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γ-catenin plays different roles in different types of tumors, and its rolein chronic myeloid leukemia (CML) cells has yet to be identified. In our study,two CML cell lines (K562, KU812) had higher γ-catenin expression levels comparedto five types of BCR-ABL-negative leukemia cells. Knockdown of the expressionof BCR-ABL resulted in downregulation of γ-catenin. Furthermore, downregulationof γ-catenin by siRNA inhibited the proliferation and colony formation of CMLcells and the expression of the c-Myc and cyclin D1 genes; downregulation of γ-cateninalso potentiated the effects of imatinib (inhibiting CML cell proliferation andinducing apoptosis) and suppressed the anti-apoptotic genes Bcl-xL and survivin.We also showed that downregulation of γ-catenin suppressed the phosphorylationof STAT5, promoted the phosphorylation of β-catenin and reduced the translocationof β-catenin into the nucleus, although there were no effects on the total levelof β-catenin expression in the whole cells. Furthermore, downregulation of γ-cateninwas found to promote glycogen synthase kinase-3β (GSK3β) and inhibit its phosphorylation.Collectively, our results suggest that γ-catenin is an oncogene protein in CMLthat can be regulated by BCR-ABL and that suppression of γ-catenin inhibits CMLcell growth and potentiates the effects of imatinib on CML cells through inhibitionof the activation of STAT5 and suppression of β-catenin by activating GSK3β.

Downregulation of γ-catenin inhibits CML cell growth and potentiates the response of CML cells to imatinib through β-catenin inhibition