| 2016 |
BAP18 acts as a coactivator of androgen receptor (AR) in both Drosophila and mammalian cells; it facilitates recruitment of the MLL1 subcomplex and AR to androgen-response elements (AREs) of AR target genes, increasing histone H3K4 trimethylation and H4K16 acetylation. BAP18 knockdown attenuates prostate cancer cell growth and xenograft tumor growth. |
Co-immunoprecipitation, ChIP assay, luciferase reporter assay, siRNA/shRNA knockdown, xenograft mouse model, Drosophila experimental system |
Nucleic acids research |
High |
27226492
|
| 2020 |
BAP18 functions as an H3K4me3 reader; it is recruited to promoter regions of CCND1 and CCND2 in oral squamous cell carcinoma cells, facilitating recruitment of MLL1 complex core subunits to increase H3K4me3 levels and activate transcription, thereby promoting G1-S phase transition and cell growth. |
ChIP assay, qPCR, western blot, lentiviral shRNA knockdown, colony formation, xenograft tumor experiment |
EBioMedicine |
Medium |
32113162
|
| 2020 |
BAP18 acts as a co-activator of ERα in breast cancer cells; it is recruited to promoter regions of estrogen-induced genes and facilitates recruitment of COMPASS-like core subunits, accompanied by enrichment of H3K4me3, in an E2-dependent manner. BAP18 promotes cell growth and modulates antiestrogen sensitivity. |
ChIP-seq, Co-IP, ChIP assay, shRNA knockdown, luciferase reporter assay |
Nucleic acids research |
High |
32986841
|
| 2022 |
BAP18 is recruited to the H3K4me3-marked promoter of S100A9 in triple-negative breast cancer cells, enhancing its promoter activity and transcription. Knockdown of BAP18 suppresses xenograft tumor growth, an effect partially rescued by S100A9 re-expression, placing S100A9 downstream of BAP18. |
ChIP assay, luciferase reporter assay, shRNA knockdown, rescue experiment (S100A9 re-expression), xenograft mouse model |
Cell death & disease |
Medium |
35484101
|
| 2023 |
BAP18 interacts with SMARCA1/BPTF and is required for CTCF recruitment to ERα-enriched enhancers; it facilitates chromatin accessibility within enhancer regions, promotes enhancer RNA transcription, and enhances enhancer-promoter looping. BAP18 depletion increases sensitivity to anti-estrogen and anti-enhancer treatment. |
Co-IP, ChIP assay, GRO-seq, ATAC-seq (chromatin accessibility), shRNA knockdown, luciferase reporter assay |
Cell death and differentiation |
High |
36828916
|
| 2021 |
BAP18 interacts with androgen receptor (AR) and enhances AR-mediated transactivation in luteinized granulosa cells; BAP18 and AR co-recruit to AREs of CYP19A1 and FSHR promoters. BAP18 also interacts with Sp1 and co-recruits to the AR gene promoter to activate AR transcription. BAP18 knockdown decreases CYP19A1 expression and impairs androgen-to-estrogen conversion. |
Co-IP, ChIP assay, siRNA knockdown, qPCR, western blot |
Molecular and cellular endocrinology |
Medium |
33662476
|
| 2023 |
BAP18 co-activates PPARα-mediated transactivation in hepatocellular carcinoma cells and facilitates recruitment of the NuA4/TIP60 complex, thereby increasing histone H4 acetylation at SCD1 loci. BAP18 promotes HCC cell proliferation and lipid accumulation. |
Co-IP, ChIP assay, shRNA knockdown, luciferase reporter assay, cell proliferation assay |
Biochimica et biophysica acta. Molecular basis of disease |
Medium |
38042310
|
| 2025 |
BAP18 recruits ACTL6A and PAF1 to Wnt target gene promoters, enhancing β-catenin-mediated transcription in NSCLC cells. Co-immunoprecipitation confirmed interaction between BAP18, β-catenin, ACTL6A, and PAF1; luciferase reporter assays showed increased β-catenin transcriptional activity. BAP18 knockdown inhibited NSCLC cell proliferation, migration, and xenograft tumor growth. |
Co-immunoprecipitation, luciferase reporter assay, RNA sequencing, shRNA knockdown, xenograft mouse model, immunohistochemistry |
The Journal of biological chemistry |
Medium |
40818609
|
| 2025 |
In AR-positive triple-negative breast cancer cells, BAP18 acts as a transcriptional corepressor of AR by associating with AR and the SIN3A/HDAC subcomplex. BAP18 facilitates SIN3A/HDAC recruitment to AREs in promoters of P21 and PTEN, reducing histone H4 acetylation at those sites and suppressing their expression. |
Co-immunoprecipitation, ChIP assay, shRNA knockdown, western blot |
Cell & bioscience |
Medium |
41163225
|
| 2022 |
BAP18 knockdown in NSCLC cell lines (A549, H1299) reduces transcriptional levels of CCND1 and CCND2, delays G1-to-S phase transition, and weakens NSCLC cell growth, indicating BAP18 regulates CCND1/2 transcription to promote cell cycle progression. |
siRNA/lentiviral shRNA knockdown, qRT-PCR, western blot, colony formation assay, cell cycle analysis |
European review for medical and pharmacological sciences |
Low |
35587057
|