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p foxm1 thr600 cst 14655 wb (Cell Signaling Technology Inc)

Name: p foxm1 thr600 cst 14655 wb
Brand: Cell Signaling Technology Inc
Rating: 93 (41 reviews)

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Cell Signaling Technology Inc p foxm1 thr600 cst 14655 wb
P Foxm1 Thr600 Cst 14655 Wb, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/p foxm1 thr600 cst 14655 wb/product/Cell Signaling Technology Inc
Average 93 stars, based on 41 article reviews

p foxm1 thr600 cst 14655 wb - by Bioz Stars, 2026-02

93/100 stars

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Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: RT-qPCR primers

Article Snippet: Primary antibodies included anti- FOXM1 (Cell Signaling Technology, CST, Danvers, MA, USA) (CST #5436, 1:1,000), p-FOXM1 (Thr600) (CST #14655, 1:1,000–1:2,000), AURKB (Abcam, Waltham, MA, USA, #2254, 1:1,000), CCNB1 (CST #4138, 1:1,000–1:2,000), CDC25B (CST #9525, 1:1,000–1:2000), PLK1 (CST #4513, 1:1,000) FOXA1 (CST #53528, 1:1,000–1:2,000)), FOXK2 (CST #12008, 1:1,000), FOXO3a (CST #12829, 1:10,000), cleaved PARP (cl-PARP) (CST #5625, 1:1,000), ubiquitin (CST #14049, 1:20,000). alpha-tubulin (CST #2144, 1:5,000), β-actin (Santa Cruz Biotechnology, Dallas, TX, USA, # 47778, 1:10,000), and Lamin B1 (CST #12586, 1:1,000).

Techniques: Sequencing

Potency and efficacy of FOXM1 inhibitors in HGSOC cell lines a

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: Potency and efficacy of FOXM1 inhibitors in HGSOC cell lines a

Techniques:

Selectivity of FOXM1 inhibitors in HGSOC cells vs. FTE cells a

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: Selectivity of FOXM1 inhibitors in HGSOC cells vs. FTE cells a

Techniques:

Protein expression and NB compound dose response in HGSOC and FTE cells. A Western blot analyses of FOXM1, FOXM1-P (P-Threonine 600), CCNB1, FOXA1, FOXK2, and FOXO3a expression in CAOV3 (HGSOC), OVCAR4 (HGSOC), and FT282-C11 (immortalized FTE cells). β-actin staining is a shown as a protein loading control. B-C Dose–response curves of CAOV3 (red), OVCAR4 (blue), and FT282-C11 (yellow) cells treated with B NB-73 or C NB-115 for 72 h. Cell viability was analyzed by CyQuant assay. Three independent trials were performed with three technical replicates per trial. Values represent mean ± SEM. Curves were created using nonlinear regression with least squares (ordinary) fit in GraphPad Prism. IC50 values are indicated below the graphs

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: Protein expression and NB compound dose response in HGSOC and FTE cells. A Western blot analyses of FOXM1, FOXM1-P (P-Threonine 600), CCNB1, FOXA1, FOXK2, and FOXO3a expression in CAOV3 (HGSOC), OVCAR4 (HGSOC), and FT282-C11 (immortalized FTE cells). β-actin staining is a shown as a protein loading control. B-C Dose–response curves of CAOV3 (red), OVCAR4 (blue), and FT282-C11 (yellow) cells treated with B NB-73 or C NB-115 for 72 h. Cell viability was analyzed by CyQuant assay. Three independent trials were performed with three technical replicates per trial. Values represent mean ± SEM. Curves were created using nonlinear regression with least squares (ordinary) fit in GraphPad Prism. IC50 values are indicated below the graphs

Techniques: Expressing, Western Blot, Staining, Control, CyQUANT Assay

$NB compound treatment suppresses FOXM1 and FOXM1-P expression in HGSOC cells. A Western blot analysis of FOXM1, FOXM1-P, and β-actin (loading control) expression in CAOV3 cells treated with the indicated concentrations of NB-73 or NB-115 for 48 h. Numerical values below the images indicate protein expression normalized by β-actin, and red numbers indicate reduced expression relative to DMSO control. B Quantified western blot data from panel A , with data from three biological replicates plotted. Two-way ANOVA with Dunnett’s multiple comparisons test, error bars indicate mean ± SD. C-D As in panels A - B , but in OVCAR4 cells treated for 72 h. E Western blot analysis of FOXM1, FOXM1-P, Lamin B1 (nuclear isolation control), α-tubulin (cytoplasm isolation control), and β-actin (overall loading control) expression in cytoplasmic and nuclear protein fractions from CAOV3 cells treated with the indicated concentrations of NB-73 and NB-115 for 48 h. Numerical values below the images indicate protein expression normalized to β-actin and red numbers indicate reduced expression relative to the DMSO control. F as in E , except in OVCAR4 cells treated for 72 h$

