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Addgene inc megfp n1 yaps127a plasmids
Megfp N1 Yaps127a Plasmids, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Elevated expression of HES1 in tumor associated macrophages. A Gene expression analysis was performed on TAMs and mammary tissue macrophages (MTMs) obtained from 16-week-old female MMTV-PyMT mice (GES56755). Canonical Notch signaling related genes with a p-value threshold lower than 0.05 were considered to be differentially expressed. The fold change was represented using a log scale. B The mean fluorescence intensity (MFI) of intracellular HES1 staining was measured in macrophages (CD11b + F4/80 + double positive) isolated from bone marrow, spleen, and tumors. Mice were subcutaneously injected with 4T1, CT26 or B16F10 cell lines to generate tumor tissues. C The intracellular HES1 staining from MMTV-PyMT mice. Macrophages from bone marrow, spleen, and tumors were analyzed by flow cytometry. D Expression of HES1 in differentiating macrophages obtained from bone marrows of normal mice. The population of differentiated macrophages were analyzed by flow cytometry based on CD11b + F4/80 + cells (also see Supplemental Fig. 3). Additionally, Hes1 mRNA levels during the differentiation of BMDMs were analyzed using qRT-PCR. Relative expression was normalized to the expression level at the beginning of the experiment, designated as ‘day1’. E Protein expression levels of HES1 during BMDM differentiation were analyzed by Western blotting. The expression levels of Notch signaling-related factors, including NICD, RBPJ, and HEY1 were also measured over the course of BMDM differentiation. F BMDMs were subjected to normoxic (20.9% O 2 ) or hypoxic (1% O 2 ) conditions for 24 h. The expression of HES1 was measured using both qRT-PCR and Western blotting. β-actin expression was used as the normalization control for both methods. The presented data are expressed as mean ± SEM, with asterisks denoting significant differences (* p < 0.05) determined by the student’s t-test

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: Elevated expression of HES1 in tumor associated macrophages. A Gene expression analysis was performed on TAMs and mammary tissue macrophages (MTMs) obtained from 16-week-old female MMTV-PyMT mice (GES56755). Canonical Notch signaling related genes with a p-value threshold lower than 0.05 were considered to be differentially expressed. The fold change was represented using a log scale. B The mean fluorescence intensity (MFI) of intracellular HES1 staining was measured in macrophages (CD11b + F4/80 + double positive) isolated from bone marrow, spleen, and tumors. Mice were subcutaneously injected with 4T1, CT26 or B16F10 cell lines to generate tumor tissues. C The intracellular HES1 staining from MMTV-PyMT mice. Macrophages from bone marrow, spleen, and tumors were analyzed by flow cytometry. D Expression of HES1 in differentiating macrophages obtained from bone marrows of normal mice. The population of differentiated macrophages were analyzed by flow cytometry based on CD11b + F4/80 + cells (also see Supplemental Fig. 3). Additionally, Hes1 mRNA levels during the differentiation of BMDMs were analyzed using qRT-PCR. Relative expression was normalized to the expression level at the beginning of the experiment, designated as ‘day1’. E Protein expression levels of HES1 during BMDM differentiation were analyzed by Western blotting. The expression levels of Notch signaling-related factors, including NICD, RBPJ, and HEY1 were also measured over the course of BMDM differentiation. F BMDMs were subjected to normoxic (20.9% O 2 ) or hypoxic (1% O 2 ) conditions for 24 h. The expression of HES1 was measured using both qRT-PCR and Western blotting. β-actin expression was used as the normalization control for both methods. The presented data are expressed as mean ± SEM, with asterisks denoting significant differences (* p < 0.05) determined by the student’s t-test

Article Snippet: The murine Hes1 reporter plasmids pHes1 (467)-luc (Addgene plasmid #41723; http://n2t.net/addgene:41723 ; RRID: Addgene_41723) and pHes1 (467 RBPj (-))-luc (Addgene plasmid #43805; http://n2t.net/addgene:43805 ; RRID: Addgene_43805) were gifts from Ryoichiro Kageyama (RIKEN Center for Brain Science, Kyoto University). pGL2 basic, pHes1 (467)-luc, or pHes1 (467 RBPj (-))-luc, together with pCMV-β-Gal, were co-transfected into BMDMs using Lipofectamine 2000.

