Abstract: Objective To investigate the effects of the γ isoform of Ca2 +/calmodulin-dependent protein kinase II (CaMKIIγ) on
colorectal cancer (CRC) cell growth in vitro and in vivo and explore the mechanisms. Methods The mRNA levels of CaMKIIγ in
5 CRC cell lines, tumor tissues and matched adjacent tissues from 20 CRC patients were examined by semi-quantitative
RT-PCR. The lentiviral vector pLenti6.3-MCS-IRES2-eGFP was used to genrate the lentivirus particle Lenti-CaMKIIγ for
transfecting SW620 cells. The proliferation ability of the transfected SW620-CaMKIIγ cells was assessed by growth curve and
colony formation assay. The expression of IKKα, IKKβ, IKKγ, p-IKKα/β, p-IκB and IκB of the transfected cells were
determined by Western blotting, and the expression and localization of nuclear factor-κB (NF-κB) p65 were detected by
immunofluorescence. In nude mouse models bearing the transfected SW620-CaMKIIγ cell xenograft, the tumor volume was
measured twice a week. Results CaMKIIγ mRNA showed high expressions in the 5 colorectal cancer cell lines. Eighteen of the
20 tumor tissues showed higher expressions of CaMKIIγ than the adjacent non-tumor tissues. The proliferation of transfected
SW620-CaMKIIγ cells was enhanced significantly. CaMKIIγ activated NF-κB signaling pathway and led to NF-κB p65 nuclear
translocation. In the tumor-bearing mouse model, the volume of the tumors generated by the transfected SW620-CaMKIIγ
cells was 1.46- and 1.68-fold higher than that of the tumors with the control cells at the 8th and 12th day, respectively.
Conclusion CaMKIIγ can effectively promote the growth of colorectal cancer cells in vitro and in vivo by activating NF-κB
signaling pathway.