Histone methylation in pancreatic cancer and its clinical implications

doi:10.3748/wjg.v27.i36.6004

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Sep 28, 2021 (publication date) through Jan 4, 2025

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Sep 28, 2021; 27(36): 6004-6024
Published online Sep 28, 2021. doi: 10.3748/wjg.v27.i36.6004

Table 1 Histone methyltransferases play a major role in pancreatic cancer

Family	Subfamily	Alias	Site	Function in pancreatic cancer
PRMTs	PRMT1	HRMT1L2, HMT2, ANM1	H4R3me2a	Increase the β-catenin protein level; Methylate Gli1 at R597[44,54]
	PRMT5	HRMT1L5, SKB1, HSL7	H3R2me2s	Silence the expression of the tumor suppressor FBW7; Promote EMT via activating EGFR/ AKT/β-catenin signaling[45,56,188,189]
KMTs	SMYD3	ZNFN3A1, ZMYND1	H4K5me3	Affect the PC progression by regulating MMP-2; Potentiate Ras signaling through methylation of MAP3K2[62,64]
	EZH2	KMT6, WVS, ENX-1	H3K27me3	Suppress miR-139-5p expression by upregulating H3K27me3; Repress the E-cadherin by tri-methylation of H3K27[78,190]

All current research on reprogramming histone methyltransferases that play a role in pancreatic cancer. EMT: Epithelial-mesenchymal transition; FBW7: F-Box and WD repeat domain containing 7; KMTs: Histone lysine methyltransferases; PC: Pancreatic cancer; PRMTs: Protein arginine N-methyltransferases.

Citation: Liu XY, Guo CH, Xi ZY, Xu XQ, Zhao QY, Li LS, Wang Y. Histone methylation in pancreatic cancer and its clinical implications. World J Gastroenterol 2021; 27(36): 6004-6024
URL: https://www.wjgnet.com/1007-9327/full/v27/i36/6004.htm
DOI: https://dx.doi.org/10.3748/wjg.v27.i36.6004