Techniques: Expressing, Gene Expression, Fluorescence, Staining, Isolation, Injection, Flow Cytometry, Quantitative RT-PCR, Western Blot, Control

Tumor promoting factors lead to HES1 expression in a Notch signaling pathway-dependent manner. A BMDMs were cultured alone or co-cultured with tumor cell lines (B16F10, E0771, MC38, or TC-1) or human embryonic kidney cell line (HEK293). Protein levels of HES1, as well as markers of pro-tumoral macrophage and the Notch signaling pathway were detected by Western blotting. Phosphorylation status of STAT3 was analyzed to confirm the efficiency of co-culture of tumor cells and BMDMs. GAPDH was used as a loading control. B BMDMs were transiently transfected with siRNA against Rbpj for at least 24 h and treated with CM obtained from B16F10 (skin) or TC-1 (lung) for 8 h. β-actin expression was used as the normalization control. C RBPJ in THP-1 was knock-down by siRNA for at least 24 h and treated with CMs from AGS (stomach) or MB231 (breast) cell lines for 8 h. β-actin was used as a loading control. D BMDMs were exposed to purified cytokines and growth factors known to promote tumor growth, and Hes1 expression was measured using qRT-PCR. E BMDMs were treated to either an inflammatory stimulus (100 ng/ml LPS with 20 ng/ml IFN-γ) or an anti-inflammatory stimulus (20 ng/ml IL-4 with 20 ng/ml IL-13) for the indicated periods. The expression levels of Hes1 were measured by qRT-PCR. F Rbpj -knocked down (at least 24 h) BMDMs were treated with 20 ng/ml IL4, 20 ng/ml EGF, or 20 ng/ml TGFβ for 8 h. β-actin was used as a loading control. G RBPJ was transiently knocked down in THP-1 cells at least for 24 h and treated with 20 ng/ml IL4, 20 ng/ml EGF, or 20 ng/ml TGFβ for 8 h. β-actin was used as a loading control

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: Tumor promoting factors lead to HES1 expression in a Notch signaling pathway-dependent manner. A BMDMs were cultured alone or co-cultured with tumor cell lines (B16F10, E0771, MC38, or TC-1) or human embryonic kidney cell line (HEK293). Protein levels of HES1, as well as markers of pro-tumoral macrophage and the Notch signaling pathway were detected by Western blotting. Phosphorylation status of STAT3 was analyzed to confirm the efficiency of co-culture of tumor cells and BMDMs. GAPDH was used as a loading control. B BMDMs were transiently transfected with siRNA against Rbpj for at least 24 h and treated with CM obtained from B16F10 (skin) or TC-1 (lung) for 8 h. β-actin expression was used as the normalization control. C RBPJ in THP-1 was knock-down by siRNA for at least 24 h and treated with CMs from AGS (stomach) or MB231 (breast) cell lines for 8 h. β-actin was used as a loading control. D BMDMs were exposed to purified cytokines and growth factors known to promote tumor growth, and Hes1 expression was measured using qRT-PCR. E BMDMs were treated to either an inflammatory stimulus (100 ng/ml LPS with 20 ng/ml IFN-γ) or an anti-inflammatory stimulus (20 ng/ml IL-4 with 20 ng/ml IL-13) for the indicated periods. The expression levels of Hes1 were measured by qRT-PCR. F Rbpj -knocked down (at least 24 h) BMDMs were treated with 20 ng/ml IL4, 20 ng/ml EGF, or 20 ng/ml TGFβ for 8 h. β-actin was used as a loading control. G RBPJ was transiently knocked down in THP-1 cells at least for 24 h and treated with 20 ng/ml IL4, 20 ng/ml EGF, or 20 ng/ml TGFβ for 8 h. β-actin was used as a loading control

Techniques: Expressing, Cell Culture, Western Blot, Phospho-proteomics, Co-Culture Assay, Control, Transfection, Knockdown, Purification, Quantitative RT-PCR

