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Proteintech runx2 rabbit monoclonal

In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, <t>Runx2,</t> OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Runx2 Rabbit Monoclonal, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1024 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/runx2+rabbit+monoclonal/Collagen+Type+I+Polyclonal+antibody/pmc12874108-276-50-54
Average 96 stars, based on 1024 article reviews

runx2 rabbit monoclonal - by Bioz Stars, 2026-11

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1) Product Images from "Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration"

Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration

Journal: Materials Today Bio

doi: 10.1016/j.mtbio.2026.102779

Figure Legend Snippet: In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, Runx2, OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Techniques Used: In Vitro, Staining, Activity Assay, Quantitative RT-PCR, Expressing

In vitro evaluation of osteogenesis related proteins and genes. (A) The relative protein expression levels of C1, Runx2 and OPN. (B–D) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. (E) Immunofluorescence staining of OPN. (F) Immunofluorescence staining of OCN. (G) The relative protein expression levels of C1, Runx2 and OPN. (H–J) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Figure Legend Snippet: In vitro evaluation of osteogenesis related proteins and genes. (A) The relative protein expression levels of C1, Runx2 and OPN. (B–D) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. (E) Immunofluorescence staining of OPN. (F) Immunofluorescence staining of OCN. (G) The relative protein expression levels of C1, Runx2 and OPN. (H–J) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Techniques Used: In Vitro, Expressing, Western Blot, Immunofluorescence, Staining

Incubation:

Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration
Article Snippet: Equal protein aliquots were resolved on 10 % SDS-PAGE gels (Bio-Rad, #4561033) at 100 V for 2 h and transferred to PVDF membranes (Millipore, #IPFL00010) via electrophoresis (300 mA, 30 min). .. Membranes were blocked with 5 % non-fat milk (BD Difco, #232100) in TBST (Beyotime, #ST673) for 1 h at 25 °C and incubated overnight at 4 °C with the following primary antibodies: Osteopontin (OPN) : • Rabbit monoclonal (Proteintech, 22952-1-AP), 1:1000 • Collagen I (COL1A1): Rabbit polyclonal (Proteintech, 14695-1-AP), 1:1000 • RUNX2: Rabbit monoclonal (Proteintech, 20700-1-AP), 1:1000 • NRF2: Rabbit monoclonal (Proteintech, 16396-1-AP), 1:2000 • NQO1: Mouse monoclonal (Proteintech, 67240-1-Ig), 1:2000 • Beta Actin: Mouse monoclonal (Proteintech, 66009-1-Ig), 1:20,000 After three 10-min TBST washes, membranes were incubated with HRP-conjugated goat anti-rabbit/mouse IgG (Beyotime, #A0208/#A0216, 1:5000) for 2 h at 25 °C. .. Protein bands were visualized using ECL Prime (Beyotime, #P0018) and imaged on a ChemiDoc MP System (Bio-Rad).

Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration
Article Snippet: Equal protein aliquots were resolved on 10 % SDS-PAGE gels (BioRad, #4561033) at 100 V for 2 h and transferred to PVDF membranes (Millipore, #IPFL00010) via electrophoresis (300 mA, 30 min). .. Membranes were blocked with 5 % non-fat milk (BD DifcoTM, #232100) in TBST (Beyotime, #ST673) for 1 h at 25 ◦C and incubated overnight at 4 ◦C with the following primary antibodies:Osteopontin (OPN): • Rabbit monoclonal (Proteintech, 22952-1-AP), 1:1000 • Collagen I (COL1A1): Rabbit polyclonal (Proteintech, 14695-1-AP), 1:1000 • RUNX2: Rabbit monoclonal (Proteintech, 20700-1-AP), 1:1000 • NRF2: Rabbit monoclonal (Proteintech, 16396-1-AP), 1:2000 • NQO1: Mouse monoclonal (Proteintech, 67240-1-Ig), 1:2000 • Beta Actin: Mouse monoclonal (Proteintech, 66009-1-Ig), 1:20,000 After three 10-min TBST washes, membranes were incubated with HRP-conjugated goat anti-rabbit/mouse IgG (Beyotime, #A0208/ #A0216, 1:5000) for 2 h at 25 ◦C. .. Protein bands were visualized using ECL Prime (Beyotime, #P0018) and imaged on a ChemiDoc MP System (Bio-Rad).

Image Search Results

The biocompatibility assay and osteogenesis assay of AC, AS, PAS, PASN groups. A ) The cell viability assay of AC, AS, PAS, and PASN scaffolds. B ) The osteogenesis-related gene expressions of ALP, COL-1, RUNX2 and OCN at 7 and 14 days. C ) Schematic diagram of BMSCs cocultured with AC, AS, PAS scaffold. D ) Immunofluorescent staining and E ) quantitative analysis of BMSCs co-cultured with different hydrogel scaffolds for 7 days, green for ALP, COL-1, RUNX2, and OCN, red (phalloidin) for F-actin and blue (DAPI) for nuclei. F ) ALP staining of BMSCs for 7 and 14 days. G ) Calcium deposition stained with alizarin red S of BMSCs for 28 days. (*P < 0.05, **P <0.01, and ***P < 0.001; “ns” denoted no significant difference, n = 3, error bars indicate means ± standard deviations)

