Table 3 The histone modification disorder of CSCs in distinct cancers
Cancer types | The measures taken to target histone modification | Dysregulation in cancer | Effects generated on CSCs and tumors |
|---|---|---|---|
Pancreatic ductal adenocarcinoma (PDAC) | apply HDAC inhibitor (domatinostat) | block the expression and function of FOXM1 | target CSC compartment and alter redox homeostasis of CSC, induce antitumor effect and make PDAC sensitive to chemotherapy drugs [54] |
HCC | apply histone demethylase JMJD2D; remove HDAC11 | enhance the expression of CSC markers (EpCAM and SOX9); facilitate histone acetylation of the LKB1 promoter region | enhance Wnt and Notch signaling transduction, promote self-renewal capability of CSC [150]; hinder cancer stemness, HCC progression and sorafenib resistance [152] |
Breast cancer | knock down or inhibit HDAC1 and HDAC3; combination of DNMT inhibitor (5-azacytidine) and HDAC inhibitor (butyrate) | results in HDAC7 downregulation and inhibit the transcription of oncogenes; target CSCs to reactivate the tumor suppressor genes | suppress the phenotype of CSCs [153]; block tumor occurrence and growth [154] |
CRC | exhaust HotairM1 (lncRNA) | lead to H3K27 trimethylation at the HOXA1 gene promoter site and epigenetic silencing | induce H3K27 acetylation at the NANOG gene enhancer site to up-regulate the expression, promote self-renewal of CSC and tumor spread [157] |