mice  (MedChemExpress)

Journal: Frontiers in Oncology

Article Title: GLIS3 drives epithelial–mesenchymal transition and cancer stem–like traits in stomach adenocarcinoma via TGFBR3–Hedgehog signaling

doi: 10.3389/fonc.2026.1826297

Figure Lengend Snippet: The GLIS3–TGFBR3–Hedgehog axis mediates the pro-EMT and pro-CSC effects of GLIS3 in STAD cells. (A) ChIP-qPCR showing significant enrichment of GLIS3 at the TGFBR3 promoter; (B) Co-immunoprecipitation assays using whole-cell lysates demonstrating that TGFBR3, SUFU, and GLI1 were detected in GLIS3 immunoprecipitates; (C) Dual-luciferase reporter assays showing reduced TGFBR3 promoter activity following GLIS3 knockdown; (D) 8×GLI luciferase reporter assays showing GLI-dependent transcriptional activity after TGFBR3 knockdown with or without vismodegib treatment in AGS and HGC-27 cells; (E) RT-qPCR and WB analyzes showing increased expression of Hedgehog pathway target genes following GLIS3 overexpression; (F) Effects of vismodegib on EMT- and CSC-related marker expression in AGS cells under complete control conditions (Vector + DMSO, Vector + vismodegib, OE-GLIS3 + DMSO, and OE-GLIS3 + vismodegib), as assessed by RT-qPCR and WB. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, P ≥ 0.05 (n = 3 independent experiments); ChIP-qPCR, Chromatin immunoprecipitation followed by quantitative PCR.

Article Snippet: For in vitro pathway inhibition, cells were treated with vismodegib (20 μM; HY-10440, MedChemExpress) or an equivalent volume of DMSO as a vehicle control for 48 h. Total RNA was extracted using TRIzol reagent (R0016, Beyotime), and cDNA was synthesized using a reverse transcription kit (11155ES, Yeasen).

Techniques: ChIP-qPCR, Immunoprecipitation, Luciferase, Activity Assay, Knockdown, Quantitative RT-PCR, Expressing, Over Expression, Marker, Control, Plasmid Preparation, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction

Journal: Frontiers in Oncology

Article Title: GLIS3 drives epithelial–mesenchymal transition and cancer stem–like traits in stomach adenocarcinoma via TGFBR3–Hedgehog signaling

doi: 10.3389/fonc.2026.1826297

Figure Lengend Snippet: Xenograft tumor model in nude mice. (A) Validation of shRNA transfection efficiency; (B) Representative images of subcutaneous tumors in nude mice; (C) Tumor volume measurements over time; (D) Body weight monitoring of mice throughout the experiment; (E) RT-qPCR analysis of key Hedgehog pathway components in tumor tissues; (F) WB of GLI1 protein levels in tumor tissues; (G) RT-qPCR analysis of EMT-related gene expression; (H) RT-qPCR analysis of CSC marker expression; (I) RT-qPCR analysis of proliferation- and apoptosis-related gene expression; (J) WB of MKI67 protein levels in tumor tissues; (K) Representative immunohistochemical staining of TGFBR3, GLI1, and E-cadherin in xenograft sections from the control, vismodegib, and sh-GLIS3 groups. * P < 0.05, ** P < 0.01, and *** P < 0.001; ns, P ≥ 0.05 (n = 3 independent experiments).

Article Snippet: For in vitro pathway inhibition, cells were treated with vismodegib (20 μM; HY-10440, MedChemExpress) or an equivalent volume of DMSO as a vehicle control for 48 h. Total RNA was extracted using TRIzol reagent (R0016, Beyotime), and cDNA was synthesized using a reverse transcription kit (11155ES, Yeasen).

Techniques: Biomarker Discovery, shRNA, Transfection, Quantitative RT-PCR, Gene Expression, Marker, Expressing, Immunohistochemical staining, Staining, Control

