GEOGenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE229949GEOGSEfalseNicotinic acid-induced histone nicotinylation suppresses hepatocellularcarcinoma metastasis by regulating PPFIA1 gene expression.Histone post-translational modifications (PTMs) controls the gene expression profile via transcriptional regulation．Aberrant histone PTMs chromatin structures lead to dysregulated gene expression and cancer progression. Nicotinic acid (vitamin B3 or vitamin PP), one of the thirteen essential vitamins, has a wide range of uses, helping to function digestive system, skin and nervous system. Here we show nicotinic acid (NA) induces histone and non-histone lysine nicotinylation, and identify 17 nicotinylation sites on core histones in HeLa cells. Also, NA-derived nicotinylation of histone lysine residues is an epigenetic modification that regulates gene transcription via altering the chromatin accessibility by generating nicotinyl-CoA. Knic inactivates oncogene PPFIA1 transcription by inhibiting its combination with transcription factors HOXB9, and PPFIA1 was found as an important role in promoting cells spreading on the extracellular matrix and is required for migration and invasion in human breast tumor cells However, the role and the molecular mechanisms of PPFIA1 control hepatocellularcarcinoma (HCC) initiation and progression are poorly understood. Here we demonstrate PPFIA1 promotes proliferation, migration, invasion and tumorigenesis of HCC in vivo and in vitro. It is worth noting that the expression of PPFIA1 is upregulated in multiple human carcinomas, including HCC. Our study also suggests that PPFIA1 is a promising potential target of NA for the future treatment strategies of HCC2026/04/13GSE229949GSM7181859GSM7181854GSM7181856GSM7181855GSM7181858GSM718185724676229949Homo sapiens