Additional compensatory mechanisms altering antisense oligonucleotide suppression of BCL2: Effects upon AKT1 and STAT3

Marvin Rubenstein*, Courtney M P Hollowell, Patrick Guinan

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Antisense oligonucleotides have targeted regulatory proteins in both in vivo and in vitro prostate cancer models. We evaluated mono- and bispecific oligonucleotides which targeted and comparably suppressed B-cell lymphoma-2 BCL- 2 (an apoptosis-inhibitory protein) expression in LNCaP cells. These oligonucleotides were administered with lipofectin as part of a nanoparticle delivery system. Treated cells compensated by suppressing caspase-3 (an apoptosis promoter) and enhancing expression of the androgen receptor and its co-Activating p300 and IL-6 proteins. This suggests a progression to increased androgen sensitivity (in LNCaP) accompanies BCL-2 suppression and a gene activation pattern associated with more advanced prostate tumors. To further evaluate compensatory mechanisms related to tumor resistance in the present study we evaluate the expressed levels of the AKT1 oncogene and STAT3 transcription factor, finding both to be enhanced.

Original languageEnglish (US)
Pages (from-to)867-870
Number of pages4
JournalIn Vivo
Volume28
Issue number5
StatePublished - Jan 1 2014

Keywords

  • Antisense
  • BCL-2
  • Prostate cancer
  • Therapy

ASJC Scopus subject areas

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

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