mc38 cell lines  (ATCC)


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    ATCC mc38 cell lines
    The impact of KRAS peptide–Lpx on tumor growth was completely dependent on CD8 + T cells while depletion of CD4 + T cells had no impact. a , b Depletion of CD4 + or CD8 + T cells before and during the growth of <t>MC38-G12D</t> tumors (solid arrow; every 2–3 days) in mice immunized with the naked peptide G12D 1–23 and CpG ( a ) or with G12D 1–23 –Lpx starting on day −8 (dashed arrow) ( b ). Significance was determined using two-way ANOVA (**** p
    Mc38 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "A nanoparticle vaccine that targets neoantigen peptides to lymphoid tissues elicits robust antitumor T cell responses"

    Article Title: A nanoparticle vaccine that targets neoantigen peptides to lymphoid tissues elicits robust antitumor T cell responses

    Journal: NPJ Vaccines

    doi: 10.1038/s41541-020-00253-9

    The impact of KRAS peptide–Lpx on tumor growth was completely dependent on CD8 + T cells while depletion of CD4 + T cells had no impact. a , b Depletion of CD4 + or CD8 + T cells before and during the growth of MC38-G12D tumors (solid arrow; every 2–3 days) in mice immunized with the naked peptide G12D 1–23 and CpG ( a ) or with G12D 1–23 –Lpx starting on day −8 (dashed arrow) ( b ). Significance was determined using two-way ANOVA (**** p
    Figure Legend Snippet: The impact of KRAS peptide–Lpx on tumor growth was completely dependent on CD8 + T cells while depletion of CD4 + T cells had no impact. a , b Depletion of CD4 + or CD8 + T cells before and during the growth of MC38-G12D tumors (solid arrow; every 2–3 days) in mice immunized with the naked peptide G12D 1–23 and CpG ( a ) or with G12D 1–23 –Lpx starting on day −8 (dashed arrow) ( b ). Significance was determined using two-way ANOVA (**** p

    Techniques Used: Mouse Assay

    Tumors respond to the peptide–lipoplex vaccine by upregulating MHC class I and II molecules and PD-L1. a MHC class I (H2D b ) expression on MC38-G12D cells before tumor implantation. b , c MHC class I and MHC class II expression on MC38-G12D tumors or CD11b + myeloid cells from mice immunized with lipoplex (Lpx) control or G12D 1–23 peptide–lipoplex. d PD-L1 expression analyzed by flow cytometric analysis on MC38-G12D tumors and tumor-infiltrating myeloid cells in mice immunized with Lpx control or G12D 1–23 peptide–Lpx. Significance was determined using a one-sided Student’s t- test ( b – d ). (* p
    Figure Legend Snippet: Tumors respond to the peptide–lipoplex vaccine by upregulating MHC class I and II molecules and PD-L1. a MHC class I (H2D b ) expression on MC38-G12D cells before tumor implantation. b , c MHC class I and MHC class II expression on MC38-G12D tumors or CD11b + myeloid cells from mice immunized with lipoplex (Lpx) control or G12D 1–23 peptide–lipoplex. d PD-L1 expression analyzed by flow cytometric analysis on MC38-G12D tumors and tumor-infiltrating myeloid cells in mice immunized with Lpx control or G12D 1–23 peptide–Lpx. Significance was determined using a one-sided Student’s t- test ( b – d ). (* p

    Techniques Used: Expressing, Tumor Implantation, Mouse Assay

    Therapeutic peptide–lipoplex vaccination in combination with checkpoint inhibition elicits potent anti-tumor responses with exhausted TILs. a Detection of mutant Adpgk-specific CD8 + TILs in mice immunized with Neo-Lpx using an MHC class I dextramer specific for Adgk. b , c TILs specific or not for Adpgk using dextramer staining were analyzed for PD-1 and Tim3 expression ( b ) and CTLA4 and Lag3 expression ( c ). d Mutant Adpgk and Copg1 27-mers with G12D 1–23 peptide were formulated lipoplexes (Neo-Lpx) to immunize mice with MC38-G12D tumors 5 days after implantation (solid arrows). Mice were immunized and/or treated with PD-1 antibody or isotype control after randomization on day 14 (dashed arrows). e Tumor growth curves of individual mice from ( d ). Significance was determined using two-way ANOVA (**** p
    Figure Legend Snippet: Therapeutic peptide–lipoplex vaccination in combination with checkpoint inhibition elicits potent anti-tumor responses with exhausted TILs. a Detection of mutant Adpgk-specific CD8 + TILs in mice immunized with Neo-Lpx using an MHC class I dextramer specific for Adgk. b , c TILs specific or not for Adpgk using dextramer staining were analyzed for PD-1 and Tim3 expression ( b ) and CTLA4 and Lag3 expression ( c ). d Mutant Adpgk and Copg1 27-mers with G12D 1–23 peptide were formulated lipoplexes (Neo-Lpx) to immunize mice with MC38-G12D tumors 5 days after implantation (solid arrows). Mice were immunized and/or treated with PD-1 antibody or isotype control after randomization on day 14 (dashed arrows). e Tumor growth curves of individual mice from ( d ). Significance was determined using two-way ANOVA (**** p