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: NB compound treatment suppresses FOXM1 and FOXM1-P expression in HGSOC cells. A Western blot analysis of FOXM1, FOXM1-P, and β-actin (loading control) expression in CAOV3 cells treated with the indicated concentrations of NB-73 or NB-115 for 48 h. Numerical values below the images indicate protein expression normalized by β-actin, and red numbers indicate reduced expression relative to DMSO control. B Quantified western blot data from panel A , with data from three biological replicates plotted. Two-way ANOVA with Dunnett’s multiple comparisons test, error bars indicate mean ± SD. C-D As in panels A - B , but in OVCAR4 cells treated for 72 h. E Western blot analysis of FOXM1, FOXM1-P, Lamin B1 (nuclear isolation control), α-tubulin (cytoplasm isolation control), and β-actin (overall loading control) expression in cytoplasmic and nuclear protein fractions from CAOV3 cells treated with the indicated concentrations of NB-73 and NB-115 for 48 h. Numerical values below the images indicate protein expression normalized to β-actin and red numbers indicate reduced expression relative to the DMSO control. F as in E , except in OVCAR4 cells treated for 72 h

Techniques: Expressing, Western Blot, Control, Isolation

NB compound treatment suppresses FOXM1 target protein and gene expression in HGSOC cells. A Western blot analysis of FOXM1 targets and β-actin expression in CAOV3 cells treated with the indicated concentrations of NB-73 or NB-115 for 48 h. Numerical values below the images indicate protein expression normalized by β-actin and red numbers indicate reduced expression relative to DMSO control. B Quantified western blot data from panel A , data from three biological replicates are plotted. Two-way ANOVA with Dunnett’s multiple comparisons test, error bars indicate mean ± SD. C-D As in panels A - B , but in OVCAR4 cells treated for 72 h. E RT-qPCR analysis of FOXM1 target gene expression in CAOV3 cells treated with the indicated concentration of NB-73 or NB-115 for 24 h. Line indicates median, two-way ANOVA with Tukey’s multiple comparison test. F As in panel E , except in OVCAR4 cells treated for 72 h

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: NB compound treatment suppresses FOXM1 target protein and gene expression in HGSOC cells. A Western blot analysis of FOXM1 targets and β-actin expression in CAOV3 cells treated with the indicated concentrations of NB-73 or NB-115 for 48 h. Numerical values below the images indicate protein expression normalized by β-actin and red numbers indicate reduced expression relative to DMSO control. B Quantified western blot data from panel A , data from three biological replicates are plotted. Two-way ANOVA with Dunnett’s multiple comparisons test, error bars indicate mean ± SD. C-D As in panels A - B , but in OVCAR4 cells treated for 72 h. E RT-qPCR analysis of FOXM1 target gene expression in CAOV3 cells treated with the indicated concentration of NB-73 or NB-115 for 24 h. Line indicates median, two-way ANOVA with Tukey’s multiple comparison test. F As in panel E , except in OVCAR4 cells treated for 72 h

Techniques: Gene Expression, Western Blot, Expressing, Control, Quantitative RT-PCR, Targeted Gene Expression, Concentration Assay, Comparison

NB-73 treatment suppresses FOXM1 protein prior to FOXM1 mRNA in CAOV3 cells. A Western blot analysis of FOXM1, FOXM1-P, and β-actin expression in CAOV3 cells treated with 2.5 μM NB-73 for the indicated time points. B RT-qPCR of FOXM1 gene expression in CAOV3 cells treated with 2.5 μM NB-73 for the indicated time points. Error bars indicate mean ± SD, unpaired t-test. C FOXM1 protein and FOXM1 mRNA from three independent experiments as described in panels A and B , plotted together. Error bars indicate mean ± SD, two-way ANOVA with Dunnett’s multiple comparisons test

