Journal: Oncology Letters

Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle

doi: 10.3892/ol.2025.15285

Figure Lengend Snippet: HAT1 levels are upregulated in human ovarian cancer tissue and higher HAT1 levels indicate a poor prognosis. (A) Representative images depicting the representative immunostaining of HAT1 in ovarian cancer tissues and healthy human tissues in The Human Protein Altas database. Scale bar=200 µm. (B) Analysis of the TNMplot database showed that HAT1 was highly expressed in ovarian cancer tissues compared with healthy controls. (C) Protein levels of HAT1 in ovarian cancer and healthy human samples from healthy controls were analyzed in the CPTAC database. (D) HAT1 protein levels were upregulated with tumor grade in ovarian cancer tissues. (E) Higher HAT1 levels were associated with an unfavorable prognosis in patients with ovarian cancer. Data are presented as the mean ± SD. **P<0.01. HAT1, histone acetyltransferase 1; CPTAC, Clinical Proteomic Tumor Analysis Consortium; HR, hazard ratio.

Article Snippet: HEY and SKOV3 cells were seeded into 96-well plates (5×10 3 /well) and treated with 0.0, 0.5, 1.0, 5, 10, 20, 30 and 50 μM) of HAT1 inhibitor JG-2016 or DMSO as indicated (Cat.HY-154944; MedChemExpress) for 72 h at room temperature.

Techniques: Immunostaining

Journal: Oncology Letters

Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle

doi: 10.3892/ol.2025.15285

Figure Lengend Snippet: HAT1 expression levels are upregulated in human ovarian cancer cell lines. (A) Relative expression levels of HAT1 were detected by reverse transcription-quantitative PCR in A2780, HEY, OVCAR3, SKOV3 and normal IOSE386 cell lines. (B) Western blot analysis of HAT1 expression in A2780, HEY, OVCAR3, SKOV3 and IOSE386 cell lines. ****P<0.0001 vs. IOSE386. HAT1, histone acetyltransferase 1.

Article Snippet: HEY and SKOV3 cells were seeded into 96-well plates (5×10 3 /well) and treated with 0.0, 0.5, 1.0, 5, 10, 20, 30 and 50 μM) of HAT1 inhibitor JG-2016 or DMSO as indicated (Cat.HY-154944; MedChemExpress) for 72 h at room temperature.

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot

Journal: Oncology Letters

Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle

doi: 10.3892/ol.2025.15285

Figure Lengend Snippet: FOXA1 transcriptionally regulates HAT1 expression levels. (A) FOXA1 binding sites in the HAT1 promoter region were predicted using the JASPAR database. MUT constructs were generated at the binding sequence regions as indicated. (B) The expression levels of FOXA1 in HEY cells transfected with an empty or FOXA1 vector. (C) HEY cells were transfected with pmirGLO reporter vectors containing either WT or MUT plasmids alongside an empty or FOXA1 vector. Luciferase activities were determined 24 h after transfection. (D) Overexpression of FOXA1 induced HAT1 expression levels. (E) cBioPortal database was adopted to analyze the correlation between FOXA1 and HAT1. Pearson's rank correlation between HAT1 and FOXA1 was analyzed in ovarian cancer tissues. (F) FOXA1 levels in ovarian cancer tissues from TCGA were determined using TNMplot database. (G) FOXA1 was enriched at the HAT1 promoter region as suggested by Cistrome DB. Data are presented as the mean ± SD of three replicates. **P<0.01 vs. vector or as indicated; ns, not significant. ChIP-seq, chromatin immunoprecipitation sequencing; FOXA1, forkhead box protein A1; HAT1, histone acetyltransferase 1; WT, wild-type; MUT, mutant.

Article Snippet: HEY and SKOV3 cells were seeded into 96-well plates (5×10 3 /well) and treated with 0.0, 0.5, 1.0, 5, 10, 20, 30 and 50 μM) of HAT1 inhibitor JG-2016 or DMSO as indicated (Cat.HY-154944; MedChemExpress) for 72 h at room temperature.

