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 language | English (US) |
|---|---|
| Pages (from-to) | 251-256 |
| Number of pages | 6 |
| Journal | In Vivo |
| Volume | 27 |
| Issue number | 2 |
| State | Published - 2013 |
Keywords
- Antisense
- BCL-2
- CD44
- Prostate cancer
- Therapy
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology
- Pharmacology