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: NB-73 treatment suppresses FOXM1 protein prior to FOXM1 mRNA in CAOV3 cells. A Western blot analysis of FOXM1, FOXM1-P, and β-actin expression in CAOV3 cells treated with 2.5 μM NB-73 for the indicated time points. B RT-qPCR of FOXM1 gene expression in CAOV3 cells treated with 2.5 μM NB-73 for the indicated time points. Error bars indicate mean ± SD, unpaired t-test. C FOXM1 protein and FOXM1 mRNA from three independent experiments as described in panels A and B , plotted together. Error bars indicate mean ± SD, two-way ANOVA with Dunnett’s multiple comparisons test

Techniques: Western Blot, Expressing, Quantitative RT-PCR, Gene Expression

NB compound treatment mediated FOXM1 suppression in HGSOC cells is rescued by MG132 co-treatment. A Western blot analysis of FOXM1 and total ubiquitin expression in OVCAR4 cells treated with the indicated compounds for 24 h. Protein quantification is provided below each protein band, and protein expression is normalized to DMSO control (lane 1). Ponceau S staining shows total protein loading. Protein levels were quantified using Fiji software . B As in panel A , except in COV318 cells treated for 24 h

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: NB compound treatment mediated FOXM1 suppression in HGSOC cells is rescued by MG132 co-treatment. A Western blot analysis of FOXM1 and total ubiquitin expression in OVCAR4 cells treated with the indicated compounds for 24 h. Protein quantification is provided below each protein band, and protein expression is normalized to DMSO control (lane 1). Ponceau S staining shows total protein loading. Protein levels were quantified using Fiji software . B As in panel A , except in COV318 cells treated for 24 h

Techniques: Western Blot, Ubiquitin Proteomics, Expressing, Control, Staining, Software

NB compound treatment mediated FOXM1 suppression in CAOV3 cells after drug washout. A Experimental schematic, created with BioRender. B-D Western blot analysis of FOXM1, FOXM1-P, CCNB1, and β-actin expression in CAOV3 cells treated as indicated in panel A , for B 24 h, C 48 h, and D 72 h post-treatment. E CyQuant cell viability assay data for CAOV3 cells treated with NB-73. The three curves compare data from no washout (72 h), 6 h drug exposure then washout (6 h), and 3 h drug exposure then washout (3 h). IC50 values for each condition are indicated in brackets. Error bars indicate mean ± SD, non-linear regression curve. F As in E , except for NB-115 treatment

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: NB compound treatment mediated FOXM1 suppression in CAOV3 cells after drug washout. A Experimental schematic, created with BioRender. B-D Western blot analysis of FOXM1, FOXM1-P, CCNB1, and β-actin expression in CAOV3 cells treated as indicated in panel A , for B 24 h, C 48 h, and D 72 h post-treatment. E CyQuant cell viability assay data for CAOV3 cells treated with NB-73. The three curves compare data from no washout (72 h), 6 h drug exposure then washout (6 h), and 3 h drug exposure then washout (3 h). IC50 values for each condition are indicated in brackets. Error bars indicate mean ± SD, non-linear regression curve. F As in E , except for NB-115 treatment

Techniques: Western Blot, Expressing, CyQUANT Assay, Viability Assay

NB compound treatment mediated FOXM1 suppression is independent of apoptosis. A Western blot analysis of FOXM1, FOXM1-P, cl-PARP, and β-actin expression in CAOV3 cells treated with the indicated compounds for 48 h. Numerical values below the images indicate protein expression normalized by β-actin and red numbers indicate reduced expression relative to DMSO control. B Quantified western blot data from panel A ; data from three biological replicates are plotted. Error bars indicate mean ± SD. C Western blot analysis of CCNB1, PLK1, AURKB, and CDC25B expression in CAOV3 cells treated with the indicated compounds for 48 h. D Quantified western blot data from panel C ; data from three biological replicates are plotted. Error bars indicate mean ± SD

Journal: Journal of Ovarian Research

Article Title: NB compounds are potent and efficacious FOXM1 inhibitors in high-grade serous ovarian cancer cells

doi: 10.1186/s13048-024-01421-4

Figure Lengend Snippet: NB compound treatment mediated FOXM1 suppression is independent of apoptosis. A Western blot analysis of FOXM1, FOXM1-P, cl-PARP, and β-actin expression in CAOV3 cells treated with the indicated compounds for 48 h. Numerical values below the images indicate protein expression normalized by β-actin and red numbers indicate reduced expression relative to DMSO control. B Quantified western blot data from panel A ; data from three biological replicates are plotted. Error bars indicate mean ± SD. C Western blot analysis of CCNB1, PLK1, AURKB, and CDC25B expression in CAOV3 cells treated with the indicated compounds for 48 h. D Quantified western blot data from panel C ; data from three biological replicates are plotted. Error bars indicate mean ± SD

