Exploration of the mechanism by which H3K27ac activates APOC1 to promote PTC proliferation.

Early studies have suggested that apolipoprotein C1 (APOC1) functions as an oncogenic factor in papillary thyroid carcinoma (PTC), where it promotes tumor cell proliferation. Here, we focus on the regulatory mechanisms underlying APOC1-mediated PTC cell growth, with particular attention to histone modification-driven changes in APOC1 expression and disease progression. Our bioinformatics analysis revealed that APOC1 was differentially expressed in PTC and might be involved in tumor-related biological processes. The influence of APOC1 on PTC cell growth and glycolysis was studied. The impact of APOC1-induced glycolytic reprogramming on PTC cell proliferation was assessed. Cells were treated with the a selective p300/CBP histone acetyltransferase inhibitor (C646) and the histone deacetylase inhibitor sodium butyrate (NaB) to modulate histone acetylation levels. Subsequently, chromatin immunoprecipitation (ChIP) assays were carried out to assess the role of histone modifications in APOC1 expression regulation. Finally, nude mouse xenograft models were used to confirm the oncogenic role of APOC1 in PTC development. Bioinformatics and experimental analyses confirmed that APOC1 expression showed a strong correlation with glycolysis-related genes and PTC cell proliferation was influenced by changes in glycolysis. Meanwhile, APOC1 expression was activated by H3K27ac. Xenograft models were subsequently used to further validate these findings in vivo. H3K27ac-mediated activation of APOC1 may promote glycolytic reprogramming in PTC cells, thereby driving their proliferation.