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Inhibition of bcr-abl and/or c-abl gene expression by small interfering, double-stranded RNAs : Cross-talk with cell proliferation factors and other oncogenes

✍ Scribed by Hideki Ohba; Zhivko Zhelev; Rumiana Bakalova; Ashraf Ewis; Toshiro Omori; Mitsuru Ishikawa; Yasuo Shinohara; Yoshinobu Baba


Publisher
John Wiley and Sons
Year
2004
Tongue
English
Weight
789 KB
Volume
101
Category
Article
ISSN
0008-543X

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✦ Synopsis


Abstract

BACKGROUND

Short, 21‐mer, double‐stranded/small interfering RNAs (ds/siRNAs) were designed to target bcrabl mRNA in chronic myelogenous leukemia (CML) with a potential also to target cabl mRNA.

METHODS

ds/siRNAs were transfected into bcrabl‐positive K‐562 cells (derived from blast‐crisis) or bcrabl‐negative/cabl‐positive Jurkat cells (derived from acute lymphoblastic leukemia) using lipofectamine. ds/siRNAs intracellular uptake was detected by fluorescent confocal microscopy using fluorescein‐labeled ds/__siRNA__s. The treatment was performed over 6 days with repetitive siRNA transfections. Efficiency of the __siRNA__s was determined 24 hours after single siRNA transfection and 6 days after repetitive siRNA transfections.

RESULTS

Two of the designed ds/__siRNA__s decreased the target mRNA levels markedly (determined by reverse transcriptase‐polymerase chain reaction analysis) and bcrabl/cabl oncoproteins (determined by flow cytometry using Fluor‐488‐labeled, anti‐cabl antibody as well as by Western blot analysis). These sequences also inhibited protein tyrosine kinase activity significantly and suppressed cell proliferation. One of the three selected ds/__siRNA__s expressed only slight effects on the bcrabl/cabl mRNA in K‐562 cells (but not on the oncoprotein level), on protein tyrosine kinase activity, and on cell proliferation. The combination of the three ds/siRNA constructs provoked stronger decreases in bcrabl/cabl mRNAs and their respective oncoproteins and produced the strongest suppression of cell proliferation.

CONCLUSIONS

The cross‐talk between siRNA interference of bcrabl oncogene and the expression of several apoptotic/antiapoptotic factors, cell proliferation factors, and other oncogenes exists and it was determined by microarray analysis in K‐562 cells that were treated over 6 days. Cancer 2004. © 2004 American Cancer Society.