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sjsa1  (ATCC)


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    ATCC sjsa1
    Gene expression changes after IL-11Rα knockdown or IL-11 exogenous expression in the OS cells. a , Four shRNA sequences (G2, C1, H8, and H2) targeting IL-11Rα were stably expressed in KRIB cells. Gene expression was measured by microarray. Processed and log2-transformed gene expression data were compared to that of control cells. The heat map shows subtracted values for the gene probes in which values for shRNA sequences C1, H8, and H2 differed on average by at least twofold from those in the control cells. The color bar shows the fold-change difference from the values in the control cells. b , Quantitative reverse-transcription PCR analysis of the mRNA expression levels of the PRC2 complex members EZH2 , EED , and SUZ12 in <t>SJSA1</t> (upper panel) and KRIB cells (lower panel). P—parental cells, E—empty vector, C1—IL-11Rα knockdown via shRNA C1, H8—IL-11Rα knockdown via shRNA H8, RQ—relative quantity. c Immunoblot of EZH2 and EED protein levels in SJSA1 and KRIB cells. β-actin served as a loading control. P—parental cells, E—empty vector, C1—IL-11Rα knockdown via shRNA C1, H8—IL-11Rα knockdown via shRNA H8, RQ—relative quantity.
    Sjsa1, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 86 stars, based on 1 article reviews
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    sjsa1 - by Bioz Stars, 2024-10
    86/100 stars

    Images

    1) Product Images from "Targeting IL-11R/EZH2 signaling axis as a therapeutic strategy for osteosarcoma lung metastases"

    Article Title: Targeting IL-11R/EZH2 signaling axis as a therapeutic strategy for osteosarcoma lung metastases

    Journal: Discover Oncology

    doi: 10.1007/s12672-024-01056-3

    Gene expression changes after IL-11Rα knockdown or IL-11 exogenous expression in the OS cells. a , Four shRNA sequences (G2, C1, H8, and H2) targeting IL-11Rα were stably expressed in KRIB cells. Gene expression was measured by microarray. Processed and log2-transformed gene expression data were compared to that of control cells. The heat map shows subtracted values for the gene probes in which values for shRNA sequences C1, H8, and H2 differed on average by at least twofold from those in the control cells. The color bar shows the fold-change difference from the values in the control cells. b , Quantitative reverse-transcription PCR analysis of the mRNA expression levels of the PRC2 complex members EZH2 , EED , and SUZ12 in SJSA1 (upper panel) and KRIB cells (lower panel). P—parental cells, E—empty vector, C1—IL-11Rα knockdown via shRNA C1, H8—IL-11Rα knockdown via shRNA H8, RQ—relative quantity. c Immunoblot of EZH2 and EED protein levels in SJSA1 and KRIB cells. β-actin served as a loading control. P—parental cells, E—empty vector, C1—IL-11Rα knockdown via shRNA C1, H8—IL-11Rα knockdown via shRNA H8, RQ—relative quantity.
    Figure Legend Snippet: Gene expression changes after IL-11Rα knockdown or IL-11 exogenous expression in the OS cells. a , Four shRNA sequences (G2, C1, H8, and H2) targeting IL-11Rα were stably expressed in KRIB cells. Gene expression was measured by microarray. Processed and log2-transformed gene expression data were compared to that of control cells. The heat map shows subtracted values for the gene probes in which values for shRNA sequences C1, H8, and H2 differed on average by at least twofold from those in the control cells. The color bar shows the fold-change difference from the values in the control cells. b , Quantitative reverse-transcription PCR analysis of the mRNA expression levels of the PRC2 complex members EZH2 , EED , and SUZ12 in SJSA1 (upper panel) and KRIB cells (lower panel). P—parental cells, E—empty vector, C1—IL-11Rα knockdown via shRNA C1, H8—IL-11Rα knockdown via shRNA H8, RQ—relative quantity. c Immunoblot of EZH2 and EED protein levels in SJSA1 and KRIB cells. β-actin served as a loading control. P—parental cells, E—empty vector, C1—IL-11Rα knockdown via shRNA C1, H8—IL-11Rα knockdown via shRNA H8, RQ—relative quantity.

    Techniques Used: Expressing, Knockdown, shRNA, Stable Transfection, Microarray, Transformation Assay, Control, Reverse Transcription, Plasmid Preparation, Western Blot

    IL-11 activates EZH2 OS cells a Immunoprecipitation assay of EZH2 in CCH-OS-D and SJSA1 cells treated with human IL11 (200 or 400 ng) for 24 h. b CCH-OS-D cells were treated with human IL-11 for 48 h and then used for immunoblot analysis of phosphorylated EZH2-Y244. β-actin was used as loading control
    Figure Legend Snippet: IL-11 activates EZH2 OS cells a Immunoprecipitation assay of EZH2 in CCH-OS-D and SJSA1 cells treated with human IL11 (200 or 400 ng) for 24 h. b CCH-OS-D cells were treated with human IL-11 for 48 h and then used for immunoblot analysis of phosphorylated EZH2-Y244. β-actin was used as loading control

    Techniques Used: Immunoprecipitation, Western Blot, Control

    IL-11 mediates H3K27 trimethylation. a KRIB and SJSA1, EZH2shRNA and vector control cells were treated with human IL-11 for 48 h, Cells were harvested and used for immunoblot with H3K27 antibody. Total H3 was used as a control. b Immunoblot analysis of EZH2 knockdown and vector control in KRIB and SJSA1 cells. β-actin was used as a loading control
    Figure Legend Snippet: IL-11 mediates H3K27 trimethylation. a KRIB and SJSA1, EZH2shRNA and vector control cells were treated with human IL-11 for 48 h, Cells were harvested and used for immunoblot with H3K27 antibody. Total H3 was used as a control. b Immunoblot analysis of EZH2 knockdown and vector control in KRIB and SJSA1 cells. β-actin was used as a loading control

