Journal: bioRxiv

Article Title: KMT5C-H4K20me3 drives changes in epigenetic landscape independent of H3K9me3

doi: 10.64898/2026.05.11.724304

Figure Lengend Snippet: A . Distribution of H3K9me3-/H4K20me3+ and H3K9me3+/H4K20me3+ across the gene bodies in HCC827 cells. TSS, transcriptional start site; TTS, transcriptional termination site. B . Heatmaps of H3K27me3, H3K27ac, H3K4me3, H4K20me1, and KMT5C peaks in HCC827 cells, clustered by H4K20me3-only, H3K9me3-only, or overlapping H4K20me3/H3K9me3 peaks. C . Normalized peak density plots of H3K27me3, H3K27ac, H3K4me3, H4K20me1, and KMT5C in HCC827 cells, clustered as in (B). D . Expression of genes associated with H3K9me3-/H4K20me3+ or H3K9me3+/H4K20me3+ peaks in HCC827 cells. RNA-seq data were obtained from GSE81167 and GSE202859. E . HOMER motif analysis of H3K9me3-/H4K20me3+ or H3K9me3+/H4K20me3+ peaks in HCC827 cells.

Article Snippet: For CUT&RUN, 0.5μg of the following primary antibodies was used: H4K20me3 (Abcam, #ab9053), H3K9me3 (ActiveMotif, #39162), H3K27me3 (Cell Signaling, #9733), H3K27ac (Abcam, #ab4729), H3K4me3 (Epicypher, #13-0041), H4K20me1 (Abcam, #ab9051), KMT5C (Sigma, #HPA052294), HA Tag (Epicypher, #13-2010), and IgG (Epicypher, #13-0042).

Techniques: Expressing, RNA Sequencing

Journal: Neoplasia (New York, N.Y.)

Article Title: BPGM as an intrinsic brake to constrain metastasis through phospho-epigenetic-mediated carnitine biosynthesis suppression

doi: 10.1016/j.neo.2026.101299

Figure Lengend Snippet: Hypoxia inhibits BPGM expression in a KDM4A/H3K9me3-dependent manner. (A) The oxygen concentration and its positive correlation with BPGM level in different stage of tumor development. (B) Hypoxia treatment decreased the mRNA level of BPGM. (C-D) Hypoxia treatment decreased the protein level of BPGM. For B-C, SK-HEP-1 and SNU-449 cells were incubated under normoxia or hypoxia for the indicated time. The BPGM level was detected by qPCR (B) or western blotting (C-D). (E) Hypoxia treatment decreased the luciferase activities of p(−2/+0.1k) promoter. Cells were co-transfected with BPGM promoter plasmid (p(−2/+0.1k)) and pRL-CML vectors for 36 hours, then untreated or treated with hypoxia for another 12 hours. The promoter activity was examined by luciferase activity assay. Basic, pGL3-basic vector. (F) Knockdown of hypoxia-inducible-factor 1α did not block the inhibitory effect of hypoxia on the luciferase activities of p(−2/+0.1k) promoter. (G-H) The histone modification features and binding sites of histone demethylase in the promoter region of BPGM gene. ChIP-seq profiles of H3K4me1, H3K4me3, H3K27ac and H3K9me3 are visualized using the UCSC genome browser ( http://genome.ucsc.edu/ ). The transcription direction and the potential promoter region of BPGM are indicated. TSS, transcription start site. (I) The level of H3K9me3 was downregulated in HCC tissues with MVI. The protein levels of H3K9me3 in human HCC tissues (“-”, n = 5; “+”, n = 5) were detected by immunofluorescence. (J) The protein level of BPGM was negatively correlated with the level of H3K9me3 in human placentae and HCC tissues. (K) Hypoxia increased H3K9me3 level but decreased BPGM level in tumor cells. SK-HEP-1 cells were incubated under normoxia or hypoxia for the indicated time. (L) H3K9me3 inhibitor blocked the inhibitory role of hypoxia on BPGM expression. SK-HEP-1 cells were incubated without or with the indicated concentration of chaetocin (Chao) under normoxia or hypoxia condition for 12 h. Scale bar, 50 μm. (M) KDM4A inhibitor suppressed BPGM expression under normoxia condition. SK-HEP-1 cells were incubated without or with the indicated dose of ML324 (KDM4A inhibitor) under normoxia condition for 12 h. (N) The model deciphers the role of hypoxia in repressing BPGM expression. Error bar: mean ± SEM. P -values are labeled above the bar chart.

Article Snippet: The antibodies used included mouse antibody against β-actin (BM0627, Boster, Wuhan, China), rabbit antibody against BPGM (17173-1-AP, Proteintech), EZH2 (F0281, Selleck), phospho-EZH2 (Thr345) (TA3584S, Abmart, Shanghai, China), phospho-CDK1 (Thr14) (AP1465, Abclonal, Wuhan, China), ubiquitin (10201-2-AP, Proteintech), HIF1α (36169, Cell Signaling Technology, CST, Beverly, MA, USA), H3K4me3 (91264, Active Motif), H3K79me3 (cat 49-1020, Thermos Fisher), H3K9me3 (61014, Active Motif), H3K27me3 (91168, Active Motif) and Histone 3 (F0057, Selleck).

Techniques: Expressing, Concentration Assay, Incubation, Western Blot, Luciferase, Transfection, Plasmid Preparation, Activity Assay, Knockdown, Blocking Assay, Modification, Binding Assay, ChIP-sequencing, Immunofluorescence, Labeling