Journal: Journal of Nanobiotechnology

Article Title: 4D printed hydrogel scaffolds with shape morphing by near-infrared to promote bone regeneration through immune and vascular coupling

doi: 10.1186/s12951-026-04386-2

Figure Lengend Snippet: The biocompatibility assay and osteogenesis assay of AC, AS, PAS, PASN groups. A ) The cell viability assay of AC, AS, PAS, and PASN scaffolds. B ) The osteogenesis-related gene expressions of ALP, COL-1, RUNX2 and OCN at 7 and 14 days. C ) Schematic diagram of BMSCs cocultured with AC, AS, PAS scaffold. D ) Immunofluorescent staining and E ) quantitative analysis of BMSCs co-cultured with different hydrogel scaffolds for 7 days, green for ALP, COL-1, RUNX2, and OCN, red (phalloidin) for F-actin and blue (DAPI) for nuclei. F ) ALP staining of BMSCs for 7 and 14 days. G ) Calcium deposition stained with alizarin red S of BMSCs for 28 days. (*P < 0.05, **P <0.01, and ***P < 0.001; “ns” denoted no significant difference, n = 3, error bars indicate means ± standard deviations)

Article Snippet: Immunofluorescence staining blocking buffer (Beyotime, China), ALP Rabbit Monoclonal Antibody (ABclonal, China), COL-1 Rabbit Monoclonal Antibody (ABclonal, China), OCN Rabbit Monoclonal Antibody (ABclonal, China), RUNX2 Rabbit Monoclonal Antibody (ABclonal, China), and Alexa Fluor 488-labeled Goat Anti-rabbit IgG (Beyotime, China) were used for Immunofluorescence Staining according to the manufacturer’s instructions.

Techniques: Viability Assay, Staining, Cell Culture

Transcriptomics Analysis of BMSCs and verification of the mechanical force sensing pathway in cells. A ) KEGG and B ) GO enrichment bubble diagram of BMSCs [n = 3, adjusted p-value (q value) of <0.05]. C )Topological graph of “focal adhesion signaling pathway mediated by PASN” in the Reactome data. D ) Heatmap analysis of BMSCs, Orange: higher expressions, blue: lower expressions [n = 3, adjusted p-value (q value) of <0.05]. E ) Immunofluorescent staining of BMSCs cultured on different hydrogel scaffolds for 3 days, green for vinculin and G ) YAP, red(phalloidin) for F-actin and blue (DAPI) for nuclei. F ) Quantitative analysis of vinculin area and H ) nucleus/ cytoplasmic ratio of YAP based on fluorescence intensities. I ) Real-time PCR analysis of the mRNA expression of VCL, Lamc, RhoA, ROCK1, ROCK2 for 3 days. J ) Expressions of RhoA, ALP, RUNX2, YAP, Lamin, Vinculin, ROCK1, and COL-1 proteins detected by western blot analysis of BMSCs. K ) Cells sense composite microenvironment by exerting contractile forces with stress fibers through focal adhesions, which activates various proteins, such as focal adhesion kinase (FAK), vinculin, RhoA and ROCK, at the adhesion site. Activation of these proteins leads to adhesion maturation and stress fiber formation and contractility, which in turn transmits forces to the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex, resulting in changes in nuclear envelope tension and nuclear pore opening. This allows the nuclear entry of proteins such as the transcription regulator YAP, leading to a downstream impact on cell phenotype. (*P < 0.05, **P < 0.01, and ***P < 0.001; “ns” denoted no significant difference, n = 3, error bars indicate means ± standard deviations)

Journal: Journal of Nanobiotechnology

Article Title: 4D printed hydrogel scaffolds with shape morphing by near-infrared to promote bone regeneration through immune and vascular coupling

doi: 10.1186/s12951-026-04386-2

Figure Lengend Snippet: Transcriptomics Analysis of BMSCs and verification of the mechanical force sensing pathway in cells. A ) KEGG and B ) GO enrichment bubble diagram of BMSCs [n = 3, adjusted p-value (q value) of <0.05]. C )Topological graph of “focal adhesion signaling pathway mediated by PASN” in the Reactome data. D ) Heatmap analysis of BMSCs, Orange: higher expressions, blue: lower expressions [n = 3, adjusted p-value (q value) of <0.05]. E ) Immunofluorescent staining of BMSCs cultured on different hydrogel scaffolds for 3 days, green for vinculin and G ) YAP, red(phalloidin) for F-actin and blue (DAPI) for nuclei. F ) Quantitative analysis of vinculin area and H ) nucleus/ cytoplasmic ratio of YAP based on fluorescence intensities. I ) Real-time PCR analysis of the mRNA expression of VCL, Lamc, RhoA, ROCK1, ROCK2 for 3 days. J ) Expressions of RhoA, ALP, RUNX2, YAP, Lamin, Vinculin, ROCK1, and COL-1 proteins detected by western blot analysis of BMSCs. K ) Cells sense composite microenvironment by exerting contractile forces with stress fibers through focal adhesions, which activates various proteins, such as focal adhesion kinase (FAK), vinculin, RhoA and ROCK, at the adhesion site. Activation of these proteins leads to adhesion maturation and stress fiber formation and contractility, which in turn transmits forces to the nucleus via the linker of nucleoskeleton and cytoskeleton (LINC) complex, resulting in changes in nuclear envelope tension and nuclear pore opening. This allows the nuclear entry of proteins such as the transcription regulator YAP, leading to a downstream impact on cell phenotype. (*P < 0.05, **P < 0.01, and ***P < 0.001; “ns” denoted no significant difference, n = 3, error bars indicate means ± standard deviations)

Techniques: Transcriptomics, Staining, Cell Culture, Fluorescence, Real-time Polymerase Chain Reaction, Expressing, Western Blot, Activation Assay

