Journal: Stem cell research & therapy

Article Title: PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.

doi: 10.1186/s13287-025-04409-z

Figure Lengend Snippet: Fig. 4 PRMT1 inhibition promotes proliferation and migration of ADSCs through RUNX1-mediated MMP-10/PlGF/TGF-β2 expression in ADSCs. (A) Pre dicted transcription factors binding to the target Mmp10, Plgf and Tgfb2 genes promoter region. The promoter region is defined as 2000 bp upstream of the target gene transcription starting point. (B) Predict possible binding sites in the gene promoter region and transcription factor RUNX1. (C, D) The relationship between PRMT1 and RUNX1 was detected by Co-IP experiment. (E, F) ADSCs were treated with Furamidine (10 µM) and Ro5-3335 (50 µM) for 48 h. Full-length blots are presented in Supplementary Fig. 4E, F. Western blotting and quantitative analysis of MMP-10, PlGF, and TGF-β2 protein levels (n = 6). Full-length blots are presented in Supplementary Fig. 5A. (G) Changes in cell proliferation were detected by CCK-8 after ADSCs were treated with Furamidine and Ro5-3335 for 24 h (n = 6). (H, I) Representative images of crystal violet staining. The migration ability of ADSCs was observed by transwell assay after treatment with Furamidine and Ro5-3335 (n = 4). Scale bar: 50 μm. All data are presented as mean ± SEM and were analyzed by one-way ANOVA, *P < 0.05

Article Snippet: The primary antibodies used in this study included: anti-PRMT1 rabbit monoclonal antibody (2449 S, 1:1000; Cell Signaling Technology, MA, USA), anti-cleaved caspase-3 rabbit polyclonal antibody (9664 S, 1:1000; Cell Signaling Technology, MA, USA), anti-MMP-10 rabbit polyclonal antibody (A3033, 1:1000; Abclonal Technology, Wuhan, China), anti-TGF-β2 rabbit polyclonal antibody (19999-1-AP, 1:1000; Proteintech, Wuhan, China), anti-PlGF rabbit polyclonal antibody (10642-1-AP, 1:1000; Proteintech, Wuhan, China), anti-RUNX1 rabbit polyclonal antibody (25315-1-AP, 1:1000; Proteintech, Wuhan, China), anti-GAPDH rabbit polyclonal antibody (10494-1-AP, 1:10000; Proteintech, Wuhan, China).

Techniques: Inhibition, Migration, Expressing, Binding Assay, Co-Immunoprecipitation Assay, Western Blot, CCK-8 Assay, Staining, Transwell Assay

Journal: Stem cell research & therapy

Article Title: PRMT1 inhibition enhances the cardioprotective effect of adipose-derived mesenchymal stem cells against myocardial infarction through RUNX1.

doi: 10.1186/s13287-025-04409-z

Figure Lengend Snippet: Fig. 8 Schematic illustration of inhibition of PRMT1 improve the therapeutic efficacy of ADSCs for MI. After MI, the level of PRMT1 in ADSCs transplanted into the infarct border zone increased under stress, and by interacting with RUNX1, the transcription-promoting effect of RUNX1 on Mmp10, Plgf and Tgfb2 was inhibited, resulting in impaired retention and survival of ADSCs, and inadequate cardioprotective effects (left). After knockdown of PRMT1, the released RUNX1 promoted the expression of Mmp10, Plgf and Tgfb2 in ADSCs, improved the retention rate of implanted ADSCs, and enhanced cardiopro tective effects of ADSCs (right). The Figure was created with BioRender software (https://biorender.com/)

Article Snippet: The primary antibodies used in this study included: anti-PRMT1 rabbit monoclonal antibody (2449 S, 1:1000; Cell Signaling Technology, MA, USA), anti-cleaved caspase-3 rabbit polyclonal antibody (9664 S, 1:1000; Cell Signaling Technology, MA, USA), anti-MMP-10 rabbit polyclonal antibody (A3033, 1:1000; Abclonal Technology, Wuhan, China), anti-TGF-β2 rabbit polyclonal antibody (19999-1-AP, 1:1000; Proteintech, Wuhan, China), anti-PlGF rabbit polyclonal antibody (10642-1-AP, 1:1000; Proteintech, Wuhan, China), anti-RUNX1 rabbit polyclonal antibody (25315-1-AP, 1:1000; Proteintech, Wuhan, China), anti-GAPDH rabbit polyclonal antibody (10494-1-AP, 1:10000; Proteintech, Wuhan, China).