    Techniques Used: Inhibition, Mutagenesis, Mouse Assay, Staining, Expressing

    Vaccination with neoantigen peptide–Lpx generates peptide-specific effector CD4 + and CD8 + T cells. a Tumors and spleens from MC38-G12D tumor-bearing mice that were immunized with the G12D 1-23 -Lpx were analyzed on day 25. Analysis of CD8 + and CD4 + T cell infiltrating the tumors determined by the CD8/CD4 ratio. b IFN-γ ELISpot of splenocytes re-stimulated with the immunizing G12D 1–23 or WT peptide in tumor-bearing mice. c Intracellular cytokine staining of CD4 + and CD8 + T cells from spleens of MC38-G12D tumor-bearing mice after G12D 1–23 peptide re-stimulation . d , e Expression of PD-1 and Ki67 based on IFN-γ production from G12D 1–23 -stimulated CD4 + and CD8 + T cells gated from c . (** p
    Figure Legend Snippet: Vaccination with neoantigen peptide–Lpx generates peptide-specific effector CD4 + and CD8 + T cells. a Tumors and spleens from MC38-G12D tumor-bearing mice that were immunized with the G12D 1-23 -Lpx were analyzed on day 25. Analysis of CD8 + and CD4 + T cell infiltrating the tumors determined by the CD8/CD4 ratio. b IFN-γ ELISpot of splenocytes re-stimulated with the immunizing G12D 1–23 or WT peptide in tumor-bearing mice. c Intracellular cytokine staining of CD4 + and CD8 + T cells from spleens of MC38-G12D tumor-bearing mice after G12D 1–23 peptide re-stimulation . d , e Expression of PD-1 and Ki67 based on IFN-γ production from G12D 1–23 -stimulated CD4 + and CD8 + T cells gated from c . (** p

