Antisense oligodeoxynucleotides targeting the serine/threonine kinase Pim-2 inhibited proliferation of DU-145 cells
Abstract
Aim: To investigate the effect of antisense oligodeoxynucleotides (ASODN) targeting
Pim-2 on cell proliferation of DU-145 cells. Methods: Three ASODN targeting
Pim-2 were designed and synthesized. After transfection with ASODN, cell
proliferation was analyzed using an MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-
carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt] assay. In
addition, Pim-2 mRNA, protein levels, and cell cycles were examined. Results:
The ASODN designed and synthesized by our laboratory significantly reduced
Pim-2 mRNA level and protein content in DU-145 cells. After transfection with
ASODN for 48 h, a marked reduction in cell viability was observed in DU-145 cells
in a dose-dependent manner. No remarkable apoptosis occurred in cells treated
with ASODN compared with control cells. However, it should be noted that G1
phase arrest was clearly observed in ASODN-treated cells. Conclusion: ASODN
targeting Pim-2 resulted in a marked reduction in DU-145 cell proliferation, and
induction of G1 phase cell cycle arrest is one of the important mechanisms for
ASODN to reduce cell growth. Moreover, antisense inhibition of Pim-2 expression
provides a new promising therapy target for prostate cancer.
Keywords:
Pim-2 on cell proliferation of DU-145 cells. Methods: Three ASODN targeting
Pim-2 were designed and synthesized. After transfection with ASODN, cell
proliferation was analyzed using an MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-
carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt] assay. In
addition, Pim-2 mRNA, protein levels, and cell cycles were examined. Results:
The ASODN designed and synthesized by our laboratory significantly reduced
Pim-2 mRNA level and protein content in DU-145 cells. After transfection with
ASODN for 48 h, a marked reduction in cell viability was observed in DU-145 cells
in a dose-dependent manner. No remarkable apoptosis occurred in cells treated
with ASODN compared with control cells. However, it should be noted that G1
phase arrest was clearly observed in ASODN-treated cells. Conclusion: ASODN
targeting Pim-2 resulted in a marked reduction in DU-145 cell proliferation, and
induction of G1 phase cell cycle arrest is one of the important mechanisms for
ASODN to reduce cell growth. Moreover, antisense inhibition of Pim-2 expression
provides a new promising therapy target for prostate cancer.