PASN scaffold induced M2 macrophage polarization which enforces BMSCs osteogenic differentiation in vitro. A ) AC, AS, PAS, PASN scaffold induced M2 macrophage polarization. B ) Flow cytometry exhibiting enhanced expression of the M2 macrophage marker CD206 and decreased expression of the M1 macrophage marker CD86 in the PASN group at 3 days as compared with PAS (n=3). C )Relative mRNA expressions of macrophage polarization-related markers at 3 days (n=3). D ) Schematic diagram of BMSCs cocultured with macrophage-laden AC scaffold, macrophage-laden AS scaffold, macrophage-laden PAS scaffold and macrophage-laden PASN scaffold. E ) ALP staining at 14 days and alizarin red staining at 28 days. F ) Relative mRNA expression of ALP, OCN, RUNX2, and COL-1 in BMSCs at the 7th and 14th day in different groups (n=3). G ) Immunofluorescent staining of BMSCs co-cultured with different hydrogel scaffolds for 7 days, green for ALP, COL-1, RUNX2, and OCN, red(phalloidin) for F-actin and blue (DAPI) for nuclei. (*P < 0.05, **P < 0.01, and ***P < 0.001; “ns” denoted no significant difference, n = 3, error bars indicate means ± standard deviations)

Journal: Journal of Nanobiotechnology

Article Title: 4D printed hydrogel scaffolds with shape morphing by near-infrared to promote bone regeneration through immune and vascular coupling

doi: 10.1186/s12951-026-04386-2

Figure Lengend Snippet: PASN scaffold induced M2 macrophage polarization which enforces BMSCs osteogenic differentiation in vitro. A ) AC, AS, PAS, PASN scaffold induced M2 macrophage polarization. B ) Flow cytometry exhibiting enhanced expression of the M2 macrophage marker CD206 and decreased expression of the M1 macrophage marker CD86 in the PASN group at 3 days as compared with PAS (n=3). C )Relative mRNA expressions of macrophage polarization-related markers at 3 days (n=3). D ) Schematic diagram of BMSCs cocultured with macrophage-laden AC scaffold, macrophage-laden AS scaffold, macrophage-laden PAS scaffold and macrophage-laden PASN scaffold. E ) ALP staining at 14 days and alizarin red staining at 28 days. F ) Relative mRNA expression of ALP, OCN, RUNX2, and COL-1 in BMSCs at the 7th and 14th day in different groups (n=3). G ) Immunofluorescent staining of BMSCs co-cultured with different hydrogel scaffolds for 7 days, green for ALP, COL-1, RUNX2, and OCN, red(phalloidin) for F-actin and blue (DAPI) for nuclei. (*P < 0.05, **P < 0.01, and ***P < 0.001; “ns” denoted no significant difference, n = 3, error bars indicate means ± standard deviations)

Techniques: In Vitro, Flow Cytometry, Expressing, Marker, Staining, Cell Culture

Journal: Materials Today Bio

Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration

doi: 10.1016/j.mtbio.2026.102779

Figure Lengend Snippet: In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, Runx2, OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Article Snippet: Membranes were blocked with 5 % non-fat milk (BD DifcoTM, #232100) in TBST (Beyotime, #ST673) for 1 h at 25 °C and incubated overnight at 4 °C with the following primary antibodies: Osteopontin (OPN) : • Rabbit monoclonal (Proteintech, 22952-1-AP), 1:1000 • Collagen I (COL1A1): Rabbit polyclonal (Proteintech, 14695-1-AP), 1:1000 • RUNX2: Rabbit monoclonal (Proteintech, 20700-1-AP), 1:1000 • NRF2: Rabbit monoclonal (Proteintech, 16396-1-AP), 1:2000 • NQO1: Mouse monoclonal (Proteintech, 67240-1-Ig), 1:2000 • Beta Actin: Mouse monoclonal (Proteintech, 66009-1-Ig), 1:20,000 After three 10-min TBST washes, membranes were incubated with HRP-conjugated goat anti-rabbit/mouse IgG (Beyotime, #A0208/#A0216, 1:5000) for 2 h at 25 °C.

Techniques: In Vitro, Staining, Activity Assay, Quantitative RT-PCR, Expressing

Journal: Materials Today Bio

Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration

doi: 10.1016/j.mtbio.2026.102779

Figure Lengend Snippet: In vitro evaluation of osteogenesis related proteins and genes. (A) The relative protein expression levels of C1, Runx2 and OPN. (B–D) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. (E) Immunofluorescence staining of OPN. (F) Immunofluorescence staining of OCN. (G) The relative protein expression levels of C1, Runx2 and OPN. (H–J) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

Techniques: In Vitro, Expressing, Western Blot, Immunofluorescence, Staining

EPCs enhance osteogenic differentiation of PBMSCs. A Alizarin red staining was used to characterize the effect of different ratios of co-cultured EPCs and PBMSCs on calcified nodule formation ( N = 3). B Viability of EPCs, PBMSCs, and EPCs/PBMSCs sheets at 1 d, 3 d, and 5 d was assayed by CCK-8 assay ( N = 3). C, D The expression of osteogenesis-related transcription factor (RUNX2) and specific markers (ALP, OCN, and COL Ⅰ) in EPCs/PBMSCs sheets was detected by RT-qPCR ( C ) and western blotting assays ( D ) at 7 d and 14 d ( N = 3). E PBMSCs and EPCs were labeled with DIO and PKH26, respectively, to observe angiogenic–osteogenic coupling of EPCs/PBMSCs sheets ( N = 3). Scale: 200 μm. F The changes in CD31-labeled neovascularization and Osx-labeled osteoblasts in EPCs/PBMSCs sheets were observed by IF staining ( N = 3). Scale: 100 μm. Original gel blots see supplementary material

