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fhd 286  (MedChemExpress)


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    MedChemExpress fhd 286
    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
    Fhd 286, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/fhd/Camibirstat/bio_rxiv__64898__2026__05__22__726988-282-10-11
    Average 94 stars, based on 4 article reviews
    fhd 286 - by Bioz Stars, 2026-09
    94/100 stars

    Images

    1) Product Images from "Spatially-Resolved Multiomic Atlas of Leiomyosarcoma Identifies Two Clinically Relevant Epigenetically-Driven Cell States"

    Article Title: Spatially-Resolved Multiomic Atlas of Leiomyosarcoma Identifies Two Clinically Relevant Epigenetically-Driven Cell States

    Journal: bioRxiv

    doi: 10.64898/2026.05.22.726988

    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, FHD-286. IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
    Figure Legend Snippet: (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, FHD-286. IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.

    Techniques Used: Western Blot, Apoptosis Assay, Staining, Immunoprecipitation, Negative Control

    Related Articles

    other:

    Article Title: Selective Sensitivity of Ph-like B-ALL to BRG1 Inhibition Reveals a Novel Targeted Therapy Strategy
    Article Snippet: FHD-286 was prepared in a vehicle composed of 1.66% DMSO (Thermo Scientific), 40% PEG400 (MedChem Express), 5% Tween 80 (MedChem Express), and 53.34% PBS.



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    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
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    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
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    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
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    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
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    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
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    digital microscope zip fhd  (TAGARNO AS)
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    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, <t>FHD-286.</t> IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.
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    Image Search Results


    (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, FHD-286. IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.

    Journal: bioRxiv

    Article Title: Spatially-Resolved Multiomic Atlas of Leiomyosarcoma Identifies Two Clinically Relevant Epigenetically-Driven Cell States

    doi: 10.64898/2026.05.22.726988

    Figure Lengend Snippet: (A) Pseudotime determined by Monocle 3 is projected onto the snRNA-seq UMAP. A trajectory was noted between clusters 7 (SMC) and 8 (MES). (B) Stacked bar graph demonstrating distribution of cells from individual tumors in different colors in clusters 7 and 8, demonstrating that many of the tumors in the cohort have a population of cells from both clusters 7 and 8. (C) Western blots demonstrating depletion of FOSL2 and subsequent enrichment in mesenchymal markers (ZEB1, NCAM1, vimentin) in an SMC cell line (Leio-012). (D) Western blots demonstrating depletion of NFIX and subsequent decrease of mesenchymal markers (ZEB1, NCAM1) and increase in smooth muscle markers (SMA, MKL1) in a MES cell line (SK-UT-1B). (E) CUT&RUN was performed to assess pathways controlled by each TF. (E) Enrichment of peaks centered on NFIX peaks identified from CUT&RUN data in SK-UT-1B. (F) Venn diagrams showing overlap of peaks identified from CUT&RUN in SK-UT-1B. (G) IGV tracks in a representative MES-defining gene showing the presence of NFIX but absence of FOSL2. (H) Enrichment of peaks centered on FOSL2 peaks identified from CUT&RUN data in Leio-012. (I) Venn diagrams showing overlap of peaks identified from CUT&RUN in Leio-012. (J) IGV tracks in a representative SMC-defining gene showing the presence of FOSL2 but absence of NFIX. (K) Dose response curves with treatment with the SMARCA4/2 inhibitor, FHD-286. IC50 values are shown on the right. (N) Western blots after immunoprecipitating NFIX from SK-UT-1B cells. (L-M) Tumor volume measurements following xenografting of SK-UT-1B (L) and SK-LMS-1 (M) into immunodeficient nude mice and treatment with FHD-286, 1.5 mg/kg given by oral gavage, days 1-5 of 7-day cycles. Treatment started at day 0 on the graph following tumor growth to 100-200 mm 3 . N = 5 mice per group. ***P value < 0.001. (N) Apoptosis assay was performed by staining cells with anti-Annexin V and propidium iodide following treatment with a range of concentrations of FHD-286. Bars represent means ± SEM. (O) Western blotting for smooth muscle (SMA) and mesenchymal (Slug) markers in SK-LMS-1 cells treated with FHD-286. (P) NFIX was immunoprecipitated from SK-UT-1B nuclear extracts and probed for other NFI TFs, SWI/SNF components (SMARCA4/2) and the PRC2 component EED as a negative control.

    Article Snippet: Chemicals used in this study include: puromycin (InvivoGen), polybrene (InvivoGen), FHD-286 (MedChemExpress), panobinostat (MedChemExpress), vorinostat (MedChemExpress), tazemetostat (MedChemExpress), azacitidine (MedChemExpress), decitabine (MedChemExpress), A-845 (MedChemExpress), JQ1 (MedChemExpress), ZEN-3694 (MedChemExpress), bomedemstat (MedChemExpress), SNDX-5613 (MedChemExpress), MI-503 (MedChemExpress), gintemetostat (MedChemExpress), GSK-J4 (MedChemExpress).

    Techniques: Western Blot, Apoptosis Assay, Staining, Immunoprecipitation, Negative Control