From: The dysregulated expression and functional effect of CaMK2 in cancer
Cancer | Cell lines | Method of selecting CSCs | The functional influence of CaMK2 on CSCs/TICs | References |
---|---|---|---|---|
Liver cancer | Huh7, MHCC97H, SNU398 | CD133+ Huh7 population and CD90+ MHCC97H population were sorted by FACS | CaMK2 inhibitor, KN93, remarkably decreased the stem cell populations and inhibited sphere formation in liver cancer cell lines | [48] |
GBM | U87MG U373MG | GSCs were enriched by neurosphere formation | Inhibiting CaMK2γ remarkably repressed the stem cell-like phenotypes as well as the expression of stemness markers by decreasing c-Met signaling pathway | [66] |
Patient-derived xenografts | BTICs and non-BTICs were isolated based on functional criteria | CaMK2 was highly expressed in non-BTICs and positively associated with the non-BTICs phenotypes | [67] | |
CML | K562 KCL22 | CD34+/CD38− leukemia stem cells were sorted from primary CML samples using FACS | CaMK2γ was highly up-regulated and activated in leukemia stem cells of CML | [57] |
Breast cancer | MCF-7, MDA-MB-231 | long-term glucose deprivation | CaMK2α inhibition using siRNAs or KN62 significantly increased apoptosis and decreased survival of CSCs | [68] |
Lung cancer | HCC827, A549, H1299 ZRLC-1 | CSCs were enriched by oncosphere culture | CaMK2γ significantly enhanced the stem-like traits and tumorigenicity of lung cancer cells in an Akt- and β-catenin-dependent manner | [69] |