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Table 2 Histone variants in breast cancer metastasis

From: A three layered histone epigenetics in breast cancer metastasis

S. no. Histone variants Role in breast cancer metastasis References
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]