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Table 1 CaMK2 expression in numerous cancer progression is prominently changed reflected by bioinformatic analyses

From: The dysregulated expression and functional effect of CaMK2 in cancer

Cancer types

Method of bioinformatic analysis

The altered CaMK2 expression in cancer

References

CRC

The integrated transcriptomic and proteomic datasets acquired from previous microarray- and mass spectrometry (MS)-based study

Both the transcription and protein levels of CaMK2δ are concordantly decreased during CRC progression

[27]

The mRNA expression profile is inverstigated using GeneChip Human Transcriptome Array 2.0

CaMK2β expression is downregulated in F. nucleatum-induced CRC

[28]

Total genome gene expression profiling is

investigated using Illumina HT-12 V4.0 Expression Beadchip oligonucleotide microarray

CaMK2γ expression is significantly reduced in rectal cancer tissues compared with colon cancer tissues

[29]

GBM

The differentially expressed genes is found and validated by microarray analysis of RNA expression profiling and qRT-PCR, respectively

CaMK2β is significantly decreased in the MMLV/PDGFB mouse gliomas

[30]

The gene expression in GBM and normal control are compared based on the data from GEPIA

The expression of CaMK2β and CaMK2γ are synchronously downregulated in GBM

[31]

Oligonucleotide-based microarray analysis and real-time RT-PCR verification

CaMK2γ transcript level in recurrent high-grade gliomas is significantly reduced as compared to primary low-grade gliomas

[32]

A prognostic prediction system was constructed and validated using microarray data from TCGA dataset, GEO dataset and a chinese Glioma Genome Atlas (CGGA) dataset

High CaMK2α mRNA expression may be a bad prognostic factor for GBM

[33]

HSCC

The differentially expressed genes that are closely related to the TPF chemosensitivity in priamry HSCC patients was screen using mRNA microarray analysis

The expressions of CaMK2α and CaMK2β were significantly increased in TPF-resistent patients compared with the TPF-sensitive patients

[34]

MTNBC

The differentially expressed proteins between the chemosensitivity group and chemoresistance group were identified and validated by TMT-based proteomics analysis and ELISA analysis

The protein level of CaMK2α in chemoresistance group was significantly higher than that in chemosensitivity group

[35]

NSCLC

A genome wide scan of single-nucleotide polymorphisms (SNPs) was conducted in patients with early-stage NSCLC

CaMK2δ rs10023113 was significantly associated with poor prognosis of early-stage NSCLC

[36]

Breast cancer

The expression microarray data obtained from the EBI database was screened and then identified using a combinational approach involving in silico mining followed by MSP and RT-PCR

The promoter of CaMK2β was hypermethylazed and the expression of CaMK2β was decrased in breast cancer

[37]

lingual SCC

The methylation of gene promoters in lingual SCC mouse model was determined using Methylated DNA immunoprecipitation sequencing

Significant methylation in CaMK2 promoter was confirmed in lingual SCC mouse model

[38]

EAC

Targeted RNA sequencing and PCR verification were performed in 40 paired EAC specimens and nonmalignant specimens frompatients

The USP54- CaMK2γ fusion transcripts was found in EACA specimens

[39]

  1. CRC colorectal cancer, GBM glioblastoma multiforme, HSCC hypopharyngeal squamous cell carcinoma, MTNBC metastatic triple negative breast cancer, NSCLC non-small cell lung cancer, SCC squamous cell carcinoma, EAC esophageal adenocarcinoma, TPF docetaxel, cisplatin and 5-fluorouracil, TMT tandem mass tag, EBI European Bioinformatics Insstitute