    Techniques Used: Mouse Assay, Enzyme-linked Immunospot, Staining, Expressing

    Vaccination with neoantigen peptide–lipoplexes enhances CD8 + T cell responses and controls tumor growth in syngeneic tumors expressing mutant KRAS. a Growth of MC38-G12D tumors in C57Bl/6 mice immunized with empty liposomes and CpG control (+Lpx Ctrl), G12D 1–23 peptide and CpG (+G12D 1–23 ), or with G12D 1–23 in lipoplexes (+G12D 1–23 –Lpx) starting 10 days before implantation and every 7 days for 3 weeks (dashed arrows) (n = 5–10). b Growth of MC38-WT tumors in mice immunized with G12D 1–23 –Lpx as indicated by the dashed arrows ( n = 5). c Growth of MC38-WT and MC38-G12D tumors in mice immunized with G12D 1–23 –Lpx starting at randomization on days 8 and 7 days later (arrows) (n = 7–9). d Mice were immunized with the mutant Adpgk and Copg1 27-mer peptides and CpG (top) and with the 27-mer complexed Lpx twice, one week apart. Splenocytes were stimulated with the immunizing peptide and the 9-mer that stimulates CD8 + T cells ( n = 3). e Growth curves of mice immunized with the Adpgk, Copg1, and G12D 1–23 SLP–Lpx (Neo-Lpx) at the indicated time points (arrows) ( n = 9–11). f Tumor-infiltrating Foxp3 + CD4 + regulatory T cells were quantified by intranuclear staining on day 23. g CT26 tumor growth in mice immunized with empty Lpx control or G12D 1–23 –Lpx on the day of randomization and 1 week later ( n = 9–10). h Naive Balb/c mice were s.c. immunized with the indicated neoantigen peptides in the naked form (top) or with Lpx (bottom) once weekly for 2 weeks and an IFN-γ ELISpot was performed to detect reactivity to the immunizing SLP or 9-mer corresponding to the predicted CD8 + T cell epitope. i Randomized CT26 tumors were immunized with empty Lpx control, CpG, and neoantigen (Neo) peptides (KRAS-G12D 1–23 , Tmem87a G63R 27-mer, and Slc4a3 T373I 27-mer), or neoantigen peptide–lipoplexes (Neo-Lpx). Mice immunized twice after randomization ( n = 7–11). Significance was determined using two-way ANOVA and one-sided Student’s t -test (**** p
    Figure Legend Snippet: Vaccination with neoantigen peptide–lipoplexes enhances CD8 + T cell responses and controls tumor growth in syngeneic tumors expressing mutant KRAS. a Growth of MC38-G12D tumors in C57Bl/6 mice immunized with empty liposomes and CpG control (+Lpx Ctrl), G12D 1–23 peptide and CpG (+G12D 1–23 ), or with G12D 1–23 in lipoplexes (+G12D 1–23 –Lpx) starting 10 days before implantation and every 7 days for 3 weeks (dashed arrows) (n = 5–10). b Growth of MC38-WT tumors in mice immunized with G12D 1–23 –Lpx as indicated by the dashed arrows ( n = 5). c Growth of MC38-WT and MC38-G12D tumors in mice immunized with G12D 1–23 –Lpx starting at randomization on days 8 and 7 days later (arrows) (n = 7–9). d Mice were immunized with the mutant Adpgk and Copg1 27-mer peptides and CpG (top) and with the 27-mer complexed Lpx twice, one week apart. Splenocytes were stimulated with the immunizing peptide and the 9-mer that stimulates CD8 + T cells ( n = 3). e Growth curves of mice immunized with the Adpgk, Copg1, and G12D 1–23 SLP–Lpx (Neo-Lpx) at the indicated time points (arrows) ( n = 9–11). f Tumor-infiltrating Foxp3 + CD4 + regulatory T cells were quantified by intranuclear staining on day 23. g CT26 tumor growth in mice immunized with empty Lpx control or G12D 1–23 –Lpx on the day of randomization and 1 week later ( n = 9–10). h Naive Balb/c mice were s.c. immunized with the indicated neoantigen peptides in the naked form (top) or with Lpx (bottom) once weekly for 2 weeks and an IFN-γ ELISpot was performed to detect reactivity to the immunizing SLP or 9-mer corresponding to the predicted CD8 + T cell epitope. i Randomized CT26 tumors were immunized with empty Lpx control, CpG, and neoantigen (Neo) peptides (KRAS-G12D 1–23 , Tmem87a G63R 27-mer, and Slc4a3 T373I 27-mer), or neoantigen peptide–lipoplexes (Neo-Lpx). Mice immunized twice after randomization ( n = 7–11). Significance was determined using two-way ANOVA and one-sided Student’s t -test (**** p

    Techniques Used: Expressing, Mutagenesis, Mouse Assay, Staining, Enzyme-linked Immunospot

    2) Product Images from "IL-9/STAT3/fatty acid oxidation–mediated lipid peroxidation contributes to Tc9 cell longevity and enhanced antitumor activity"

    Article Title: IL-9/STAT3/fatty acid oxidation–mediated lipid peroxidation contributes to Tc9 cell longevity and enhanced antitumor activity