    Techniques Used: Plasmid Preparation, Control, Western Blot, Knockdown

    GSK126 inhibits proliferation and H3K27me3 of OS cells. a OS cell lines were treated for 48 h with GSK126, and their proliferation was assessed using the WST-1 assay. GSK126 inhibited the proliferation of KRIB, HOS, and SJSA-1 cells. Half-maximal inhibitory concentrations (IC 50 ) values are available in Table S4. b and c Treatment with GSK126 induced apoptosis and cell-cycle arrest in OS cells. b Results of annexin V–fluorescein isothiocyanate/propidium iodide analysis of the indicated OS cell lines after 24 h of treatment with GSK126 ( P < .01). The error bars represent standard error of the mean. c, Results of flow cytometric analysis of the cell-cycle progression in OS cell lines after 24 h of treatment with GSK126. GSK126 induced sub-G1 arrest in KRIB, SJSA1, and CCH-OS-D cells and S-phase arrest in HOS cells ( P < .05). The error bars represent standard error of the mean ** P < 0.01; *** P < 0.001; **** P < 0.0001. d Evaluation of H3K27me3 in SJSA1, KRIB and CCH-OS-D cell lines following GSK126 treatment for 72 h. Total histone H3 is shown as a loading control
    Figure Legend Snippet: GSK126 inhibits proliferation and H3K27me3 of OS cells. a OS cell lines were treated for 48 h with GSK126, and their proliferation was assessed using the WST-1 assay. GSK126 inhibited the proliferation of KRIB, HOS, and SJSA-1 cells. Half-maximal inhibitory concentrations (IC 50 ) values are available in Table S4. b and c Treatment with GSK126 induced apoptosis and cell-cycle arrest in OS cells. b Results of annexin V–fluorescein isothiocyanate/propidium iodide analysis of the indicated OS cell lines after 24 h of treatment with GSK126 ( P < .01). The error bars represent standard error of the mean. c, Results of flow cytometric analysis of the cell-cycle progression in OS cell lines after 24 h of treatment with GSK126. GSK126 induced sub-G1 arrest in KRIB, SJSA1, and CCH-OS-D cells and S-phase arrest in HOS cells ( P < .05). The error bars represent standard error of the mean ** P < 0.01; *** P < 0.001; **** P < 0.0001. d Evaluation of H3K27me3 in SJSA1, KRIB and CCH-OS-D cell lines following GSK126 treatment for 72 h. Total histone H3 is shown as a loading control

    Techniques Used: WST-1 Assay, Control

    RNA sequencing of OS cells treated with GSK126. a - c Principal component analysis of RNA expression levels of genes for GSK126-sensitive cell lines HOS and SJSA1 ( a and b ) and the GSK126-resistant cell line CCH-OS-D c . subjected to no treatment (control, C), treatment with dimethyl sulfoxide (DMSO, vehicle), or treatment with GSK126 at 1 or 2 µM. d and e Venn diagrams showing the intersection of significantly upregulated and downregulated genes (upon GSK126 treatment, both 1 or 2 µM, as compared to control and DMSO) of the 3 cell lines. f Bar plot of the Gene Ontology enriched pathways
    Figure Legend Snippet: RNA sequencing of OS cells treated with GSK126. a - c Principal component analysis of RNA expression levels of genes for GSK126-sensitive cell lines HOS and SJSA1 ( a and b ) and the GSK126-resistant cell line CCH-OS-D c . subjected to no treatment (control, C), treatment with dimethyl sulfoxide (DMSO, vehicle), or treatment with GSK126 at 1 or 2 µM. d and e Venn diagrams showing the intersection of significantly upregulated and downregulated genes (upon GSK126 treatment, both 1 or 2 µM, as compared to control and DMSO) of the 3 cell lines. f Bar plot of the Gene Ontology enriched pathways

    Techniques Used: RNA Sequencing Assay, RNA Expression, Control

    Inhibition of OS lung metastases by GSK126 in vivo. a Luciferase imaging of mice injected with SJSA1 cells comparing day 3, when primary tumors had developed, and day 21, after primary tumors had been removed by amputation but before treatment initiation. The bottom panels shows luciferase imaging and lung tumors for mice treated with control-, vehicle (cyclodextrin)-, and EZH2 inhibitor (EZH2i; GSK126) by day 48 after the start of the regimen. b Quantification of luciferase activity. c number of tumor nodules in control-treated versus GSK126-treated mice. d Survival curves for all mice. e Weight of lungs in control- and GSK126-treated mice. F Representative images of H&E staining of explanted lungs treated with Vehicle and GSK126. Scale bar: 100 μm
    Figure Legend Snippet: Inhibition of OS lung metastases by GSK126 in vivo. a Luciferase imaging of mice injected with SJSA1 cells comparing day 3, when primary tumors had developed, and day 21, after primary tumors had been removed by amputation but before treatment initiation. The bottom panels shows luciferase imaging and lung tumors for mice treated with control-, vehicle (cyclodextrin)-, and EZH2 inhibitor (EZH2i; GSK126) by day 48 after the start of the regimen. b Quantification of luciferase activity. c number of tumor nodules in control-treated versus GSK126-treated mice. d Survival curves for all mice. e Weight of lungs in control- and GSK126-treated mice. F Representative images of H&E staining of explanted lungs treated with Vehicle and GSK126. Scale bar: 100 μm

    Techniques Used: Inhibition, In Vivo, Luciferase, Imaging, Injection, Control, Activity Assay, Staining



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