Techniques: Western Blot, Expressing, Control

DDX56 positively regulates MELK-mediated FOXM1 signaling (A) The correlation analysis of DDX56 with MELK and FOXM1 in HCC samples according to ENCORI prediction. (B) The protein levels of MELK, p -FOXM1, and FOXM1 in HepG2 and Huh7 cells after DDX56 overexpression or knockdown. (C) The protein levels of MELK were determined by western blotting in HepG2 and Huh7 cells after shMELK transfection. (D) The protein levels of MELK, p -FOXM1, and FOXM1 in HepG2 and Huh7 cells after transfection. (E) Dual luciferase in HepG2 and Huh7 cells transfected with WT, MUT 3′-UTR of MELK or FOXM1. (F) ChIP assay showing enrichment of DDX56 binding to the MELK or FOXM1 promoter in HepG2 and Huh7 cells. DDX56 binding at the MELK or FOXM1 promoter region is shown relative to input. IgG was used as a negative control (top). Agarose gel electrophoresis of PCR fragments after ChIP (bottom). (G and H) The mRNA expression of MELK and FOXM1 (G) and their correlation with DDX56 expression (H) in HCC tissues. Data are represented as means ± SD of triplicate experiments. # p < 0.05, ∗∗;## p < 0.01, ∗∗∗;### p < 0.001 indicate statistical significance.

Journal: iScience

Article Title: DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2024.109827

Figure Lengend Snippet: DDX56 positively regulates MELK-mediated FOXM1 signaling (A) The correlation analysis of DDX56 with MELK and FOXM1 in HCC samples according to ENCORI prediction. (B) The protein levels of MELK, p -FOXM1, and FOXM1 in HepG2 and Huh7 cells after DDX56 overexpression or knockdown. (C) The protein levels of MELK were determined by western blotting in HepG2 and Huh7 cells after shMELK transfection. (D) The protein levels of MELK, p -FOXM1, and FOXM1 in HepG2 and Huh7 cells after transfection. (E) Dual luciferase in HepG2 and Huh7 cells transfected with WT, MUT 3′-UTR of MELK or FOXM1. (F) ChIP assay showing enrichment of DDX56 binding to the MELK or FOXM1 promoter in HepG2 and Huh7 cells. DDX56 binding at the MELK or FOXM1 promoter region is shown relative to input. IgG was used as a negative control (top). Agarose gel electrophoresis of PCR fragments after ChIP (bottom). (G and H) The mRNA expression of MELK and FOXM1 (G) and their correlation with DDX56 expression (H) in HCC tissues. Data are represented as means ± SD of triplicate experiments. # p < 0.05, ∗∗;## p < 0.01, ∗∗∗;### p < 0.001 indicate statistical significance.

Article Snippet: p -FOXM1 , Cell Signaling Technology , Cat# 14170; RRID: AB_2798411.

Techniques: Over Expression, Knockdown, Western Blot, Transfection, Luciferase, Binding Assay, Negative Control, Agarose Gel Electrophoresis, Expressing

DDX56 regulates HCC cell proliferation via MELK-FOXM1 signaling pathway (A) The protein levels of FOXM1 and p -FOXM1 were determined by western blotting in HepG2 and Huh7 cells after shFOXM1 transfection. (B–D) CCK-8 (B), colony formation (C), EdU (D; scale bar: 50 μm) assays for the cell proliferation analysis in HepG2 and Huh7 cells after transfection. Data are represented as means ± SD of triplicate experiments. # p < 0.05, ## p < 0.01, ∗∗∗;### p < 0.001 indicate statistical significance.

Journal: iScience

Article Title: DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2024.109827

Figure Lengend Snippet: DDX56 regulates HCC cell proliferation via MELK-FOXM1 signaling pathway (A) The protein levels of FOXM1 and p -FOXM1 were determined by western blotting in HepG2 and Huh7 cells after shFOXM1 transfection. (B–D) CCK-8 (B), colony formation (C), EdU (D; scale bar: 50 μm) assays for the cell proliferation analysis in HepG2 and Huh7 cells after transfection. Data are represented as means ± SD of triplicate experiments. # p < 0.05, ## p < 0.01, ∗∗∗;### p < 0.001 indicate statistical significance.