Techniques: Expressing, Binding Assay, Construct, Generated, Sequencing, Transfection, Plasmid Preparation, Luciferase, Over Expression, ChIP-sequencing, Mutagenesis

Journal: Oncology Letters

Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle

doi: 10.3892/ol.2025.15285

Figure Lengend Snippet: Relationship between HAT1 and DNA replication and pyrimidine metabolism pathways. (A) LinkedOmics database suggested that differentially expressed genes of HAT1 were enriched in several biological processes, such as ‘DNA replication’, ‘pyrimidine metabolism’ and ‘RNA transport’. (B) Gene set enrichment analysis revealed that genes altered by HAT1 were positively associated with ‘DNA replication’ as well as ‘pyrimidine metabolism’ pathways. (C) cBioPortal database was used to analyze the correlations between HAT1 and regulatory proteins of the DNA replication pathway. Pearson's rank correlation between HAT1 and DNA replication-related proteins (PCNA, RPA1 and POLA1) was analyzed in ovarian cancer tissues. (D) Pearson's rank correlation between HAT1 and pyrimidine metabolism-related proteins (TK1, RRM1 and RRM2) was analyzed in ovarian cancer tissues as suggested in the cBioPortal database. HAT1, histone acetyltransferase 1; PCNA, proliferating cell nuclear antigen; RPA1, replication protein A1; POLA1, DNA polymerase α catalytic subunit; TK1, thymidine kinase 1; RRM, ribonucleoside-diphosphate reductase subunit M; NES, normalized enrichment score; FDR, false discovery rate.

Article Snippet: HEY and SKOV3 cells were seeded into 96-well plates (5×10 3 /well) and treated with 0.0, 0.5, 1.0, 5, 10, 20, 30 and 50 μM) of HAT1 inhibitor JG-2016 or DMSO as indicated (Cat.HY-154944; MedChemExpress) for 72 h at room temperature.

Techniques:

Journal: Oncology Letters

Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle

doi: 10.3892/ol.2025.15285

Figure Lengend Snippet: Inhibition of HAT1 suppresses cell viability and colony formation in vitro . (A) Western blot analysis of HAT1 expression in HEY and SKOV3 cells transfected with HAT1 siRNA or NC siRNA. (B) Cell Counting Kit-8 assays were performed to determine cell viability after HAT1 was knocked down in HEY and SKOV3 cells. (C) HEY and SKOV3 cells were treated with HAT1 inhibitor JG-2016 for 72 h, which significantly inhibited cell viability. (D) Knockdown of HAT1 decreased the colony formation capacity of HEY and SKOV3 cells. Data are presented as the mean ± SD of three replicates. *P<0.05 and **P<0.01 vs. siNC in figure 5B and DMSO group in figure 5C. HAT1, histone acetyltransferase 1; si, small interfering; NC, negative control.

Article Snippet: HEY and SKOV3 cells were seeded into 96-well plates (5×10 3 /well) and treated with 0.0, 0.5, 1.0, 5, 10, 20, 30 and 50 μM) of HAT1 inhibitor JG-2016 or DMSO as indicated (Cat.HY-154944; MedChemExpress) for 72 h at room temperature.

Techniques: Inhibition, In Vitro, Western Blot, Expressing, Transfection, Cell Counting, Knockdown, Negative Control

Journal: Oncology Letters

Article Title: Histone acetyltransferase 1 promotes ovarian cancer progression by regulating cell proliferation and the cell cycle

doi: 10.3892/ol.2025.15285

Figure Lengend Snippet: HAT1 knockdown inhibits cell proliferation. (A) EdU assays of HEY cells were performed showing that suppression of HAT1 attenuated cell proliferation activities. Scale bar, 20 µm. (B) Cell cycle analysis was carried out on the HAT1 knockdown and siNC cell lines, and the distribution of G 0 /G 1 , S and G 2 /M percentages were analyzed. (C) Western blot analysis of cell cycle-related protein expression after knockdown of HAT1. (D) Pearson's rank correlation between HAT1 and CDK2, CDK4 and cyclin E was analyzed in ovarian cancer tissues. Data are presented as the mean ± SD of three replicates. **P<0.01 vs. siNC. HAT1, histone acetyltransferase 1; si, small interfering; NC, negative control; CDK, cyclin-dependent kinase.

Article Snippet: HEY and SKOV3 cells were seeded into 96-well plates (5×10 3 /well) and treated with 0.0, 0.5, 1.0, 5, 10, 20, 30 and 50 μM) of HAT1 inhibitor JG-2016 or DMSO as indicated (Cat.HY-154944; MedChemExpress) for 72 h at room temperature.

Techniques: Knockdown, Cell Cycle Assay, Western Blot, Expressing, Negative Control