From: Lactylation modification in cancer: mechanisms, functions, and therapeutic strategies
Lactyltransferase | Substrate | Modification Site | Delactylase | Biological Function | Cancer | PMID |
---|---|---|---|---|---|---|
EP300 | NMNAT1 | K128 | HDAC1 | Enhance the nuclear localization of NMNAT1 and maintain its activity, thereby collectively contributing to the maintenance of NAD levels in the nucleus. | Pancreatic Ductal Adenocarcinoma | [26] |
EP300 | H3 | K18 | HDAC2 | Promote the transcription of TTK protein kinase (TTK) and BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B). | Pancreatic Ductal Adenocarcinoma | [27] |
HBO1 | H3 | K9 | —— | HBO1 is highly enriched at the transcription start sites of actively transcribed genes and may directly participate in H3K9la-mediated gene regulation, thereby promoting tumorigenesis. | Cervical cancer | [31] |
KAT8 | eEF1A2 | K408 | —— | eEF1A2K408la stimulates translation elongation, thereby enhancing protein synthesis in colorectal cancer cells. | Colorectal cancer | [32] |
KAT5 | PIK3C3 | K356 | —— | Promote enzymatic activity and activate autophagy in muscle cells and cancer cells. | —— | [33] |
TIP60 | NBS1 | K388 | HDAC3 | Promote homologous recombination-driven DNA repair and chemotherapy resistance in cancer cells. | Gastric cancer | [34] |
CBP | MRE11 | K673 | SIRT1/SIRT2 | Promote DNA repair and chemotherapeutic resistance in cancer cells. | —— | [35] |
KAT2A | H3 | K14/K18 | —— | Promote the expression of Wnt/β-catenin, NF-κB, and PD-L1, as well as the growth of brain tumors and immune evasion. | Glioblastoma Multiforme | [36] |
AARS1 | YAP/TEAD1 | K90/K108 | SIRT1 | Activate the expression of downstream target genes to promote the proliferation of tumor cells. | Gastric cancer | [37] |
AARS1 | p53 | K120/K139 | SIRT1 | Block p53 liquid-liquid phase separation, bind to DNA, and induce its target genes promotes tumorigenesis. | Breast cancer | [38] |
AARS2 | PDHA1/CPT2 | K336/K457 | SIRT3 | Lactylation of mitochondrial proteins integrates interconnected metabolism and hypoxia to restrict oxidative phosphorylation. | —— | [40] |