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: Patient-derived PanNET tumoroids express HH signaling proteins and respond to HH pathway activation and inhibition. A Combined fluorescence and phase-contrast images of 21-day-old human PanNET tumoroids (PanNET3) stained for chromogranin A (CHGA) and HH proteins (PTCH1, SHH). B Four patient-derived PanNET tumoroid lines (PanNET1–4) were exposed to recombinant human SHH N-terminal peptide (100 ng/mL) or the SMO inhibitor vismodegib (VISMO, 20 µM) for 72 h and changes in mRNA expression were analyzed by RT-qPCR. mRNA changes were normalized to HPRT1 expression and DMSO vehicle control. ( n = 4 unique patient lines). * = p < 0.05, ** = p < 0.01, **** = p < 0.0001 by Two-way ANOVA with Sidak post-test. C EdU labeling showing proliferation of dissociated PanNET3 cells following 5-day exposure to: the HH agonists SHH-N (100 ng/mL) and SAG (10 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 1 µM). D Quantitation of the percentage of EdU-positive PanNET tumor cells following 5-day treatment. ( n = 3 replicates from one patient tumoroid line). * = p < 0.05, by One-way ANOVA with Tukey post-test. E SHH or SAG were co-administered with the respective pharmacologic inhibitors and EdU uptake was evaluated after 7 days. F Immunofluorescent images of CHGA, SHH, and PTCH1 expression in a second PanNET tumoroid line (PanNET5). G , H EdU labeling was evaluated in PanNET5 tumoroids following 7-day treatment with SHH-N (200 ng/mL) and SAG (20 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 5 µM). I Crystal violet staining of human BON-1 PanNET cells after 48 h treatment. J BrdU incorporation in BON-1 cells after 48 h treatment with HH agonists SHH-N and SAG, ( K ) SMO inhibitors vismodegib and sonidegib, and ( L ) inhibitors of GLI1/2 signaling. M Immunofluorescent images of CHGA, SHH, and PTCH1 expression in tumoroids derived from a metastatic ileal NET (IL-NET-met1). N , O EdU labeling was assayed in the IL-NET-met1 tumoroid line following 7-day treatment with the same drug concentrations used for PanNET5. * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Derivative Assay, Activation Assay, Inhibition, Fluorescence, Staining, Recombinant, Expressing, Quantitative RT-PCR, Control, Labeling, Quantitation Assay, BrdU Incorporation Assay

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: HH signaling regulates the growth of GFAP ΔMen1 and Sox10 ΔMen1 pancreatic NET tumoroids. A Phase contrast and ( B ) fluorescence images of PanNET tumoroids from Sox10-Cre; Men1 FL/FL ; LSL-tdTomato mice. Tumoroids were imaged after 72 h exposure to: the HH agonists SHH-N (100 ng/mL) and SAG (10 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 1 µM). C TdTomato fluorescence intensity was used to measure PanNET tumoroid growth in the presence of HH pathway agonists or ( D ) inhibitors of the canonical and ( E ) non-canonical HH signaling pathways. Fluorescence signal is compared to DMSO vehicle control. ( n = 3 replicates in two unique mouse PanNET tumoroid lines). ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. F BrdU incorporation was used to measure tumoroid proliferation in GFAP ΔMen1 and Sox10 ΔMen1 PanNET tumoroids after 72 h treatment. ( n = 4). ** = p < 0.01, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. G Relative fold-change in Chga mRNA levels in PanNET tumoroids following 72 h treatment. ( n = 5). H Western blot analysis of HH pathway proteins in PanNET tumoroids after 72 h treatment. I Quantitation of SHH protein expression normalized to beta-actin and DMSO vehicle control from the western blot analysis in panel ( H ). ( n = 3). J Western blot analysis and ( K ) associated quantitation of phosphorylated and total ERK and AKT growth pathways in PanNET tumoroids after 72 h treatment. ( n = 3). * = p < 0.05, ** = p < 0.01, *** = p < 0.001 by Kruskal-Wallis test

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Fluorescence, Protein-Protein interactions, Control, BrdU Incorporation Assay, Western Blot, Quantitation Assay, Expressing

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: GFAP ΔMen1 DNETs and jejunal NETs are sensitive to HH pathway activation and inhibition. A Phase contrast and ( B ) fluorescence images of DNET tumoroids from a GFAP-Cre; Men1 FL/FL ; LSL-tdTomato mouse. Tumoroids were imaged after 72 h exposure to: the HH agonists SHH-N (100 ng/mL) and SAG (10 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 1 µM). C TdTomato fluorescence intensity was used to measure DNET tumoroid growth in the presence of HH pathway inhibitors. Fluorescence signal is compared to DMSO vehicle control. ( n = 3 replicates using one mouse DNET tumoroid line). ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. D Relative BrdU incorporation in a second GFAP ΔMen1 DNET tumoroid line and ( E ) a jejunal tumoroid line (J-NET) after 72 h treatment. ( n = 4). ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. F Western blot analysis of SHH, ERK, and AKT growth pathways in J-NET tumoroids after 72 h treatment. G Western blot quantitation of SHH and ( H ) phosphorylated and total ERK and AKT proteins normalized to GAPDH and DMSO vehicle control. ( n = 3). * = p < 0.05 by Kruskal-Wallis test. I Crystal violet staining of mouse STC-1 SI-NET cells after 48 h treatment with agonists and inhibitors of the HH signaling pathway. J BrdU incorporation in STC-1 cells after 48 h treatment with HH agonists SHH-N and SAG, ( K ) SMO inhibitors vismodegib and sonidegib, and ( L ) inhibitors of GLI1/2 signaling. * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Activation Assay, Inhibition, Fluorescence, Control, BrdU Incorporation Assay, Western Blot, Quantitation Assay, Staining

