The inhibitor displayed a Ki value of 23 nM and effectively reduced cellular Nα-acetylation on histone H4, leading to reduced migration in lung cancer cells by modulating the expression of E-cadherin, N-cadherin, and vimentin. Our findings demonstrate that the CPP-conjugated NatD inhibitor serves as a valuable chemical probe for elucidating the biological roles of NatD in lung cancer, laying the groundwork for future therapeutic strategies targeting NatD.

Our study highlights the pivotal functions of NAT10 in the progression of PC and reveals the underlying epigenetic mechanism that NAT10 promotes metastasis via ZEB1/MT1-MMP axis.

We show that in 22Rv1 prostate cancer cells EZH2 occupies a large set of gene loci lacking H3K27me3, and these non-canonical genomic sites are instead co-occupied by p300, RNA Pol II and BRD4, and are rich in histone marks associated with transcriptional activation. Our findings shed light on the potential basis for such a high degree genetic co-localization through the direct association of p300TAZ2 with EZH2TADs.

Furthermore, significant associations are found among low nuclear ACAT1 levels, decreased S60 phosphorylation, and reduced NK cell infiltration, as well as poor prognosis in CRC. Our findings reveal an unexpected function of ACAT1 as a nuclear acetyltransferase and elucidate its role in NK cell-dependent antitumor immunity through p50 acetylation.

Our findings suggest that NAT10-mediated acetylation of JARID2 mRNA up-regulates its protein levels, thereby promoting stemness and contributing to the malignancy of GBM. Targeting this NAT10-JARID2 axis may represent a novel therapeutic approach for treatment of GBM.

Eventually, the oncogenic effect of NAT10/ac4C/LDHA axis was confirmed in xenograft experiments. NAT10 promoted the GC progression by mediating the ac4C modification of LDHA mRNA, which could serve as a potential therapeutic target for GC.

Collectively, these results indicate that a novel sialylated IgG-integrin β4-FAK-Src-Erk-p300-c-Myc signaling pathway promotes colorectal cancer liver metastasis, thus providing potential therapeutic targets for colorectal cancer liver metastasis.

NAT10 exerts a critical role in cervical cancer progression via acetylating SLC7A5 mRNA and could represent a key prognostic and therapeutic target in cervical cancer.

Our findings highlight the critical crosstalk between glucose homeostasis and the ac4C epitranscriptome in gastric carcinogenesis. This finding offers a potential strategy of targeting NAT10/HK2 axis for the treatment of GC patients, especially those with highly active glucose metabolism.

MG149 suppresses ATC progression and metastasis by inhibiting the acetylation of c-Myc mediated by KAT5.

Additionally, NAT10 impedes autophagy flux by preventing the fusion of autophagosomes with lysosomes and suppressing GABARAP transcription, which is regulated by EZH2-mediated H3K27me3. In summary, our study elucidates the biological significance and molecular mechanisms of the NAT10/SGK2/EZH2 axis in the pathogenesis of lung cancer, potentially providing novel prognostic markers and therapeutic targets for its treatment.

MG149 suppresses ATC progression and metastasis by inhibiting the acetylation of c-Myc mediated by KAT5.