Superinduction of wild-type p53 protein after 2-methoxyestradiol treatment of Ad5p53-transduced cells induces tumor cell apoptosis

We describe a unique approach to inducing apoptosis in human lung cancer cell lines, whereby cells are transduced with Ad5p53 at low MOIs and treated with 2-MeOE2, resulting in apoptosis irrespective of their p53 status

Tapas Mukhopadhyay; Jack A Roth

2002

Scholarcy highlights

  • The p53 gene is the most commonly mutated gene in human cancer, and mutation in its protein often inactivates the protein's tumor suppressor function
  • We describe a unique approach to inducing apoptosis in human lung cancer cell lines, whereby cells are transduced with Ad5p53 at low MOIs and treated with 2-MeOE2, resulting in apoptosis irrespective of their p53 status
  • The results indicated that 5 mM 2-MeOE2 induced high levels of wt p53 protein in this cell line
  • Even though 1 mM 2-MeOE2 induced an increase in wt p53 protein levels, it had no e€ect on the proliferation of the H460 cells
  • The 5 mM concentration of 2-MeOE2 by itself had no e€ect on either cell viability or apoptosis of normal bronchial cells but did induce apoptosis in tumor cells containing wt p53
  • We studied the e€ect on wt p53 induction in more detail
  • An earlier report indicated that treating the estrogen-dependent MCF-7 cell line with 2-MeOE2 caused G2/M arrest associated with depolymerization of tubulin

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