Table 2.
Occurrence and Potential treatment of H3K14-related diseases
| The name of the disease | Mechanism of impact | Potential therapeutic targets/measures | Reference |
|---|---|---|---|
| Cutaneous T Cell Lymphoma (CTCL) | Genome-wide H3K9/14ac (H3ac) and H3K27ac levels were significantly increased | HDACi | 97 |
| Renal Cell Carcinoma (RCC) | Renal oxidative stress, high DNA methylation, low H3 acetylation | Raise the level of oxidative stress | 98 |
| Acute promyelocytic leukemia (APL) | The PML-RARA fusion protein recruits HDAC/HMT to form an inhibitory complex that blocks differentiation gene expression. Belinostat and 3-Deazaneplanocin A directly disrupt the complex and reverse the apparent silencing by H3K14ac elevation | HDAC inhibitor combined with HMT inhibitor; EGCG | 85, 99 |
| Breast cancer | Increased expression of ATP-binding cassette (ABC) -type transporters |
RNAi down-regulated the expression of HATs PCAF and GCN5 | 100 |
| Abdominal Aortic Aneurysm (AAA) | There is increased acetylation of H3K14 and DNA hypomethylation |
mRNA levels of DNMT and HDAC | 101, 102 |
| Glioma | IDH1 mutations can lead to a wide range of DNA and histone methylation; Overexpression of HCMV IE86 protein | The joint HDACi cAMP agonist, ATF5expression | 10, 103, 104 |
| Nasopharyngeal carcinoma | Upregulation of AFAP1-AS1, H3K14acetylation and protein binding to the brominated domain of TIF1α | Enhanced KAT2Bacetyltransferase activation and YAP mRNA stabilization | 31 |
| Periodontitis | Cut GCN5 activated PDLSCs Wnt/beta Catenin signaling pathway, H3K14ac level is low | Up-regulation of GCN5 | 83, 105 |
| Mastitis | H3K14 high acetylation, lipopolysaccharide |
Metformin activates AMPK signaling pathway to reverse H3K14hyperacetylation | 106-108 |
| Acute necrotizing pancreatitis (AP) | The key initiating cytokine TNF-AP was strongly up-regulated and H3K14 acetylation was increased | 109 | |
| Asthma | PMCS, increasethe CD4 + T cells inthe IL - 4 gene promoter H3K14 acetylation and H3K27me3 | Notch Signaling pathway | 20, 110 |
| Diabetes | SIRT2 expression was decreased, EPB41L4A-AS1 binding to GCN5, andH3K14 level was increased. Claudin-5 is deficient | Upregulation of SIRT2; EPB41L4A-AS1; Ketoβ-hydroxybutyricacid (BHB) therapy | 30, 61, 111, 112 |
| Neurodegenerative disease Friedreich's ataxia | FXN introns within the GAA x TTC triplets amplification result in transcriptional silencing, with histone H3 acetylation | HDACi | 53 |
| Intrauterine growth retardation (IUGR) | Prenatal caffeine exposure increased the mRNA expression of DNAmethyltransferases Dnmt1, Dnmt3a, HDAC1, and HDAC2, and decreased the acetylation level of H3K14 | DNA methylation and histone acetylation | 113, 114 |
| Tuberculosis (TB) | HDAC1 gene/protein expression increases, H3K14Ac decrease | Downregulation of HDAC | 115 |