Journal: Stem Cell Research & Therapy

Article Title: SLIT3/ROBO1 axis contributes to angiogenic–osteogenic coupling in endothelial progenitor cells and peripheral blood mesenchymal stem cells

doi: 10.1186/s13287-026-04960-3

Figure Lengend Snippet: EPCs enhance osteogenic differentiation of PBMSCs. A Alizarin red staining was used to characterize the effect of different ratios of co-cultured EPCs and PBMSCs on calcified nodule formation ( N = 3). B Viability of EPCs, PBMSCs, and EPCs/PBMSCs sheets at 1 d, 3 d, and 5 d was assayed by CCK-8 assay ( N = 3). C, D The expression of osteogenesis-related transcription factor (RUNX2) and specific markers (ALP, OCN, and COL Ⅰ) in EPCs/PBMSCs sheets was detected by RT-qPCR ( C ) and western blotting assays ( D ) at 7 d and 14 d ( N = 3). E PBMSCs and EPCs were labeled with DIO and PKH26, respectively, to observe angiogenic–osteogenic coupling of EPCs/PBMSCs sheets ( N = 3). Scale: 200 μm. F The changes in CD31-labeled neovascularization and Osx-labeled osteoblasts in EPCs/PBMSCs sheets were observed by IF staining ( N = 3). Scale: 100 μm. Original gel blots see supplementary material

Article Snippet: Blocked PVDF membranes were incubated in hybridization bags (10483064, Cytiva, China) with antibodies including Rabbit ALP mAb (1:2000; bsm-52252R, Bioss, China), Rabbit RUNX2 pAb (1:1000; 20700-1-Ap.

Techniques: Staining, Cell Culture, CCK-8 Assay, Expressing, Quantitative RT-PCR, Western Blot, Labeling

Effect of the SLIT3/ROBO1 axis on angiogenic–osteogenic coupling in EPCs/PBMSCs sheets. A Representative pictures of alizarin red staining for each group of EPCs/PBMSCs sheets ( N = 3). B Representative images of gel bolt for osteogenesis-related markers (ALP, RUNX2, and OCN) and vascular-related markers (CD31) ( N = 3). C The effects of the SLIT3/ROBO1 axis on vascular-osteogenic coupling of EPCs/PBMSCs sheets were observed by IF staining ( N = 3). Scale: 100 μm. The co-localization of CD31 and EMCN was analyzed using Image J and the Coloc 2 plugin, characterized by the Person’s Coefficient and the Overlap Coefficient. Original gel blots see supplementary material

Journal: Stem Cell Research & Therapy

Article Title: SLIT3/ROBO1 axis contributes to angiogenic–osteogenic coupling in endothelial progenitor cells and peripheral blood mesenchymal stem cells

doi: 10.1186/s13287-026-04960-3

Figure Lengend Snippet: Effect of the SLIT3/ROBO1 axis on angiogenic–osteogenic coupling in EPCs/PBMSCs sheets. A Representative pictures of alizarin red staining for each group of EPCs/PBMSCs sheets ( N = 3). B Representative images of gel bolt for osteogenesis-related markers (ALP, RUNX2, and OCN) and vascular-related markers (CD31) ( N = 3). C The effects of the SLIT3/ROBO1 axis on vascular-osteogenic coupling of EPCs/PBMSCs sheets were observed by IF staining ( N = 3). Scale: 100 μm. The co-localization of CD31 and EMCN was analyzed using Image J and the Coloc 2 plugin, characterized by the Person’s Coefficient and the Overlap Coefficient. Original gel blots see supplementary material

Techniques: Staining

Expression and survival analysis of RUNX2 in FP-RMS and FN-RMS. A, Analysis of RUNX2 expression in a cohort of 2486 pediatric cancers showing expression of RUNX2 in OS as well as FP-RMS and NRSTS compared to expression in other pediatric solid tumors. OS, osteosarcoma (n=112), FP-RMS, fusion-positive rhabdomyosarcoma (n=16), FN-RMS, fusion-negative rhabdomyosarcoma, NRSTS (n=28), non-rhabdomyosarcoma soft tissue sarcoma (n=13), EWS, Ewing sarcoma (n=5), NBL, neuroblastoma (n=198), GLM, glioblastoma (n=182), EPDY, ependymoma (n=92), MBL, medulloblastoma (n=31). Other pediatric solid tumors shown for comparison. B, Cluster plot of RUNX2 expression in pediatric bone and soft tissue sarcomas. C, RUNX2 expression in FP-RMS tumors compared to myoblasts. Myoblast (n=3), myotube (n=3), skeletal muscle (n=14), FN cell line (n=12), FN tumor (n=63), FP cell line (n=16), FP tumor (n=39). D,E,F,G Kaplan-Meier plot demonstrates the correlation between RUNX2 and survival in all RMS (n=146), FP-RMS and FN-RMS combined (n=114), FP-RMS (n=50), and FN-RMS (n=64).

