Table 2 Histone variants in breast cancer metastasis

1.

H2A.Z

Over-expressed in breast cancer metastasis

H2A.Z enrichment is found at p53/p21 and TFF1 gene promoters

Regulate cell cycle via c-myc

H2A.Z depletion imitates EMT

[87, 90,91,92,93,94]

2.

MacroH2A

Act as tumour suppressor

Recruits EZH2 which causes H3K27 tri-methylation around LOX transcription start site

HER2 interaction with MacroH2A causes activation of ERBB2

SKP-SCF complex is found to be an upstream regulator of MacroH2A and CDK8 as downstream effector

mH2A.1 is found to be associated with the upregulation of EMT specific markers- Twist1 and Snail and downregulation of mesenchymal markers like E-cadherin

[40, 95, 96, 101, 102]

3.

H2A.X

Found at the site of double Strand breakage, telomeric erosion

Forms ɣH2A.X upon phosphorylation by ATM at SER139

Higher ɣH2A.X level is associated with Breast Cancer as well as TNBC

Reported to function via TRAF6-ATM–H2AX pathway mediated by HIF1α

[107, 108, 110, 111]

4.

H2B

Hypomethylation and upregulation of HIST1H2BJ is found in brain metastasis of breast cancer

Hypomethylated and upregulated HIST1H2BE is found to be associated with breast cancer cell lines

[112, 114]

5.

CENP-A

Over-expression in breast cancer tissue samples

Higher CENP-A expression is found in estrogen negative breast cancer condition than estrogen positive condition

Positive correlation of CENP-A has been observed with ki-67 expression

[116, 117]

6.

H4G

Over-expressed in breast cancer cell lines

[115]

7.

H1

Over-expressed in cancer cells

[118]