Table 2 The calcium/calmodulin-stimulated protein kinase II regulates the cellular proliferation, migration, invasion and metastasis in various cancer types

CRC

HCT116 cells

HT29 cells

CaMK2γ significantly inhibites cell cycle arrest, decreases apoptosis, thus promoting cell growth

[40]

HCT116 cells

CaMK2 activity is required for cellular proliferation, migration and invasion

[41]

Breast cancer

11q13-amplified breast cancer cells

CaMK2 signaling is required for the ANO1-mediated cell survival and proliferation

[42]

MDA-MB-231 cells

MCF-7 cells

CaMK2α activation positively regulates cellular growth, migration and invasion

[43]

MDA-MB-231 cells

The dephosphorylation of CaMK2α at T253 accelerates the metaphase–anaphase transition and increases cell proliferation

[44]

Gastric cancer

BGC-803 cells

CaMK2α activation promotes proliferation and metastasis

[45]

BGC-823 cells

Inhibition of CaMK2β decreases cell viability, survival and migration

[46]

Hepatocarcinoma

Hep3B cells

HepG2 cells

Inhibiting CaMK2 activity using KN-62 decreased the protein synthesis and functionally activity of HIF-1α in hepatocellular carcinoma cells

[47]

Huh7, MHCC97H; SNU398; SK-Hep-1

Inhibiting CaMK2γ with KN93 and shRNAs significantly reduced survival and proliferation in carcinoma cells, wheras, overexpression of CaMK2γ exerts an opposite effect

[48]

Prostate cancer

C4-2B cells

Inhibition of CaMK2 activity results in significant inhibition of cell proliferation

[49]

LNCaP cells

Overexpression of CaMK2 (α and β isofroms) decreases apoptosis and promotes cell growth

[50]

KN-93 synergistically increases cell death in combination with low doses of doxorubicin and converts the phenotype of prostate cancer cells from TRAIL-resistant to TRAIL-sensitive

[52]

C4-2B4 cells

PC3-mm2 cells

CaMK2 activation promotes cell survival, growth, migration and metastasis in vivo and vitro

[51]

PC3 cells

Inhibition of CaMK2 (α isoform) using AIP or a dominant negative mutant significantly mitigates H₂O₂-induced cell death

[53]

Osteosarcoma

MG-63 cells

143B cells

Inhibiting CaMK2α using KN93, specific siRNA or the K42M kinase-dead construct (CaMK2α K42M) significantly decreases growth of osteosarcoma cells through the induction of p21-dependent cell cycle arrest

[54]

MG-63, 143B, HOS, MNNG/HOS cells

Knockdown of CaMK2α decreases proliferation, migration and invasion in vitro and tumor burden in vivo; wheras, overexpression of CaMK2α has the opposite effects

[55]

Myeloid leukemia

K562 cells

Inhibition of CaMK2 activity with pharmacologic agents, dominant-negative constructs or shRNAs reduces the proliferation of myeloid leukemia cells

[56]

overexpression of CaMK2γ greatly reversed berbamine-induced growth inhibition of myeloid leukemia cells in vivo and vitro

[57]

T cell lymphoma

H9 cells, SU-DHL-1 cells, JB6 cells, and Jurkat cells

CaMK2γ promotes lymphomagenesis and cellular proliferation of T cell lymphoma by regulating c-Myc protein expression

[58]

OSCC

HSC-3 and SAS cells

CaMK2 signaling may be involved in OSCC progression

[59]

GBM

U87MG, U251 and LN229 cells

CaMK2α might exert an inhibitory effect on cell survival and progression of GBM

[60]