GSE135908
BAP18 is involved in upregulation of CCND1/2 transcription to promote cell growth in oral squamous cell carcinoma
Oral squamous cell carcinoma (OSCC) is a common malignant tumor worldwide and lack of biomarker for early diagnosis and therapy targets. Cyclin D proteins participating in controlling the cell cycle play crucial roles in cancer cell proliferation. However, the upstream regulatory protein for cyclin D proteins remains to be elusive. In this study, we have demonstrated that BPTF associated protein 18 kDa (BAP18) acting as a reader of histone H3K4me3 is highly expressed in OSCC tissues compared with that in benign. RNA-seq data showed that BAP18 depletion obviously influenced the expression of a series of genes, involved in multiple biological processes. We thus provided the evidence to demonstrate that knockdown of BAP18 extremely decreases CCND1 and CCND2 (CCND1/2) gene transcription. ChIP assay data demonstrated that BAP18 recruited to the promoter regions of CCND1/2, and facilitated the recruitment of the core subunits of MLL1/WDR5 complex to the same promoter regions, consequently increasing histone H3K4me3 levels. Furthermore, BAP18 depletion delayed G1-S phase transition and inhibited cell growth in OSCC. Our data suggested that BAP18 involved in modulation of CCND1/2 transcription promotes OSCC progression and could be a potential therapeutic target for OSCC treatment. Overall design: Examination the total RNA change of BAP18 depletion in Tca-8113 cells