Article Snippet: p -FOXM1 , Cell Signaling Technology , Cat# 14170; RRID: AB_2798411.

Techniques: Western Blot, Transfection, CCK-8 Assay

DDX56 regulates EMT process and stemness via MELK-FOXM1 signaling pathway in HCC cells (A–C) Wound healing (A) and transwell (B and C) assays for the cell migration and invasion analysis in HepG2 and Huh7 cells after transfection. (D) The sphere formation abilities of HepG2 and Huh7 cells after transfection. Data are represented as means ± SD of triplicate experiments. ∗∗;## p < 0.01, ∗∗∗;### p < 0.001 indicate statistical significance.

Journal: iScience

Article Title: DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2024.109827

Figure Lengend Snippet: DDX56 regulates EMT process and stemness via MELK-FOXM1 signaling pathway in HCC cells (A–C) Wound healing (A) and transwell (B and C) assays for the cell migration and invasion analysis in HepG2 and Huh7 cells after transfection. (D) The sphere formation abilities of HepG2 and Huh7 cells after transfection. Data are represented as means ± SD of triplicate experiments. ∗∗;## p < 0.01, ∗∗∗;### p < 0.001 indicate statistical significance.

Article Snippet: p -FOXM1 , Cell Signaling Technology , Cat# 14170; RRID: AB_2798411.

Techniques: Migration, Transfection

DDX56 regulates MELK-FOXM1 signaling pathway and promotes tumor growth and lung metastasis in vivo (A) Representative photographs showing the dissected tumors and growth curves of xenograft-bearing nude mice. (B) Tumor weights of xenograft-bearing nude mice. (C) Immunohistochemical staining of DDX56, MELK, FOXM1 and Ki-67 expression in the dissected tumors (scale bar: 50 μm). (D) Representative images of H&E staining from the lung metastasis model (scale bar: 100 μm). (E and F) HepG2 cells with DDX56 knockdown were transplanted into the left lobe of the mouse liver; representative images showing livers with tumor lesions (E) and IHC staining showing DDX56 expression in mouse liver with tumor lesions (F; scale bars: 100 μm; 50 μm). Data are represented as means ± SD of triplicate experiments. ∗ p < 0.05, ∗∗∗ p < 0.001 indicate statistical significance.

Journal: iScience

Article Title: DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2024.109827

Figure Lengend Snippet: DDX56 regulates MELK-FOXM1 signaling pathway and promotes tumor growth and lung metastasis in vivo (A) Representative photographs showing the dissected tumors and growth curves of xenograft-bearing nude mice. (B) Tumor weights of xenograft-bearing nude mice. (C) Immunohistochemical staining of DDX56, MELK, FOXM1 and Ki-67 expression in the dissected tumors (scale bar: 50 μm). (D) Representative images of H&E staining from the lung metastasis model (scale bar: 100 μm). (E and F) HepG2 cells with DDX56 knockdown were transplanted into the left lobe of the mouse liver; representative images showing livers with tumor lesions (E) and IHC staining showing DDX56 expression in mouse liver with tumor lesions (F; scale bars: 100 μm; 50 μm). Data are represented as means ± SD of triplicate experiments. ∗ p < 0.05, ∗∗∗ p < 0.001 indicate statistical significance.

Article Snippet: p -FOXM1 , Cell Signaling Technology , Cat# 14170; RRID: AB_2798411.

Techniques: In Vivo, Immunohistochemical staining, Staining, Expressing, Knockdown, Immunohistochemistry

Schematic illustrating the carcinogenic mechanism of DDX56 in HCC We propose that DDX56 maintains cancer cell stemness and EMT in hepatocellular carcinoma via the MELK-FOXM1 signaling.

Journal: iScience

Article Title: DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2024.109827

Figure Lengend Snippet: Schematic illustrating the carcinogenic mechanism of DDX56 in HCC We propose that DDX56 maintains cancer cell stemness and EMT in hepatocellular carcinoma via the MELK-FOXM1 signaling.

Article Snippet: p -FOXM1 , Cell Signaling Technology , Cat# 14170; RRID: AB_2798411.

Techniques:

Journal: iScience

Article Title: DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma

doi: 10.1016/j.isci.2024.109827

Figure Lengend Snippet:

Article Snippet: p -FOXM1 , Cell Signaling Technology , Cat# 14170; RRID: AB_2798411.

Techniques: Recombinant, In Vitro, Reporter Assay, cDNA Synthesis, shRNA, Software

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