Techniques: Inhibition, Drug discovery, Knockdown, Expressing, Software

Journal: Journal of Virology

Article Title: RUNX3 inhibits KSHV lytic replication by binding to the viral genome and repressing transcription

doi: 10.1128/jvi.01567-23

Figure Lengend Snippet: RUNX3 expression is upregulated by NF-κB during KSHV lytic reactivation. (A–D) iSLK.RGB cells were treated with or without doxycycline (Dox). The kinetics of RUNX family expression in iSLK.RGB cells. (A) The mRNA of RUNX1 during the induction of lytic reactivation in iSLK.RGB cells were analyzed by qPCR. (B) The mRNA of RUNX2 during the induction of lytic reactivation in iSLK.RGB cells were analyzed by qPCR. (C) The mRNA of RUNX3 during the induction of lytic reactivation in iSLK.RGB cells were analyzed by qPCR. (D) iSLK.RGB cells were induced with Dox for indicated times. The expression levels of RTA and RUNX family were examined by western blotting. (E and F) BCBL1 cells were treated with or without 12-O-tetradecanoylphorbol-13-acetate (TPA) and sodium butyrate (NaB). The kinetics of RUNX3 expression in BCBL1 cells. (E) BCBL1 cells were induced with TPA and NaB for indicated times. The mRNA of RUNX3 during the induction of lytic reactivation in BCBL1 cells were analyzed by qPCR. (F) The expression levels of RTA and RUNX3 were examined by western blotting. (G–J) RUNX3 induction is mediated primarily by NF-κB pathways during KSHV lytic reactivation. (G) iSLK.RGB cells were treated with or without 10 µM BAY11-7082 for 6 h in advance and then treated with or without Dox for 24 h. The expression of RUNX3 was detected by western blots. (H) The mRNA expression of RUNX3 was determined by qPCR analysis. iSLK.RGB cells were transfected with control siRNA and two siRNAs specific to human NF-κB p65. Twenty-four hours after transfection, cells were treated with Dox for the indicated times. The knockdown efficiency and RUNX3 expression were determined by western blots (I) and qPCR (J). Data were shown as mean ± SD (error bars) from at least three independent experiments, and statistical analysis was done by using multiple unpaired student’s t test (A, B, C, E, and J) and unpaired student’s t test (H). ns, not significant; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Article Snippet: The primary antibodies were used in this study: anti-RUNX1 rabbit polyclonal antibody (ABclonal, A2055), anti-RUNX2 rabbit monoclonal antibody (ABclonal, A11753), anti-RUNX3 rabbit monoclonal antibody (Abcam, ab224641), anti-DDDDK-Tag mouse monoclonal antibody (ABclonal, AE005), anti-α-tubulin mouse monoclonal antibody (Sigma, T6199), anti-RTA rabbit monoclonal antibody (prepared in our laboratory), HA antibody (Sigma, H9658), anti-GAPDH mouse monoclonal antibody (ABclonal, AC033), anti-UBC rabbit polyclonal antibody (ABclonal, A3207), anti-BrdU mouse monoclonal antibody (ABclonal, A1482), NF-kB p65/RelA rabbit polyclonal antibody (ABclonal, A2547), and the Phospho-NF-κB p65 rabbit monoclonal antibody (CST, #3033).

Techniques: Expressing, Western Blot, Transfection, Control, Knockdown

Journal: Journal of Virology

Article Title: RUNX3 inhibits KSHV lytic replication by binding to the viral genome and repressing transcription

doi: 10.1128/jvi.01567-23

Figure Lengend Snippet: Primers for PCR amplification, qPCR, and ChIP-qPCR analysis

Article Snippet: The primary antibodies were used in this study: anti-RUNX1 rabbit polyclonal antibody (ABclonal, A2055), anti-RUNX2 rabbit monoclonal antibody (ABclonal, A11753), anti-RUNX3 rabbit monoclonal antibody (Abcam, ab224641), anti-DDDDK-Tag mouse monoclonal antibody (ABclonal, AE005), anti-α-tubulin mouse monoclonal antibody (Sigma, T6199), anti-RTA rabbit monoclonal antibody (prepared in our laboratory), HA antibody (Sigma, H9658), anti-GAPDH mouse monoclonal antibody (ABclonal, AC033), anti-UBC rabbit polyclonal antibody (ABclonal, A3207), anti-BrdU mouse monoclonal antibody (ABclonal, A1482), NF-kB p65/RelA rabbit polyclonal antibody (ABclonal, A2547), and the Phospho-NF-κB p65 rabbit monoclonal antibody (CST, #3033).

Techniques: Amplification, Sequencing

Journal: Journal of translational medicine

Article Title: RUNX1 knockdown induced apoptosis and impaired EMT in high-grade serous ovarian cancer cells.

doi: 10.1186/s12967-023-04762-8

Figure Lengend Snippet: Fig. 5 RUNX1 knockdown affects EMT in ovarian cancer cells via the EGFR-AKT-STAT3 axis. Western blot detected the signaling molecules change pattern in the RUNX1 KD cells that involved in the EMT related signaling pathway (A and B). Western blot detected the signaling molecules change pattern after Ro5-3335 (a RUNX1 inhibitor) treatment that involved in the EMT related signaling pathway (C and D). Western blot detected of EMT-related molecules in RUNX1 knockdown cell lines (E and F). Western blot detected of EMT-related molecules after Ro5-3335 treatment (G and H). The expression of EMT-related molecules was analyzed by immunofluorescence in RUNX1 knockdown cell lines (I and J). *p < 0.05, **p < 0.01 and ***p < 0.001 as compared with control cells expressing a scramble shRNA control, paired t test

Article Snippet: Sections were incubated overnight with RUNX1 antibody (Cusabio, China) at 4 °C.

Techniques: Knockdown, Western Blot, Expressing, Immunofluorescence, Control, shRNA