The development of hematopoietic stem cells is normal in mice with myeloid specific Hes1 knock out. A Bone marrow cells from wild-type (WT) or Hes1 conditional knockout (cKO) mice were cultured and differentiated into BMDMs for 7 days in vitro. On day 7, samples were collected, and macrophages were identified by flow cytometry (CD11b + F4/80 + ). Representative flow cytometry plots of fully differentiated BMDMs from WT and Hes1 -cKO mice are shown. B Total number of bone marrow cells from WT and Hes1 cKO littermates before differentiation. C The number of differentiated BMDMs and cell viability after differentiation. D Flow cytometry analysis of bone marrow cells for stem cells (cKit + , Sca1 + , or ckit int Sca1 int ), lymphocytes (T cells: CD3 + ; B cells: B220 + ) and myeloid cells (neutrophils: CD11b + Ly-6G + ; monocytes/macrophages: CD11b + Gr1 − ) in the bone marrow. Six to eight-week-old mice were used. E Flow cytometry for lymphocytes (T cells: CD3 + ; B cells: B220 + ), myeloid cells (neutrophils: CD11b + Ly-6G + ; monocytes/macrophages: CD11b + Gr1 − ) and T cell subpopulation (CD3 + CD4 + T cells; CD3 + CD8 + T cells) in the spleen. Six to eight-week-old mice were used. F The CBC in peripheral blood of six to eight-week-old mice to analyze overall health and conditions depending on Hes1 deficiency

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: The development of hematopoietic stem cells is normal in mice with myeloid specific Hes1 knock out. A Bone marrow cells from wild-type (WT) or Hes1 conditional knockout (cKO) mice were cultured and differentiated into BMDMs for 7 days in vitro. On day 7, samples were collected, and macrophages were identified by flow cytometry (CD11b + F4/80 + ). Representative flow cytometry plots of fully differentiated BMDMs from WT and Hes1 -cKO mice are shown. B Total number of bone marrow cells from WT and Hes1 cKO littermates before differentiation. C The number of differentiated BMDMs and cell viability after differentiation. D Flow cytometry analysis of bone marrow cells for stem cells (cKit + , Sca1 + , or ckit int Sca1 int ), lymphocytes (T cells: CD3 + ; B cells: B220 + ) and myeloid cells (neutrophils: CD11b + Ly-6G + ; monocytes/macrophages: CD11b + Gr1 − ) in the bone marrow. Six to eight-week-old mice were used. E Flow cytometry for lymphocytes (T cells: CD3 + ; B cells: B220 + ), myeloid cells (neutrophils: CD11b + Ly-6G + ; monocytes/macrophages: CD11b + Gr1 − ) and T cell subpopulation (CD3 + CD4 + T cells; CD3 + CD8 + T cells) in the spleen. Six to eight-week-old mice were used. F The CBC in peripheral blood of six to eight-week-old mice to analyze overall health and conditions depending on Hes1 deficiency

Techniques: Knock-Out, Cell Culture, In Vitro, Flow Cytometry

Hes1 -cKO leads to reduced tumor growth. A Six to eight-week-old mice were utilized in the study to evaluate tumor growth in both WT and Hes1 deficient mice after subcutaneous injection of B16F10, E0771, MC-38 and TC-1 cells. Each group comprised of five WT/ Hes1 -cKO mice. ( B ) Weight of tumors generated in ( A ). C Survival of mice bearing tumors in LysM-Hes1 + / + PyMT (n = 10) and LysM-Hes1 fl/fl PyMT mice (n = 14). D Different immune cell populations from the spleen and tumor tissue of TC-1 tumor-bearing mice. Immune cells were sorted and followed by qRT-PCR to measure the expression level of Hes1 in each sorted population. E Cells sorted from TC-1 tumor-bearing mice and protein lysates from each sorted population were analyzed by Western blotting. β-actin was used as a loading control. F Tumor growth was measured in mice treated with anti-CSF-1R (CSF1R antibody) or an isotype control antibody, as shown in Supplemental Fig. 6B. Each group included two to three tumors per mouse. Six to eight-week-old mice (n = 3) were used for the study. G The numbers of CD45 + Gr1 − CD11b + F4/80 + CD206 + macrophages were quantified in WT mice treated with α-CSF1. The graphs depict the mean ± SEM of data from more than 2 independent experiments

