Table 1.

Potential role of H3K4 HMTs in drug-resistant cancers.

Enzyme	Cancer Types	Proposed Mechanism
MLL1	Chemotherapy resistant MLL leukemia Castration-resistant prostate cancer Anti-PD-L1/PD-1 resistant pancreatic cancer	Increases MDR-1 expression [170] Activates androgen receptor signaling [135] Increases PD-L1 expression [173]
MLL3	Tamoxifen-resistant breast cancer Anti-PD-L1/PD-1 resistant prostate cancer	Increases ERα expression [111] Increases PD-l expression [179]
SETD1A	Tamoxifen-resistant breast cancer Tamoxifen-resistant breast cancer Triple-negative breast cancer Castration-resistant prostate cancer Sorafenib resistant hepatocarcinoma	Increases ERα expression [111] Activates ERα signaling and EGFR expression [119] Activates MMP expression [113] Activates FOXM1 signaling via binding with E2F1 [143] Activates Yes-associate protein [180]
SETD1B	Triple-negative breast cancer	Regulates adiponectin receptor 1 signaling [116]
SMYD2	Triple-negative breast cancer Oxaliplatin-resistant colon cancer Cisplatin-resistant non-small cell lung cancer Chemotherapy resistant renal cell carcinoma	Activates STAT3 and the p65 [117] Increases MDR-1 expression [134] Inhibits p53 signaling [188] Increases MDR-1 expression [189]
SMYD3	Cisplatin-resistant breast cancer	Increases WNT10B expression and promote the EMT [120,121]
SET7/9	Anti-estrogen-resistant breast cancer Castration-resistant prostate cancer	Controls the stability of E2F1 and DNMT1 [126] Alters chromatin accessibility via frameshift mutation [142]