No compensation in CD44 stem cell marker following BCL-2 suppression by antisense oligonucleotides

Marvin Rubenstein*, Courtney M P Hollowell, Patrick Guinan

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Scopus citations

Abstract

Antisense oligonucleotides have previously been used to target regulatory proteins in prostate cancer models. We evaluated mono- and bispecific oligonucleotides which comparably suppressed expression of B-cell lymphoma-2 (BCL- 2) in LNCaP cells. Cells compensated by suppressing caspase- 3 (an apoptosis promoter), and enhancing the expression of androgen receptor and co-activating p300 and interleukin-6 (IL- 6) proteins. This suggests that increased androgen sensitivity accompanies BCL-2 suppression with a pattern associated with more advanced tumors. To further evaluate tumor resistance and compensatory mechanisms we evaluated the stem cellassociated CD44 expression and found it to be unaffected by treatment, suggesting that this tumor population is not activated or expanded by suppressive BCL-2 therapy.

Original languageEnglish (US)
Pages (from-to)251-256
Number of pages6
JournalIn Vivo
Volume27
Issue number2
StatePublished - Mar 1 2013

Keywords

  • Antisense
  • BCL-2
  • CD44
  • Prostate cancer
  • Therapy

ASJC Scopus subject areas

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

Fingerprint Dive into the research topics of 'No compensation in CD44 stem cell marker following BCL-2 suppression by antisense oligonucleotides'. Together they form a unique fingerprint.

Cite this