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: Expression and survival analysis of RUNX2 in FP-RMS and FN-RMS. A, Analysis of RUNX2 expression in a cohort of 2486 pediatric cancers showing expression of RUNX2 in OS as well as FP-RMS and NRSTS compared to expression in other pediatric solid tumors. OS, osteosarcoma (n=112), FP-RMS, fusion-positive rhabdomyosarcoma (n=16), FN-RMS, fusion-negative rhabdomyosarcoma, NRSTS (n=28), non-rhabdomyosarcoma soft tissue sarcoma (n=13), EWS, Ewing sarcoma (n=5), NBL, neuroblastoma (n=198), GLM, glioblastoma (n=182), EPDY, ependymoma (n=92), MBL, medulloblastoma (n=31). Other pediatric solid tumors shown for comparison. B, Cluster plot of RUNX2 expression in pediatric bone and soft tissue sarcomas. C, RUNX2 expression in FP-RMS tumors compared to myoblasts. Myoblast (n=3), myotube (n=3), skeletal muscle (n=14), FN cell line (n=12), FN tumor (n=63), FP cell line (n=16), FP tumor (n=39). D,E,F,G Kaplan-Meier plot demonstrates the correlation between RUNX2 and survival in all RMS (n=146), FP-RMS and FN-RMS combined (n=114), FP-RMS (n=50), and FN-RMS (n=64).

Article Snippet: Membranes were immunoblotted with primary monoclonal antibodies anti-RUNX2 (Cell Signaling Technology, #8486S, RRID:AB_10949892), anti-FOXO1 (Cell Signaling, #2880S, RRID:AB_2106495) and anti-β-ACTIN (Cell Signaling Technology, #4970, RRID:AB_2223172).

Techniques: Expressing, Comparison

RUNX2 dependency analysis and characterization in RMS. A, Expression of RUNX2 in normal skeletal muscle. Skeletal muscle myocyte expressing RUNX2 (n=504), total cells (n=20772). B, Volcano plot showing gene dependencies in FP-RMS cell lines relative to all other cancer cell lines. Box in upper right -hand corner are all the genes in the dataset and larger figure is a zoom in on the dashed box Supplemental Table 5 . C, (Left side) Box plot of the CERES dependency score demonstrating RUNX2 specific dependencies in FP-RMS compared to all cancer types analyzed together. FP-RMS (n=8), RMS (n=13), Solid Tumor (n=1019), All Cancer. (Right side) Characterization of RUNX2 gene effect on FP-RMS cell lines compared to all sarcomas, and all other cancer. FP-RMS (n=8), RMS (n=13), Solid Tumor (n=1019), All Cancer. D, Immunoblot of PAX3::FOXO1, FOXO1, and RUNX2 protein expression in OS, FP-RMS, and FN-RMS cell lines.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: RUNX2 dependency analysis and characterization in RMS. A, Expression of RUNX2 in normal skeletal muscle. Skeletal muscle myocyte expressing RUNX2 (n=504), total cells (n=20772). B, Volcano plot showing gene dependencies in FP-RMS cell lines relative to all other cancer cell lines. Box in upper right -hand corner are all the genes in the dataset and larger figure is a zoom in on the dashed box Supplemental Table 5 . C, (Left side) Box plot of the CERES dependency score demonstrating RUNX2 specific dependencies in FP-RMS compared to all cancer types analyzed together. FP-RMS (n=8), RMS (n=13), Solid Tumor (n=1019), All Cancer. (Right side) Characterization of RUNX2 gene effect on FP-RMS cell lines compared to all sarcomas, and all other cancer. FP-RMS (n=8), RMS (n=13), Solid Tumor (n=1019), All Cancer. D, Immunoblot of PAX3::FOXO1, FOXO1, and RUNX2 protein expression in OS, FP-RMS, and FN-RMS cell lines.

Techniques: Expressing, Western Blot

RUNX2 knockdown in human FP-RMS cells (Rh30) impairs classical oncogenic phenotypes in vitro . A, qRT-PCR for RUNX2 quantification in the negative control (NT) Rh30 cells and the three independent knockdown cells (sh1, sh2, sh4). Each black dot represents an independent biological replicate. B, Normalized RUNX2 protein expression in the negative control (NT) Rh30 cells and the three independent knockdown cells (sh1, sh2, sh4) measured at 0 h, 24 h and 48 h. C, Cell growth in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent biological replicates. D, Colony formation in negative control and RUNX2 stable knockdown Rh30 cells. E, Colony numbers in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent technical replicates. F, RUNX2 knockdown through three independent stably expressed shRUNX2 lentiviral preparations (sh1, sh2, sh4) plus negative control (shNT) in Rh30 cells. Black arrows point to visible areas of differentiation. Cells were imaged at 20X magnification and captured at 48 h and 72 h. Scale bars are 25 µm. G,H, qRT-PCR for known drivers of mesenchymal stem cell differentiation; MYOD1 and OC , following RUNX2 stable knockdown. Black dots are independent biological replicates. I, Cell viability of negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent technical replicates. J, Quantification of caspase 3/7 mediated apoptosis in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent technical replicates. K, Cell cycle analysis in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent biological replicates consisting of three technical replicates each.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: RUNX2 knockdown in human FP-RMS cells (Rh30) impairs classical oncogenic phenotypes in vitro . A, qRT-PCR for RUNX2 quantification in the negative control (NT) Rh30 cells and the three independent knockdown cells (sh1, sh2, sh4). Each black dot represents an independent biological replicate. B, Normalized RUNX2 protein expression in the negative control (NT) Rh30 cells and the three independent knockdown cells (sh1, sh2, sh4) measured at 0 h, 24 h and 48 h. C, Cell growth in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent biological replicates. D, Colony formation in negative control and RUNX2 stable knockdown Rh30 cells. E, Colony numbers in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent technical replicates. F, RUNX2 knockdown through three independent stably expressed shRUNX2 lentiviral preparations (sh1, sh2, sh4) plus negative control (shNT) in Rh30 cells. Black arrows point to visible areas of differentiation. Cells were imaged at 20X magnification and captured at 48 h and 72 h. Scale bars are 25 µm. G,H, qRT-PCR for known drivers of mesenchymal stem cell differentiation; MYOD1 and OC , following RUNX2 stable knockdown. Black dots are independent biological replicates. I, Cell viability of negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent technical replicates. J, Quantification of caspase 3/7 mediated apoptosis in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent technical replicates. K, Cell cycle analysis in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent biological replicates consisting of three technical replicates each.

