Fig. 2

Regulatory roles of lysine acylation in tumorigenesis. Lysine acylation exerts profound effect on diverse tumour formation. In glioblastoma, H3K79succ promotes gene expression and tumour growth. In lung cancer, Ksucc of SOD1 impedes its anti-tumor effect while desuccinylation of PKM2 boost tumour growth. In breast cancer, hypersuccinylation causes GLS degradation and impedes glutamine consumption of tumour cells. In renal cell carcinoma, SDHA is desuccinylated and fosters tumour proliferation. In prostate cancer, Ksucc of LDHA increases its activity in promoting tumour metastasis and histone hypocrotonylation induced by BRD4 inhibitors hampers tumour proliferation and migration. In ocular melanoma, H3K18la drives oncogenesis. In ESCC, restoring Ksucc level restricts cell growth, migration and invasion. In GC, elevated Ksucc of S100A10 and LDHA enhances tumour invasion and migration whereas desuccinylation of OGDH suppresses tumorigenesis. In colorectal cancer, Ksucc of PKM2 and Kcr of ENO1 promotes cell survival and tumour development and desuccinylation of CS and SHMT2 accelerates colon cancer growth. Kpr induced by propionate suppresses the development of colon cancer. Demalonylation of SDHA and TPI prompts the recurrence of CRC and GLUD1 can be deglutaryled to promote colorectal carcinogenesis. In liver cancer, Ksucc of H3K122 and PGM1 are required for liver cancer growth. Repressed Khib of ENO1 causes proliferation defective of liver cancer cells and H3K9bhb participates in the promotion of HCC stemness and progression. Increasing Kcr level leads to undermined liver cancer cell migration and proliferation. In PDAC, Ksucc of H3K79, H3K122, PGM1 and GLS promotes cell proliferation, migration and invasion