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: Patient-derived PanNET tumoroids express HH signaling proteins and respond to HH pathway activation and inhibition. A Combined fluorescence and phase-contrast images of 21-day-old human PanNET tumoroids (PanNET3) stained for chromogranin A (CHGA) and HH proteins (PTCH1, SHH). B Four patient-derived PanNET tumoroid lines (PanNET1–4) were exposed to recombinant human SHH N-terminal peptide (100 ng/mL) or the SMO inhibitor vismodegib (VISMO, 20 µM) for 72 h and changes in mRNA expression were analyzed by RT-qPCR. mRNA changes were normalized to HPRT1 expression and DMSO vehicle control. ( n = 4 unique patient lines). * = p < 0.05, ** = p < 0.01, **** = p < 0.0001 by Two-way ANOVA with Sidak post-test. C EdU labeling showing proliferation of dissociated PanNET3 cells following 5-day exposure to: the HH agonists SHH-N (100 ng/mL) and SAG (10 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 1 µM). D Quantitation of the percentage of EdU-positive PanNET tumor cells following 5-day treatment. ( n = 3 replicates from one patient tumoroid line). * = p < 0.05, by One-way ANOVA with Tukey post-test. E SHH or SAG were co-administered with the respective pharmacologic inhibitors and EdU uptake was evaluated after 7 days. F Immunofluorescent images of CHGA, SHH, and PTCH1 expression in a second PanNET tumoroid line (PanNET5). G , H EdU labeling was evaluated in PanNET5 tumoroids following 7-day treatment with SHH-N (200 ng/mL) and SAG (20 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 5 µM). I Crystal violet staining of human BON-1 PanNET cells after 48 h treatment. J BrdU incorporation in BON-1 cells after 48 h treatment with HH agonists SHH-N and SAG, ( K ) SMO inhibitors vismodegib and sonidegib, and ( L ) inhibitors of GLI1/2 signaling. M Immunofluorescent images of CHGA, SHH, and PTCH1 expression in tumoroids derived from a metastatic ileal NET (IL-NET-met1). N , O EdU labeling was assayed in the IL-NET-met1 tumoroid line following 7-day treatment with the same drug concentrations used for PanNET5. * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Derivative Assay, Activation Assay, Inhibition, Fluorescence, Staining, Recombinant, Expressing, Quantitative RT-PCR, Control, Labeling, Quantitation Assay, BrdU Incorporation Assay

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: HH signaling regulates the growth of GFAP ΔMen1 and Sox10 ΔMen1 pancreatic NET tumoroids. A Phase contrast and ( B ) fluorescence images of PanNET tumoroids from Sox10-Cre; Men1 FL/FL ; LSL-tdTomato mice. Tumoroids were imaged after 72 h exposure to: the HH agonists SHH-N (100 ng/mL) and SAG (10 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 1 µM). C TdTomato fluorescence intensity was used to measure PanNET tumoroid growth in the presence of HH pathway agonists or ( D ) inhibitors of the canonical and ( E ) non-canonical HH signaling pathways. Fluorescence signal is compared to DMSO vehicle control. ( n = 3 replicates in two unique mouse PanNET tumoroid lines). ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. F BrdU incorporation was used to measure tumoroid proliferation in GFAP ΔMen1 and Sox10 ΔMen1 PanNET tumoroids after 72 h treatment. ( n = 4). ** = p < 0.01, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. G Relative fold-change in Chga mRNA levels in PanNET tumoroids following 72 h treatment. ( n = 5). H Western blot analysis of HH pathway proteins in PanNET tumoroids after 72 h treatment. I Quantitation of SHH protein expression normalized to beta-actin and DMSO vehicle control from the western blot analysis in panel ( H ). ( n = 3). J Western blot analysis and ( K ) associated quantitation of phosphorylated and total ERK and AKT growth pathways in PanNET tumoroids after 72 h treatment. ( n = 3). * = p < 0.05, ** = p < 0.01, *** = p < 0.001 by Kruskal-Wallis test

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Fluorescence, Protein-Protein interactions, Control, BrdU Incorporation Assay, Western Blot, Quantitation Assay, Expressing