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI153247

    Persistence of adoptively transferred CD8 + T cells in the TME is negatively correlated with their lipid peroxidation. ( A and B ) Thy1.1 + Pmel-1 Tc1 or Tc9 cells were i.v. injected into Thy1.2 + B6 mice bearing 10-day s.c. B16 tumors with adjuvant treatments (CTX, dendritic cells, and rhIL-2). Tumor growth curve ( n = 5), Thy1.1 + percentages in CD8 + T cells, and Thy1.1 + CD8 + T cell numbers in tumors on day 45 after tumor injection ( n = 8). ( C and D ) GSEA of indicated gene sets on day 24 after tumor injection. GO, Gene Ontology; NES, normalized enrichment score. ( E ) Lipid content (BODIPY 495/503 staining), ( F ) total ROS level (CM-H 2 DCFDA staining), ( G ) lipid ROS, and ( H ) PD-1 and LAG-3 expression of transferred Tc1 and Tc9 cells on day 45 after tumor injection ( n = 10, two pooled independent experiments). ( I ) Tumor-infiltrating Tc9 cells were divided into PD-1 + and PD-1 – groups and analyzed for the level of lipid ROS ( n = 10). ( J and K ) Thy1.1 + Pmel-1 Tc1 or Tc9 cells were i.v. injected into Thy1.2 + B6 mice bearing 10-day MC38-gp100 tumors with adjuvant treatments. Shown are Thy1.1 + percentages in CD8 + T cells, Thy1.1 + CD8 + T cell numbers, and relative lipid ROS levels of Tc1 and Tc9 cells in tumors on day 40 after tumor injection ( n = 6). ( L and M ) Thy1.1 + Pmel-1 Tc1 or Tc9 cells were i.v. injected into Thy1.2 + B6 mice bearing 12-day lung metastatic B16 tumors. Shown are Thy1.1 + percentages in CD8 + T cells, Thy1.1 + CD8 + T cell numbers, and relative lipid ROS levels of Tc1 and Tc9 cells in tumors on day 17 after tumor injection ( n = 6). Data are presented as mean ± SEM. Tumor-infiltrating Thy1.1 + CD8 + T cell number was normalized to 100 mg tumor tissue. * P
    Figure Legend Snippet: Persistence of adoptively transferred CD8 + T cells in the TME is negatively correlated with their lipid peroxidation. ( A and B ) Thy1.1 + Pmel-1 Tc1 or Tc9 cells were i.v. injected into Thy1.2 + B6 mice bearing 10-day s.c. B16 tumors with adjuvant treatments (CTX, dendritic cells, and rhIL-2). Tumor growth curve ( n = 5), Thy1.1 + percentages in CD8 + T cells, and Thy1.1 + CD8 + T cell numbers in tumors on day 45 after tumor injection ( n = 8). ( C and D ) GSEA of indicated gene sets on day 24 after tumor injection. GO, Gene Ontology; NES, normalized enrichment score. ( E ) Lipid content (BODIPY 495/503 staining), ( F ) total ROS level (CM-H 2 DCFDA staining), ( G ) lipid ROS, and ( H ) PD-1 and LAG-3 expression of transferred Tc1 and Tc9 cells on day 45 after tumor injection ( n = 10, two pooled independent experiments). ( I ) Tumor-infiltrating Tc9 cells were divided into PD-1 + and PD-1 – groups and analyzed for the level of lipid ROS ( n = 10). ( J and K ) Thy1.1 + Pmel-1 Tc1 or Tc9 cells were i.v. injected into Thy1.2 + B6 mice bearing 10-day MC38-gp100 tumors with adjuvant treatments. Shown are Thy1.1 + percentages in CD8 + T cells, Thy1.1 + CD8 + T cell numbers, and relative lipid ROS levels of Tc1 and Tc9 cells in tumors on day 40 after tumor injection ( n = 6). ( L and M ) Thy1.1 + Pmel-1 Tc1 or Tc9 cells were i.v. injected into Thy1.2 + B6 mice bearing 12-day lung metastatic B16 tumors. Shown are Thy1.1 + percentages in CD8 + T cells, Thy1.1 + CD8 + T cell numbers, and relative lipid ROS levels of Tc1 and Tc9 cells in tumors on day 17 after tumor injection ( n = 6). Data are presented as mean ± SEM. Tumor-infiltrating Thy1.1 + CD8 + T cell number was normalized to 100 mg tumor tissue. * P

    Techniques Used: Injection, Mouse Assay, Staining, Expressing

    3) Product Images from "TIGIT predominantly regulates the immune response via regulatory T cells"

    Article Title: TIGIT predominantly regulates the immune response via regulatory T cells

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI81187

    TIGIT restrains antitumor immune responses. ( A ) Growth of B16F10 melanoma or MC38 colon carcinoma in WT or Tigit –/– mice ( n = 5–6). Data are representative of 3 independent experiments. *** P
    Figure Legend Snippet: TIGIT restrains antitumor immune responses. ( A ) Growth of B16F10 melanoma or MC38 colon carcinoma in WT or Tigit –/– mice ( n = 5–6). Data are representative of 3 independent experiments. *** P

    Techniques Used: Mouse Assay

    4) Product Images from "HX008: a humanized PD-1 blocking antibody with potent antitumor activity and superior pharmacologic properties"

    Article Title: HX008: a humanized PD-1 blocking antibody with potent antitumor activity and superior pharmacologic properties

