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β estradiol  (MedChemExpress)


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    Structured Review

    MedChemExpress β estradiol
    <t>β-Estradiol</t> <t>induces</t> an iCAF-like phenotype in vitro that is enriched for CLECs. A, Human foreskin fibroblasts (BJ) were treated with indicated concentration of β-estradiol for 72 hours and transcript levels of markers for previously described CAF subtypes were assessed by qRT-PCR. B, As for A , the expression of CAF phenotype markers in pancreatic stellate cells (PS-1) or patient-derived CAFs (P361 and P371) was evaluated by FACS. Bar plots show mean ± SD of geometric mean fluorescence intensity (gMFI). Three biological replicates were included. Statistical significance was assessed by two-way ANOVA. C, Uniform Manifold Approximation and Projection (UMAP) plot of the fibroblast population from a human scRNA-seq dataset (PRJCA001063; ref. ). CAF subtype annotations are provided as described in Materials and Methods. D, Same Uniform Manifold Approximation and Projection plot depiction as in C . Dot colors indicate z -scores of ER pathway and CLEC signatures. E, Violin plot showing quantifications of the data shown in D . F, Violin plot showing the expression of Clec3b in previously determined CAF subsets in a KPC mouse PDAC scRNA-seq set ( GSE129455 ; ref. ). G, Kaplan–Meier survival analysis for bulk RNA-seq CLEC3B expression and patient survival using two independent PDAC cohorts ( GSE183795 , ref. , and GSE36924 , ref. ) as well as the CPCT-02 metastatic cohort . Groups are separated by median. P value is by the log-rank test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P < 0.001; ****, P < 0.0001.
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    Images

    1) Product Images from "Estrogen Production in Pancreatic Cancer Shapes a Tumor-Suppressive Stromal Microenvironment"

    Article Title: Estrogen Production in Pancreatic Cancer Shapes a Tumor-Suppressive Stromal Microenvironment

    Journal: Cancer Research

    doi: 10.1158/0008-5472.CAN-24-4707

    β-Estradiol induces an iCAF-like phenotype in vitro that is enriched for CLECs. A, Human foreskin fibroblasts (BJ) were treated with indicated concentration of β-estradiol for 72 hours and transcript levels of markers for previously described CAF subtypes were assessed by qRT-PCR. B, As for A , the expression of CAF phenotype markers in pancreatic stellate cells (PS-1) or patient-derived CAFs (P361 and P371) was evaluated by FACS. Bar plots show mean ± SD of geometric mean fluorescence intensity (gMFI). Three biological replicates were included. Statistical significance was assessed by two-way ANOVA. C, Uniform Manifold Approximation and Projection (UMAP) plot of the fibroblast population from a human scRNA-seq dataset (PRJCA001063; ref. ). CAF subtype annotations are provided as described in Materials and Methods. D, Same Uniform Manifold Approximation and Projection plot depiction as in C . Dot colors indicate z -scores of ER pathway and CLEC signatures. E, Violin plot showing quantifications of the data shown in D . F, Violin plot showing the expression of Clec3b in previously determined CAF subsets in a KPC mouse PDAC scRNA-seq set ( GSE129455 ; ref. ). G, Kaplan–Meier survival analysis for bulk RNA-seq CLEC3B expression and patient survival using two independent PDAC cohorts ( GSE183795 , ref. , and GSE36924 , ref. ) as well as the CPCT-02 metastatic cohort . Groups are separated by median. P value is by the log-rank test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P < 0.001; ****, P < 0.0001.
    Figure Legend Snippet: β-Estradiol induces an iCAF-like phenotype in vitro that is enriched for CLECs. A, Human foreskin fibroblasts (BJ) were treated with indicated concentration of β-estradiol for 72 hours and transcript levels of markers for previously described CAF subtypes were assessed by qRT-PCR. B, As for A , the expression of CAF phenotype markers in pancreatic stellate cells (PS-1) or patient-derived CAFs (P361 and P371) was evaluated by FACS. Bar plots show mean ± SD of geometric mean fluorescence intensity (gMFI). Three biological replicates were included. Statistical significance was assessed by two-way ANOVA. C, Uniform Manifold Approximation and Projection (UMAP) plot of the fibroblast population from a human scRNA-seq dataset (PRJCA001063; ref. ). CAF subtype annotations are provided as described in Materials and Methods. D, Same Uniform Manifold Approximation and Projection plot depiction as in C . Dot colors indicate z -scores of ER pathway and CLEC signatures. E, Violin plot showing quantifications of the data shown in D . F, Violin plot showing the expression of Clec3b in previously determined CAF subsets in a KPC mouse PDAC scRNA-seq set ( GSE129455 ; ref. ). G, Kaplan–Meier survival analysis for bulk RNA-seq CLEC3B expression and patient survival using two independent PDAC cohorts ( GSE183795 , ref. , and GSE36924 , ref. ) as well as the CPCT-02 metastatic cohort . Groups are separated by median. P value is by the log-rank test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P < 0.001; ****, P < 0.0001.