Techniques: Knockdown, In Vitro, Quantitative RT-PCR, Negative Control, Expressing, Stable Transfection, Cell Differentiation, Cell Cycle Assay

RUNX2 knockdown in human FP-RMS cells (Rh4) impairs classical oncogenic phenotypes in vitro. A, qRT-PCR for RUNX2 quantification in the negative control (NT) Rh4 cells and the three independent knockdown cells (sh1, sh2, sh4). Black dots are technical replicates. B, Normalized RUNX2 protein expression in the negative control (NT) Rh4 cells and the three independent knockdown cells (sh1, sh2, sh4) measured at 48 h. This blot is identical to . C, Cell growth in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent biological replicates. D, RUNX2 knockdown through three independent stably expressed shRUNX2 lentiviral preparations (sh1, sh2, sh4) plus negative control (shNT) in Rh4 cells. Black arrows point to visible areas of differentiation. Cells were imaged at 20X magnification and captured at 24 h. Scale bars are 50 µm.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: RUNX2 knockdown in human FP-RMS cells (Rh4) impairs classical oncogenic phenotypes in vitro. A, qRT-PCR for RUNX2 quantification in the negative control (NT) Rh4 cells and the three independent knockdown cells (sh1, sh2, sh4). Black dots are technical replicates. B, Normalized RUNX2 protein expression in the negative control (NT) Rh4 cells and the three independent knockdown cells (sh1, sh2, sh4) measured at 48 h. This blot is identical to . C, Cell growth in negative control and RUNX2 stable knockdown Rh30 cells. Black dots are independent biological replicates. D, RUNX2 knockdown through three independent stably expressed shRUNX2 lentiviral preparations (sh1, sh2, sh4) plus negative control (shNT) in Rh4 cells. Black arrows point to visible areas of differentiation. Cells were imaged at 20X magnification and captured at 24 h. Scale bars are 50 µm.

Techniques: Knockdown, In Vitro, Quantitative RT-PCR, Negative Control, Expressing, Stable Transfection

Additional in vivo experiments and expanded analyses. A, Tumor volume spider plot in mice engrafted with sh2 doxycycline inducible RUNX2 knockdown Rh30 cells and with or without access to doxycycline chow (see ). Each line represents a single mouse. B, Tumor volume spider plot in mice engrafted with sh4 doxycycline inducible RUNX2 knockdown Rh30 cells and with or without access to doxycycline chow. Each line represents a single mouse. C, Tumors excised from the mice and weighed (g). Black dots represent independent biological replicates. D, Tumor volume spider plot in mice engrafted with wild type Rh30 cells with or without CADD522 treatment (see ). Each line represents a single mouse. Stars above each day represent a significant difference between means of control versus treated tumors on that day.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: Additional in vivo experiments and expanded analyses. A, Tumor volume spider plot in mice engrafted with sh2 doxycycline inducible RUNX2 knockdown Rh30 cells and with or without access to doxycycline chow (see ). Each line represents a single mouse. B, Tumor volume spider plot in mice engrafted with sh4 doxycycline inducible RUNX2 knockdown Rh30 cells and with or without access to doxycycline chow. Each line represents a single mouse. C, Tumors excised from the mice and weighed (g). Black dots represent independent biological replicates. D, Tumor volume spider plot in mice engrafted with wild type Rh30 cells with or without CADD522 treatment (see ). Each line represents a single mouse. Stars above each day represent a significant difference between means of control versus treated tumors on that day.

Techniques: In Vivo, Knockdown, Control

Transcriptomic alterations following RUNX2 stable knockdown in vitro. A,B, Data reduction to two-dimensions via biplot PCA shows consistent groups along the PC1 axis that correspond to Rh30 and Rh4 cells RUNX2 knockdown at 0 h post selection (light red), 24 h post selection (olive), 48 h post selection (green), and negative control (NT) cells at identical time points (turquoise-0 h, blue-24 h, and pink-48 h). C,D, Differentially expressed genes between shNT and sh4 RUNX2 knockdown Rh30 and Rh4 cells at 0 h post selection. X-axis= -Log 2 FC. Y-axis= -Log10 AdjP. E,F, Heat map based hierarchical cluster analysis following gene set enrichment analysis (GSEA) of Rh30 and Rh4 cells at selected timepoints (x-axis), and cancer hallmark (n=49) and NCI (n=546) gene-sets (y-axis). Key represents normalized enrichment score (NES). G,H Enrichment plots for Rh30 and Rh4 cells following RUNX2 knockdown at 0 h post selection. Selected gene-sets characterize the effect of RUNX2 knockdown on differentiation, cell cycle, apoptosis, and FP-RMS regulatory circuitry. Enrichment score (ES), P -values, and false discovery rate (FDR) are shown.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: Transcriptomic alterations following RUNX2 stable knockdown in vitro. A,B, Data reduction to two-dimensions via biplot PCA shows consistent groups along the PC1 axis that correspond to Rh30 and Rh4 cells RUNX2 knockdown at 0 h post selection (light red), 24 h post selection (olive), 48 h post selection (green), and negative control (NT) cells at identical time points (turquoise-0 h, blue-24 h, and pink-48 h). C,D, Differentially expressed genes between shNT and sh4 RUNX2 knockdown Rh30 and Rh4 cells at 0 h post selection. X-axis= -Log 2 FC. Y-axis= -Log10 AdjP. E,F, Heat map based hierarchical cluster analysis following gene set enrichment analysis (GSEA) of Rh30 and Rh4 cells at selected timepoints (x-axis), and cancer hallmark (n=49) and NCI (n=546) gene-sets (y-axis). Key represents normalized enrichment score (NES). G,H Enrichment plots for Rh30 and Rh4 cells following RUNX2 knockdown at 0 h post selection. Selected gene-sets characterize the effect of RUNX2 knockdown on differentiation, cell cycle, apoptosis, and FP-RMS regulatory circuitry. Enrichment score (ES), P -values, and false discovery rate (FDR) are shown.