    Journal: mAbs

    doi: 10.1080/19420862.2020.1724751

    Antitumor response of HX008 in HuGEMM Model. Human PD-1 knock-in mice were subcutaneously implanted with MC38 cells (1 × 10 6 per mouse) and were randomized into treatment groups after mean tumor volume reached 134 mm 3 . Single i.v. administration of HX008 (5 mg/kg or 10 mg/kg, n = 8/group) or positive control pembrolizumab (10 mg/kg, n = 8) and isotype control (10 mg/kg, n = 8) were performed twice weekly as indicated, six times in total. Tumor volume was measured twice a week and mice were euthanized at maximum allowed tumor burden. (a) tumor growth curves. (b) group mean tumor volume measured on Day 13 post dose. (c) individual tumor growth curves in each treatment group. The number of total free mice per group was indicated. (d) Body weight of HuGEMM MC38 bearing mice during the treatment. For comparisons between groups in the study, we used one-way ANOVA with the Dunn-Sidak post hoc test. Data were shown as SEM of 8 mice per group; ***, P
    Figure Legend Snippet: Antitumor response of HX008 in HuGEMM Model. Human PD-1 knock-in mice were subcutaneously implanted with MC38 cells (1 × 10 6 per mouse) and were randomized into treatment groups after mean tumor volume reached 134 mm 3 . Single i.v. administration of HX008 (5 mg/kg or 10 mg/kg, n = 8/group) or positive control pembrolizumab (10 mg/kg, n = 8) and isotype control (10 mg/kg, n = 8) were performed twice weekly as indicated, six times in total. Tumor volume was measured twice a week and mice were euthanized at maximum allowed tumor burden. (a) tumor growth curves. (b) group mean tumor volume measured on Day 13 post dose. (c) individual tumor growth curves in each treatment group. The number of total free mice per group was indicated. (d) Body weight of HuGEMM MC38 bearing mice during the treatment. For comparisons between groups in the study, we used one-way ANOVA with the Dunn-Sidak post hoc test. Data were shown as SEM of 8 mice per group; ***, P

