ArticleEBioMedicine2020
BAP18 is involved in upregulation of CCND1/2 transcription to promote cell growth in oral squamous cell carcinoma.
Article in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Dissecting the role of epigenetic regulation in oral squamous cell carcinoma microenvironment: mechanisms and therapeutics.Frontiers in immunology · 2026Review
- Uncovering functional divergence and cellular clusters with specific gene signatures in HNSCC clonal spheroids.Cell communication and signaling : CCS · 2025Article
- BAP18, as a corepressor of AR together with the SIN3A/HDAC complex, promotes AR-positive triple-negative breast cancer progression.Cell & bioscience · 2025Article
- Pembrolizumab promotes degradation of cyclin dependent kinase 6 and suppresses ovarian cancer progression in vitro.Scientific reports · 2025Article
- Interaction between stromal cells and tumor cells promotes GCB-DLBCL cell survival via the CD40/RANK-KDM6B-NF-κB axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- RBAP48 facilitates the oral squamous cell carcinoma process in an androgen receptor-dependent and independent manners.Communications biology · 2025Article
- BAP18 facilitates CTCF-mediated chromatin accessible to regulate enhancer activity in breast cancer.Cell death and differentiation · 2023Article
- Long non-coding RNA TFAP2A-AS1 plays an important role in oral squamous cell carcinoma: research includes bioinformatics analysis and experiments.BMC oral health · 2022Article
- Chromatin complexes subunit BAP18 promotes triple-negative breast cancer progression through transcriptional activation of oncogene S100A9.Cell death & disease · 2022Article
- Article
- Circ_0000745 strengthens the expression of CCND1 by functioning as miR-488 sponge and interacting with HuR binding protein to facilitate the development of oral squamous cell carcinoma.Cancer cell international · 2021Article
- Identifying an lncRNA-Related ceRNA Network to Reveal Novel Targets for a Cutaneous Squamous Cell Carcinoma.Biology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a reader of histone H3K4me3, BPTF associated protein of 18 kDa (BAP18) is involved in modulation of androgen receptor action in prostate cancer. However, the function of BAP18 on oral squamous cell carcinoma (OSCC) and its molecular mechanism remains to be elusive.
methodsOSCC-derived cell lines carrying silenced BAP18 were established by Lentiviral infection. Quantitative PCR (qPCR), western blot, and ChIP assay were performed to detect gene transcription regulation and the possible mechanism. Colony formation, cell growth curve and xenograft tumor experiments were performed to examine cell growth and proliferation.
findingsOur study demonstrated that BAP18 was highly expressed in OSCC samples compared with that in benign. BAP18 depletion obviously influenced the expression of a series of genes, including cell cycle-related genes. We thus provided the evidence to demonstrate that BAP18 depletion significantly decreases CCND1 and CCND2 (CCND1/2) transcription. In addition, BAP18 is recruited to the promoter regions of CCND1/2, thereby facilitating the recruitment of the core subunits of MLL1 complex to the same regions, to increase histone H3K4me3 levels. Furthermore, BAP18 depletion delayed G1-S phase transition and inhibited cell growth in OSCC-derived cell lines.
interpretationThis study suggests that BAP18 is involved in modulation of CCND1/2 transcription and promotes OSCC progression. BAP18 could be a potential target for OSCC treatment and diagnosis. FUND: This work was funded by National Natural Science Foundation of China (31871286, 81872015, 31701102, 81702800, 81902889), Foundation for Special Professor of Liaoning Province, and Supported project for young technological innovation-talents in Shenyang (No. RC170541).
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