the growth of H322a spheroids, however, was significantly inhibited by the addition of wt-p53 virus stocks. Transduction of cells by the wt-p53 retroviral vector and penetration of multiple cell layers in H322a spheroids was demonstrated by in situ polymerase chain reaction/hybridization with the neomycin-resistant neo probe. Apoptotic changes indicating programmed cell death were observed in H322a spheroids treated with the wt-p53 virus. These results suggest that retroviral vectors can penetrate into multiple cell layers of three-dimensional tumor masses and induce potentially therapeutic effects.

Original languageEnglish
Pages (from-to)4129-4133
Number of pages5
JournalCancer Research
Volume53
Issue number18
Publication statusPublished - Sep 1993
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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    Fujiwara, T., Grimm, E. A., Mukhopadhyay, T., De Cai, W., Owen-Schaub, L. B., & Roth, J. A. (1993). A Retroviral Wild-type p53 Expression Vector Penetrates Human Lung Cancer Spheroids and Inhibits Growth by Inducing Apoptosis. Cancer Research, 53(18), 4129-4133.