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: Hes1 -cKO leads to reduced tumor growth. A Six to eight-week-old mice were utilized in the study to evaluate tumor growth in both WT and Hes1 deficient mice after subcutaneous injection of B16F10, E0771, MC-38 and TC-1 cells. Each group comprised of five WT/ Hes1 -cKO mice. ( B ) Weight of tumors generated in ( A ). C Survival of mice bearing tumors in LysM-Hes1 + / + PyMT (n = 10) and LysM-Hes1 fl/fl PyMT mice (n = 14). D Different immune cell populations from the spleen and tumor tissue of TC-1 tumor-bearing mice. Immune cells were sorted and followed by qRT-PCR to measure the expression level of Hes1 in each sorted population. E Cells sorted from TC-1 tumor-bearing mice and protein lysates from each sorted population were analyzed by Western blotting. β-actin was used as a loading control. F Tumor growth was measured in mice treated with anti-CSF-1R (CSF1R antibody) or an isotype control antibody, as shown in Supplemental Fig. 6B. Each group included two to three tumors per mouse. Six to eight-week-old mice (n = 3) were used for the study. G The numbers of CD45 + Gr1 − CD11b + F4/80 + CD206 + macrophages were quantified in WT mice treated with α-CSF1. The graphs depict the mean ± SEM of data from more than 2 independent experiments

Techniques: Injection, Generated, Quantitative RT-PCR, Expressing, Western Blot, Control

Hes1 deficiency suppressed the expression of tumor-promoting factors. A Heat map showing the expression levels of TAM signature genes in WT and Hes1 -cKO TAMs. TAMs are sorted from the TC-1 tumor model based on CD11b + F4/80 + Gr1 − and six to eight-week-old mice were used. B qRT-PCR analysis of gene expression in TAMs sorted from WT and Hes1 -cKO mice with the TC-1 tumor model, including cytokine ( Il6 , Il10 , Il12 , Ifng , and Tnfa ), metabolic enzyme ( Arg1 and Nos2 ), immune checkpoint ( Pdl1 ), co-stimulatory molecules ( Cd80 and Cd86 ), other pro-tumoral factors ( Vegfa , Mmp9 , and Lgals9 ). C BMDMs were treated with either inflammatory stimuli (100 ng/mL LPS and 20 ng/mL IFN-γ) or anti-inflammatory stimuli (20 ng/mL IL-4) for 8 h. Protein levels are analyzed by Western blotting and β-actin was used as a loading control. Non-specific bands are marked with an asterisk. D THP1 cells were transiently transfected with siRNA against HES1 (at least 24 h) and treated with tumor CM from AGS cells (stomach cancers) for 8 h. qRT-PCR was conducted to measure the gene expression. E THP1 cells were transiently transfected with siRNA against HES1 (at least 24 h) and treated with tumor CM from AGS cells (stomach cancers) for 8 h. Protein levels are analyzed and quantified by Western blotting. β-actin was used as a loading control

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: Hes1 deficiency suppressed the expression of tumor-promoting factors. A Heat map showing the expression levels of TAM signature genes in WT and Hes1 -cKO TAMs. TAMs are sorted from the TC-1 tumor model based on CD11b + F4/80 + Gr1 − and six to eight-week-old mice were used. B qRT-PCR analysis of gene expression in TAMs sorted from WT and Hes1 -cKO mice with the TC-1 tumor model, including cytokine ( Il6 , Il10 , Il12 , Ifng , and Tnfa ), metabolic enzyme ( Arg1 and Nos2 ), immune checkpoint ( Pdl1 ), co-stimulatory molecules ( Cd80 and Cd86 ), other pro-tumoral factors ( Vegfa , Mmp9 , and Lgals9 ). C BMDMs were treated with either inflammatory stimuli (100 ng/mL LPS and 20 ng/mL IFN-γ) or anti-inflammatory stimuli (20 ng/mL IL-4) for 8 h. Protein levels are analyzed by Western blotting and β-actin was used as a loading control. Non-specific bands are marked with an asterisk. D THP1 cells were transiently transfected with siRNA against HES1 (at least 24 h) and treated with tumor CM from AGS cells (stomach cancers) for 8 h. qRT-PCR was conducted to measure the gene expression. E THP1 cells were transiently transfected with siRNA against HES1 (at least 24 h) and treated with tumor CM from AGS cells (stomach cancers) for 8 h. Protein levels are analyzed and quantified by Western blotting. β-actin was used as a loading control

