No compensation in VEGF expression follows antisense suppression of BCL-2 activity

Marvin Rubenstein*, Courtney M P Hollowell, Patrick Guinan

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Antisense oligonucleotides (oligos) have been employed against prostate cancer models targeting growth-regulatory proteins, and at least one oligo (against bcl-2) has reached clinical trial. We previously found that, in LNCaP cells, mono- and bispecific oligos, which comparably suppressed the expression of bcl-2, compensated with suppression of caspase-3 (apoptosis promoter) activity, and enhanced the expression of the androgen receptor (AR) and its p300 and IL-6 co-activators. In addition, prostate-specific membrane antigen (PSMA) and (possibly its regulator) interferon (IFN) were elevated. A total of 14 proteins distributed between regulators of apoptosis, androgen regulation, differentiation antigens and autocrine-mediated growth have previously been examined. We extend these findings to include vascular endothelial growth factor (VEGF), a promoter of angiogenesis, which is not significantly altered through compensation, and therefore would not need additional regulation for suppressive bcl-2 therapy to be effective (like caspase-3).

Original languageEnglish (US)
Pages (from-to)937-940
Number of pages4
JournalIn Vivo
Volume26
Issue number6
StatePublished - Nov 1 2012

Keywords

  • Antisense
  • Bcl-2
  • Prostate cancer
  • VEGF

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology

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