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: GFAP ΔMen1 DNETs and jejunal NETs are sensitive to HH pathway activation and inhibition. A Phase contrast and ( B ) fluorescence images of DNET tumoroids from a GFAP-Cre; Men1 FL/FL ; LSL-tdTomato mouse. Tumoroids were imaged after 72 h exposure to: the HH agonists SHH-N (100 ng/mL) and SAG (10 nM); inhibitors of the canonical HH signaling pathway vismodegib (20 µM) and sonidegib (10 nM); or inhibitors of the GLI1/2 effectors GANT61 (10 µM) and itraconazole (ITZ, 1 µM). C TdTomato fluorescence intensity was used to measure DNET tumoroid growth in the presence of HH pathway inhibitors. Fluorescence signal is compared to DMSO vehicle control. ( n = 3 replicates using one mouse DNET tumoroid line). ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. D Relative BrdU incorporation in a second GFAP ΔMen1 DNET tumoroid line and ( E ) a jejunal tumoroid line (J-NET) after 72 h treatment. ( n = 4). ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test. F Western blot analysis of SHH, ERK, and AKT growth pathways in J-NET tumoroids after 72 h treatment. G Western blot quantitation of SHH and ( H ) phosphorylated and total ERK and AKT proteins normalized to GAPDH and DMSO vehicle control. ( n = 3). * = p < 0.05 by Kruskal-Wallis test. I Crystal violet staining of mouse STC-1 SI-NET cells after 48 h treatment with agonists and inhibitors of the HH signaling pathway. J BrdU incorporation in STC-1 cells after 48 h treatment with HH agonists SHH-N and SAG, ( K ) SMO inhibitors vismodegib and sonidegib, and ( L ) inhibitors of GLI1/2 signaling. * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by One-way ANOVA with Dunnett post-test

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Activation Assay, Inhibition, Fluorescence, Control, BrdU Incorporation Assay, Western Blot, Quantitation Assay, Staining

Journal: Molecular Cancer

Article Title: Hedgehog signaling drives glial cell plasticity and oncogenic reprogramming in gastroenteropancreatic neuroendocrine neoplasms

doi: 10.1186/s12943-026-02611-y

Figure Lengend Snippet: Loss of Men1 in enteric glial cells stimulates GLI1/2-dependent transcriptional reprogramming. A Combined fluorescence and phase contrast images of 5-day-old primary enteric glial cell (EGC) cultures from Sox10-CreER T2 ; LSL-tdTomato mice and CreER T2 negative controls. Top panel shows TdTomato+ EGCs after 48 h exposure to 4-hydroxytamoxifen 4-OHT (2 µM). B TdTomato + EGCs were sorted by FACS to enrich for a pure SOX10 + cell population. C Combined fluorescence and phase contrast images of FACS-enriched SOX10-tdTomato + EGCs. D Fluctuations in HH pathway mRNA levels were evaluated in SOX10-tdTomato + EGCs 72 h following siRNA-mediated Men1 silencing. siRNA treatment consisted of four pooled siRNAs targeting the Men1 gene ( si -Men1 , 25 nM) or non-targeting (si-NT, 25 nM) controls. ( n = 5). E Immunofluorescence images of SHH expression in si-NT and si-Men1 treated EGCs (SHH = red pseudo-color, DAPI = blue). Inset shows higher power image. F Western blot analysis of si-NT and si-Men1 EGCs after 72 h treatment. SHH-FL = 55 kDa full length peptide; SHH- N = 22 kDa N-terminal peptide. ( n = 3). G Quantitation of protein expression in panel (F) normalized to GAPDH loading control. ( n = 3). H Relative fold-change in glial lineage transcripts and ( I ) neuroendocrine and neural progenitor transcripts in si-NT and si-Men1 treated EGCs. ( n = 6). J qPCR analysis of HH pathway genes and ( K ) neuroendocrine and neural progenitor transcriptsin si-NT and si-Men1 EGCs after 72 h treatment with GANT61 (10 µM) or vismodegib (VISMO 20 µM). ( n = 3). For all plots, * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001 by Two-way ANOVA with Sidak post-test. L Immunofluorescence images of si-NT and si-Men1 EGCs after 96 h siRNA knockdown and 72 h treatment with vehicle or GANT61. Menin = green, GFAP = magenta, SHH = yellow. M Significant GSEA pathways in enteric glial cells following 5-days of si- Men1 knockdown compared to non-targeting control. GSEA was performed on Men1 -depleted cells and cells co-treated with ( N ) si- Men1 , si- Gli1 , and si- Gli2 , and ( O ) cells co-treated with si- Men1 and GANT61 (10 µM). P – R KEGG pathway enrichment analysis comparing the same groups as shown in panels ( M – O ). S Heatmap showing significant DEGs mapped to the cell cycle, HH signaling, epigenetic regulation, neural stem cell (NSC) reprogramming, neuronal and neuroendocrine differentiation

Article Snippet: Drug compounds used in the studies include: human recombinant SHH N-terminal peptide (R&D Systems, Cat# 1845-GMP), SAG (Tocris, Cat# 4366), vismodegib (Tocris, Cat# 7710), sonidegib (Tocris, Cat# 7826), GANT61 (Tocris, Cat# 3191), and itraconazole (Tocris, Cat# 5981).

Techniques: Fluorescence, Immunofluorescence, Expressing, Western Blot, Quantitation Assay, Control, Knockdown