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

Expression of Arg1 is regulated by HES1. A Hes1 -targeted siRNA was transfected into BMDMs, which were then treated with EO771 tumor conditioned media for up to 8 h. The abundance of Arg1 mRNA was measured using qRT-PCR. B BMDMs obtained from WT or Hes1 -cKO mice were treated with either EO771 or MC-38 CM for 8 h. Western botting analyzed protein levels of HES1, ARG1, ARG2, p-STAT6 (Y641), and STAT6. β-actin was used as a loading control. C BMDMs were treated with EO771 CM for 8 h. mRNA for Arg1 was measured by qRT-PCR. D Western blot analysis was performed to compare the expression of EO771 CM induced proteins in WT and Hes1 -cKO BMDMs after 8 h of stimulation. The intensity of the protein bands was quantified and normalized to β-actin. E The effect of HES1 overexpression on ARG1 protein expression in BMDMs. BMDMs were transfected with increasing amounts of Hes1 for 24 h and protein levels were detected by Western blots. F The luciferase activity was measured in BMDMs transfected with the putative HES1 binding sites on Arg1 promoter. Wil-type or Hes1 -cKO BMDMs were treated with EO771 CM for 8 h. G BMDMs were overexpressed with Hes1 for 24 h followed by EO771 CM for 8 h. H RAW 264.7 cells were treated with EO771 CM for 8 h and chromatin immunoprecipitation was performed and analyzed by qRT-PCR

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: Expression of Arg1 is regulated by HES1. A Hes1 -targeted siRNA was transfected into BMDMs, which were then treated with EO771 tumor conditioned media for up to 8 h. The abundance of Arg1 mRNA was measured using qRT-PCR. B BMDMs obtained from WT or Hes1 -cKO mice were treated with either EO771 or MC-38 CM for 8 h. Western botting analyzed protein levels of HES1, ARG1, ARG2, p-STAT6 (Y641), and STAT6. β-actin was used as a loading control. C BMDMs were treated with EO771 CM for 8 h. mRNA for Arg1 was measured by qRT-PCR. D Western blot analysis was performed to compare the expression of EO771 CM induced proteins in WT and Hes1 -cKO BMDMs after 8 h of stimulation. The intensity of the protein bands was quantified and normalized to β-actin. E The effect of HES1 overexpression on ARG1 protein expression in BMDMs. BMDMs were transfected with increasing amounts of Hes1 for 24 h and protein levels were detected by Western blots. F The luciferase activity was measured in BMDMs transfected with the putative HES1 binding sites on Arg1 promoter. Wil-type or Hes1 -cKO BMDMs were treated with EO771 CM for 8 h. G BMDMs were overexpressed with Hes1 for 24 h followed by EO771 CM for 8 h. H RAW 264.7 cells were treated with EO771 CM for 8 h and chromatin immunoprecipitation was performed and analyzed by qRT-PCR

Techniques: Expressing, Transfection, Quantitative RT-PCR, Western Blot, Control, Over Expression, Luciferase, Activity Assay, Binding Assay, Chromatin Immunoprecipitation

The improved TME by Hes1 deficiency. A Representative IHC images (100x, 300x) showing HES1, CD45, CD3e, CD11b, F4/80, ARG1 and CD163 staining of tumors from TC-1 tumor-bearing WT and Hes1 -cKO mice. Scale bars: 200 μm. B Tumors were collected from TC-1 tumor-bearing WT or Hes1 -cKO mice and processed into single cells. Flow cytometry was performed to assess the extent of immune cell infiltration into the tumors. Representative graphs from at least three independent experiments of 3–4 animals per group are presented. The error bars represent the standard error of the mean. C Percentage and MFI of TNFα, IL-12, CD80, CD206, or ARG1 expression in total myeloid cells isolated from TC-1 tumors and measured by flow cytometry. D T cell subpopulation analyzed by flow cytometry. For ex vivo stimulation, CD4 + or CD8 + T cells from each harvested tumor were treated with Cell Activation Cocktail containing GolgiStop for 4 h