    Techniques Used: In Vitro, Concentration Assay, Quantitative RT-PCR, Expressing, Derivative Assay, Fluorescence, RNA Sequencing



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    <t>β-Estradiol</t> <t>induces</t> an iCAF-like phenotype in vitro that is enriched for CLECs. A, Human foreskin fibroblasts (BJ) were treated with indicated concentration of β-estradiol for 72 hours and transcript levels of markers for previously described CAF subtypes were assessed by qRT-PCR. B, As for A , the expression of CAF phenotype markers in pancreatic stellate cells (PS-1) or patient-derived CAFs (P361 and P371) was evaluated by FACS. Bar plots show mean ± SD of geometric mean fluorescence intensity (gMFI). Three biological replicates were included. Statistical significance was assessed by two-way ANOVA. C, Uniform Manifold Approximation and Projection (UMAP) plot of the fibroblast population from a human scRNA-seq dataset (PRJCA001063; ref. ). CAF subtype annotations are provided as described in Materials and Methods. D, Same Uniform Manifold Approximation and Projection plot depiction as in C . Dot colors indicate z -scores of ER pathway and CLEC signatures. E, Violin plot showing quantifications of the data shown in D . F, Violin plot showing the expression of Clec3b in previously determined CAF subsets in a KPC mouse PDAC scRNA-seq set ( GSE129455 ; ref. ). G, Kaplan–Meier survival analysis for bulk RNA-seq CLEC3B expression and patient survival using two independent PDAC cohorts ( GSE183795 , ref. , and GSE36924 , ref. ) as well as the CPCT-02 metastatic cohort . Groups are separated by median. P value is by the log-rank test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P < 0.001; ****, P < 0.0001.
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    β-Estradiol induces an iCAF-like phenotype in vitro that is enriched for CLECs. A, Human foreskin fibroblasts (BJ) were treated with indicated concentration of β-estradiol for 72 hours and transcript levels of markers for previously described CAF subtypes were assessed by qRT-PCR. B, As for A , the expression of CAF phenotype markers in pancreatic stellate cells (PS-1) or patient-derived CAFs (P361 and P371) was evaluated by FACS. Bar plots show mean ± SD of geometric mean fluorescence intensity (gMFI). Three biological replicates were included. Statistical significance was assessed by two-way ANOVA. C, Uniform Manifold Approximation and Projection (UMAP) plot of the fibroblast population from a human scRNA-seq dataset (PRJCA001063; ref. ). CAF subtype annotations are provided as described in Materials and Methods. D, Same Uniform Manifold Approximation and Projection plot depiction as in C . Dot colors indicate z -scores of ER pathway and CLEC signatures. E, Violin plot showing quantifications of the data shown in D . F, Violin plot showing the expression of Clec3b in previously determined CAF subsets in a KPC mouse PDAC scRNA-seq set ( GSE129455 ; ref. ). G, Kaplan–Meier survival analysis for bulk RNA-seq CLEC3B expression and patient survival using two independent PDAC cohorts ( GSE183795 , ref. , and GSE36924 , ref. ) as well as the CPCT-02 metastatic cohort . Groups are separated by median. P value is by the log-rank test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P < 0.001; ****, P < 0.0001.

    Journal: Cancer Research

    Article Title: Estrogen Production in Pancreatic Cancer Shapes a Tumor-Suppressive Stromal Microenvironment

    doi: 10.1158/0008-5472.CAN-24-4707

    Figure Lengend Snippet: β-Estradiol induces an iCAF-like phenotype in vitro that is enriched for CLECs. A, Human foreskin fibroblasts (BJ) were treated with indicated concentration of β-estradiol for 72 hours and transcript levels of markers for previously described CAF subtypes were assessed by qRT-PCR. B, As for A , the expression of CAF phenotype markers in pancreatic stellate cells (PS-1) or patient-derived CAFs (P361 and P371) was evaluated by FACS. Bar plots show mean ± SD of geometric mean fluorescence intensity (gMFI). Three biological replicates were included. Statistical significance was assessed by two-way ANOVA. C, Uniform Manifold Approximation and Projection (UMAP) plot of the fibroblast population from a human scRNA-seq dataset (PRJCA001063; ref. ). CAF subtype annotations are provided as described in Materials and Methods. D, Same Uniform Manifold Approximation and Projection plot depiction as in C . Dot colors indicate z -scores of ER pathway and CLEC signatures. E, Violin plot showing quantifications of the data shown in D . F, Violin plot showing the expression of Clec3b in previously determined CAF subsets in a KPC mouse PDAC scRNA-seq set ( GSE129455 ; ref. ). G, Kaplan–Meier survival analysis for bulk RNA-seq CLEC3B expression and patient survival using two independent PDAC cohorts ( GSE183795 , ref. , and GSE36924 , ref. ) as well as the CPCT-02 metastatic cohort . Groups are separated by median. P value is by the log-rank test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P < 0.001; ****, P < 0.0001.

    Article Snippet: In short, cells were seeded around 50% confluence in 96-well plates (proliferation) or six-well plates (flow cytometry and qRT-PCR) and exposed to β-estradiol (MedChemExpress, HY-B0141) or a vehicle control for 72 hours; medium containing charcoal-stripped serum (Gibco; 12676029) was utilized.

    Techniques: In Vitro, Concentration Assay, Quantitative RT-PCR, Expressing, Derivative Assay, Fluorescence, RNA Sequencing