Techniques: Knockdown, In Vitro, Selection, Negative Control

Doxycycline inducible RUNX2 knockdown in Rh30 FP-RMS cells. A, qRT-PCR for RUNX2 72 h after 1 µg/mL doxycycline treatment. Black dots represent technical replicates. B, RUNX2 protein expression in RUNX2 knockdown cells (sh2, sh4) following treatment with 1 µg/mL doxycycline for 140 h. C, Doxycycline inducible knockdown of RUNX2 in Rh30 cells using two different shRNA constructs (sh2, sh4). Black arrows point to visible differentiated phenotypes. Cells were imaged at 10X magnification. Scale bars are 100 µm. D, qRT-PCR for PAX3::FOXO1 expression 72 h after 1 µg/mL doxycycline treatment in the RUNX2 knockdown cells (sh2, sh4). Black dots are technical replicates. E, Tumor volume growth curves in mice engrafted with sh2 doxycycline inducible RUNX2 knockdown Rh30 cells and with or without access to doxycycline chow. Stars above each day represent a significant difference between means of control versus treated tumors on that day. F, Tumors excised from the mice and weighed (g). Black dots represent independent biological replicates. G, Representative H&E images of excised tumors taken at 40X magnification plus immunohistochemistry for Ki-67 and CC3. Scale bars are 50 µm. H,I, Three representative tumors from each group (one shown) stained for Ki-67 and CC3 and quantified using ImageJ. J, qRT-PCR for RUNX2, MYOD1, OC, and PAX3::FOXO1 expression following RUNX2 knockdown in vivo . Blak dots represent independent biological replicates.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: Doxycycline inducible RUNX2 knockdown in Rh30 FP-RMS cells. A, qRT-PCR for RUNX2 72 h after 1 µg/mL doxycycline treatment. Black dots represent technical replicates. B, RUNX2 protein expression in RUNX2 knockdown cells (sh2, sh4) following treatment with 1 µg/mL doxycycline for 140 h. C, Doxycycline inducible knockdown of RUNX2 in Rh30 cells using two different shRNA constructs (sh2, sh4). Black arrows point to visible differentiated phenotypes. Cells were imaged at 10X magnification. Scale bars are 100 µm. D, qRT-PCR for PAX3::FOXO1 expression 72 h after 1 µg/mL doxycycline treatment in the RUNX2 knockdown cells (sh2, sh4). Black dots are technical replicates. E, Tumor volume growth curves in mice engrafted with sh2 doxycycline inducible RUNX2 knockdown Rh30 cells and with or without access to doxycycline chow. Stars above each day represent a significant difference between means of control versus treated tumors on that day. F, Tumors excised from the mice and weighed (g). Black dots represent independent biological replicates. G, Representative H&E images of excised tumors taken at 40X magnification plus immunohistochemistry for Ki-67 and CC3. Scale bars are 50 µm. H,I, Three representative tumors from each group (one shown) stained for Ki-67 and CC3 and quantified using ImageJ. J, qRT-PCR for RUNX2, MYOD1, OC, and PAX3::FOXO1 expression following RUNX2 knockdown in vivo . Blak dots represent independent biological replicates.

Techniques: Knockdown, Quantitative RT-PCR, Expressing, shRNA, Construct, Control, Immunohistochemistry, Staining, In Vivo

PAX3::FOXO1 and RUNX2 reciprocally regulate one another in FP-RMS. A,B, Stable knockdown of PAX3 :: FOXO1 in Rh4 cells affect on RUNX2 and RUNX1 expression. C,D, qRT-PCR for PAX3::FOXO1 and RUNX2 expression in PAX3::FOXO1 transient knockdown Rh30 cells. Black dots are independent biological replicates. E, Genome browser view of RUNX2 . Peaks for the top 9 rows reflect degree of DNA-binding of H3K27ac, H3K9ac, H3K4me3, H3K27me3, P300, MYOD1, and PAX3::FOXO1 using ChIP-seq. Row 10 is open chromatin peaks from ATAC-seq, and rows 11 and 12 are mRNA-seq reads. All rows are in Rh4 cells, counts are in reads per million. F, PAX3::FOXO1, FOXO1, and RUNX2 protein expression in negative control (NT) and puromycin selected RUNX2 knockdown Rh4 cells after 48 h selection. G, PAX3::FOXO1, FOXO1 and RUNX2 protein expression in negative control (NT) and puromycin selected RUNX2 knockdown Rh30 cells after 72 h selection. H, PAX3::FOXO1, FOXO1 and RUNX2 protein expression in negative control (NT) and puromycin selected RUNX2 knockdown Rh30 cells 144 h after selection.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: PAX3::FOXO1 and RUNX2 reciprocally regulate one another in FP-RMS. A,B, Stable knockdown of PAX3 :: FOXO1 in Rh4 cells affect on RUNX2 and RUNX1 expression. C,D, qRT-PCR for PAX3::FOXO1 and RUNX2 expression in PAX3::FOXO1 transient knockdown Rh30 cells. Black dots are independent biological replicates. E, Genome browser view of RUNX2 . Peaks for the top 9 rows reflect degree of DNA-binding of H3K27ac, H3K9ac, H3K4me3, H3K27me3, P300, MYOD1, and PAX3::FOXO1 using ChIP-seq. Row 10 is open chromatin peaks from ATAC-seq, and rows 11 and 12 are mRNA-seq reads. All rows are in Rh4 cells, counts are in reads per million. F, PAX3::FOXO1, FOXO1, and RUNX2 protein expression in negative control (NT) and puromycin selected RUNX2 knockdown Rh4 cells after 48 h selection. G, PAX3::FOXO1, FOXO1 and RUNX2 protein expression in negative control (NT) and puromycin selected RUNX2 knockdown Rh30 cells after 72 h selection. H, PAX3::FOXO1, FOXO1 and RUNX2 protein expression in negative control (NT) and puromycin selected RUNX2 knockdown Rh30 cells 144 h after selection.