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: The improved TME by Hes1 deficiency. A Representative IHC images (100x, 300x) showing HES1, CD45, CD3e, CD11b, F4/80, ARG1 and CD163 staining of tumors from TC-1 tumor-bearing WT and Hes1 -cKO mice. Scale bars: 200 μm. B Tumors were collected from TC-1 tumor-bearing WT or Hes1 -cKO mice and processed into single cells. Flow cytometry was performed to assess the extent of immune cell infiltration into the tumors. Representative graphs from at least three independent experiments of 3–4 animals per group are presented. The error bars represent the standard error of the mean. C Percentage and MFI of TNFα, IL-12, CD80, CD206, or ARG1 expression in total myeloid cells isolated from TC-1 tumors and measured by flow cytometry. D T cell subpopulation analyzed by flow cytometry. For ex vivo stimulation, CD4 + or CD8 + T cells from each harvested tumor were treated with Cell Activation Cocktail containing GolgiStop for 4 h

Techniques: Staining, Flow Cytometry, Expressing, Isolation, Ex Vivo, Activation Assay

Synergistic anti-tumor effect of HES1 inhibition. A TC-1 cells were subcutaneously injected WT and Hes1 -cKO mice followed by PD-1 blocking antibody. Either isotype control or α-PD1 antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. B MC-38 cells were injected intraperitoneally followed by 200 μg of isotype control or α-PD1 antibodies on days 7, 10 and 13 post tumor implantations. C TC-1 cells were subcutaneously injected WT and Hes1 -cKO mice followed by PD-1 blocking antibody. Either isotype control or α-PD1 antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. IFN-γ producing CD4 + or CD8 + T cells isolated from TC-1 tumors and analyzed by flow cytometry. D WT and Hes1- cKO mice were injected subcutaneously with TC-1 cells and treated with either αCD4 or isotype control antibodies to deplete CD4 + T cells. Antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. Tumor growth and weight were monitored and measured over time. E WT and Hes1 -cKO mice were injected with TC-1 cells subcutaneously, and the effect of CD8 + T cell depletion on tumor growth and weight was evaluated. αCD8 or isotype control antibodies were administered to deplete CD8 + T cells. Antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. Tumor growth curve and weight were monitored

Journal: Experimental Hematology & Oncology

Article Title: Disrupting Notch signaling related HES1 in myeloid cells reinvigorates antitumor T cell responses

doi: 10.1186/s40164-024-00588-2

Figure Lengend Snippet: Synergistic anti-tumor effect of HES1 inhibition. A TC-1 cells were subcutaneously injected WT and Hes1 -cKO mice followed by PD-1 blocking antibody. Either isotype control or α-PD1 antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. B MC-38 cells were injected intraperitoneally followed by 200 μg of isotype control or α-PD1 antibodies on days 7, 10 and 13 post tumor implantations. C TC-1 cells were subcutaneously injected WT and Hes1 -cKO mice followed by PD-1 blocking antibody. Either isotype control or α-PD1 antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. IFN-γ producing CD4 + or CD8 + T cells isolated from TC-1 tumors and analyzed by flow cytometry. D WT and Hes1- cKO mice were injected subcutaneously with TC-1 cells and treated with either αCD4 or isotype control antibodies to deplete CD4 + T cells. Antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. Tumor growth and weight were monitored and measured over time. E WT and Hes1 -cKO mice were injected with TC-1 cells subcutaneously, and the effect of CD8 + T cell depletion on tumor growth and weight was evaluated. αCD8 or isotype control antibodies were administered to deplete CD8 + T cells. Antibodies (200 μg) was injected intraperitoneally on days 7, 10 and 13 after tumor implantations. Tumor growth curve and weight were monitored

Techniques: Inhibition, Injection, Blocking Assay, Control, Isolation, Flow Cytometry

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