Techniques: Knockdown, Expressing, Quantitative RT-PCR, Binding Assay, ChIP-sequencing, Negative Control, Selection

Rh30 cells treated with the RUNX2 small molecule inhibitor CADD522 in vitro and in vivo. A, qRT-PCR for RUNX2 performed following 24 h of treatment with 0.5 μM and 1.0 μM of CADD522 in vitro . Black dots are independent biological replicates. B, CADD522 treatment effects on colony formation in vitro . Cells were treated with a 12 μM dose every other day for 14 d. C, Colony number after CADD522 treatment. Black dots represent technical replicates. D, Rh30 cells stained with the myogenic marker sarcomere myosin (MF20) when treated with a negative control (DMSO) and different CADD522 concentrations over 72 h. Images were captured at 20X magnification. Scale bars are 50 µm. E, Quantification of MF20 positive cells (dark brown) versus MF20 negative cells (light brown) following CADD522 treatment. F, G, H qRT-PCR for MYOD1, OC, and PAX3::FOXO1 performed following 24 h of treatment with 0.5 μM and 1.0 μM of CADD522 in vitro . Black dots are independent biological replicates. I, Tumor volume growth curves with (n=9) or without 10 mg/kg CADD522 (n=8). J, Kaplan-Meier survival curve for mice treated with 10 mg/kg CADD522. Stars above each day represent a significant difference between means of control versus treated tumors on that day. K, H&E stains on excised tumors and immunohistochemistry (IHC) for Ki-67 and CC3 with and without CADD522 treatment. Images were captured at 40X magnification. Scale bars are 50 µm. L,M, Ki-67 and CC3 quantification. N, qRT-PCR for RUNX2, MYOD1, OC, and PAX3::FOXO1 expression following CADD522 treatment in vivo . Black dots represent independent biological replicates

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: Rh30 cells treated with the RUNX2 small molecule inhibitor CADD522 in vitro and in vivo. A, qRT-PCR for RUNX2 performed following 24 h of treatment with 0.5 μM and 1.0 μM of CADD522 in vitro . Black dots are independent biological replicates. B, CADD522 treatment effects on colony formation in vitro . Cells were treated with a 12 μM dose every other day for 14 d. C, Colony number after CADD522 treatment. Black dots represent technical replicates. D, Rh30 cells stained with the myogenic marker sarcomere myosin (MF20) when treated with a negative control (DMSO) and different CADD522 concentrations over 72 h. Images were captured at 20X magnification. Scale bars are 50 µm. E, Quantification of MF20 positive cells (dark brown) versus MF20 negative cells (light brown) following CADD522 treatment. F, G, H qRT-PCR for MYOD1, OC, and PAX3::FOXO1 performed following 24 h of treatment with 0.5 μM and 1.0 μM of CADD522 in vitro . Black dots are independent biological replicates. I, Tumor volume growth curves with (n=9) or without 10 mg/kg CADD522 (n=8). J, Kaplan-Meier survival curve for mice treated with 10 mg/kg CADD522. Stars above each day represent a significant difference between means of control versus treated tumors on that day. K, H&E stains on excised tumors and immunohistochemistry (IHC) for Ki-67 and CC3 with and without CADD522 treatment. Images were captured at 40X magnification. Scale bars are 50 µm. L,M, Ki-67 and CC3 quantification. N, qRT-PCR for RUNX2, MYOD1, OC, and PAX3::FOXO1 expression following CADD522 treatment in vivo . Black dots represent independent biological replicates

Techniques: In Vitro, In Vivo, Quantitative RT-PCR, Staining, Marker, Negative Control, Control, Immunohistochemistry, Expressing

Schematic to show PAX3::FOXO1 transcriptionally upregulates RUNX2 expression at the chromatin to prevent FP-RMS terminal differentiation and apoptosis via the defined PAX3::FOXO1 core regulatory circuitry.

Journal: bioRxiv

Article Title: RUNX2 inhibition disrupts a PAX3::FOXO1-RUNX2 feed-forward loop and dismantles oncogenic gene programs in fusion-positive rhabdomyosarcoma

doi: 10.1101/2025.07.21.665972

Figure Lengend Snippet: Schematic to show PAX3::FOXO1 transcriptionally upregulates RUNX2 expression at the chromatin to prevent FP-RMS terminal differentiation and apoptosis via the defined PAX3::FOXO1 core regulatory circuitry.

Techniques: Expressing

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