    Techniques Used: Knock-In, Mouse Assay, Positive Control

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    ATCC mc38 cells
    Blocking C5aR signaling promotes the anti-tumor efficacy of checkpoint blockade. (A-B) Tumor cells (3 × 10 4 B16F10 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT or C5aR −/− mice on day 0. The mice were treated with anti-PD-L1 antibodies or the corresponding isotype control on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 10–13 mice/group). (C) Tumor cells (5 × 10 5 <t>MC38</t> cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT or C5aR −/− mice on day 0. The mice were treated with anti-PD-L1 antibodies or the corresponding isotype control on days 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 5–6 mice/group). (D-E) Tumor cells (3 × 10 4 B16F10 cells in 100 μl phosphate-buffered saline) were subcutaneously injected into the flanks of WT mice on day 0. For pharmacological blockade of C5aR signaling, the C5aR antagonist (C5aRa) (PMX53, GL Biochem; 1 mg/kg daily) was subcutaneously injected into C57BL/6 mice on days 4 to 14. PD-L1 antibodies or the corresponding isotype control were injected on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 9–10 mice/group). (F-G) Tumor cells (3 × 10 4 B16F10 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT mice on day 0. For pharmacological blockade of C5aR signaling, the C5aR antagonist (C5aRa) (PMX53, GL Biochem; 1 mg/kg daily) was subcutaneously injected into C57BL/6 mice on days 4 to 14. PD-1 antibodies or the corresponding isotype control were injected on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 10 mice/group). Two-way ANOVA (B, C, E, G) was used to evaluate statistical significance (*p
    Mc38 Cells, 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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    98
    ATCC colon adenocarcinoma mc38 cell lines
    Long-term anti-tumor immunity in TA99-treated mice relies on a specific T-cell memory response. C57BL/6N (A, B), athymic nude (C, D) and NSG (E, F) mice engrafted with 5.10 4 B16F10 melanoma cells received 6 injections (i.p.) of TA99 mAb (TA99), isotype control (IC) or PBS (PBS). The mean tumor sizes ± SEM (A, C, E) and Kaplan-Meier survival curves (B, D, F) are shown. Kaplan-Meier survival curves for tumor-free TA99-treated C57BL/6N (G) and athymic nude (H) mice after a second injection (s.c.) of 5.10 4 B16F10 cells on the opposite flank (challenge). (I) Tumor-free TA99-treated C57BL/6N mice were challenged (s.c.) with 5.10 5 <t>MC38</t> colon adenocarcinoma cells (MC38). For G, H and I, a group of newly grafted C57BL/6N or athymic nude mice was used as control. *p
    Colon Adenocarcinoma Mc38 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    86
    ATCC murine colon adenocarcinoma cell line mc38
    Treatment of mouse CIK cells with CD3/CD28-coated beads results in increased CKR expression, enhanced trafficking and enhanced anti-tumour effect. ( A ) Levels of the CKR CXCR3 are increased after exposure to beads for 24 h in a day 14 culture (N.B. cellular cytotoxivity was unchanged, data not shown). ( B ) Transwell assay was used to follow movement of CIK cells (day 14, with or without bead treatment) towards lower wells containing recombinant IP-10 (Biolegend). Numbers of cells in the lower wells were determined by flow cytometry after 3 h. ( C ) Trafficking of bead-treated mCIK cells is significantly improved for in vivo delivery to subcutaneous <t>MC38</t> tumours following tail-vein delivery of mCIK cells bound to NHS Cy5.5. CIK delivery to the tumour at 24 h after injection was determined by fluorescence imaging (using the FMT2500, Perkin Elmer) ( n =4). Significantly greater CIK cell fluorescence was found in the tumour for CIK cell preparations that had been pretreated with CD3/CD25-coated beads ( P =0.01). ( D ) Tumour volumes were also measured at the time of killing for these same groups (at day 7 post treatment), and an increased therapeutic effect was seen for bead-treated CIK cells ( n =8, P =0.003).
    Murine Colon Adenocarcinoma Cell Line Mc38, 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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    98
    ATCC mouse crc cell lines
    S100P integrates to SLC2A5 promoter and reduces its methylation levels to promote SLC2A5 transcription. a Representative IHC images of tissue microarray (TMA), showing the positive expression of S100P in the nucleus. Scale bar, 20 μm (40×). The histogram shows the proportion of nuclear S100P-positive or nuclear S100P negative samples in S100P-positive <t>CRC</t> tissues. b IF analysis of subcellular localisation of S100P in SW480 and <t>Caco2</t> cells. Scale bar, 10 μm (100×). c Heatmap shows methylation mass spectrometry sequencing of the SLC2A5 promoter in SW480-LV-S100P or SW480-LV-NC cells. d Schematic representation of the SLC2A5 promoter, showing the translational start site. The five regions used for chromatin immunoprecipitation (ChIP) are also indicated. e ChIP analysis showing the occupancy of S100P on the SLC2A5 promoter in SW480 or Caco2 cells with S100P overexpression or control vector. Data are shown as fold enrichment relative to input and mean ± SEM ( n = 3). *** P
    Mouse Crc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Blocking C5aR signaling promotes the anti-tumor efficacy of checkpoint blockade. (A-B) Tumor cells (3 × 10 4 B16F10 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT or C5aR −/− mice on day 0. The mice were treated with anti-PD-L1 antibodies or the corresponding isotype control on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 10–13 mice/group). (C) Tumor cells (5 × 10 5 MC38 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT or C5aR −/− mice on day 0. The mice were treated with anti-PD-L1 antibodies or the corresponding isotype control on days 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 5–6 mice/group). (D-E) Tumor cells (3 × 10 4 B16F10 cells in 100 μl phosphate-buffered saline) were subcutaneously injected into the flanks of WT mice on day 0. For pharmacological blockade of C5aR signaling, the C5aR antagonist (C5aRa) (PMX53, GL Biochem; 1 mg/kg daily) was subcutaneously injected into C57BL/6 mice on days 4 to 14. PD-L1 antibodies or the corresponding isotype control were injected on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 9–10 mice/group). (F-G) Tumor cells (3 × 10 4 B16F10 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT mice on day 0. For pharmacological blockade of C5aR signaling, the C5aR antagonist (C5aRa) (PMX53, GL Biochem; 1 mg/kg daily) was subcutaneously injected into C57BL/6 mice on days 4 to 14. PD-1 antibodies or the corresponding isotype control were injected on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 10 mice/group). Two-way ANOVA (B, C, E, G) was used to evaluate statistical significance (*p

    Journal: Oncoimmunology

    Article Title: Blocking C5aR signaling promotes the anti-tumor efficacy of PD-1/PD-L1 blockade

    doi: 10.1080/2162402X.2017.1349587

    Figure Lengend Snippet: Blocking C5aR signaling promotes the anti-tumor efficacy of checkpoint blockade. (A-B) Tumor cells (3 × 10 4 B16F10 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT or C5aR −/− mice on day 0. The mice were treated with anti-PD-L1 antibodies or the corresponding isotype control on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 10–13 mice/group). (C) Tumor cells (5 × 10 5 MC38 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT or C5aR −/− mice on day 0. The mice were treated with anti-PD-L1 antibodies or the corresponding isotype control on days 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 5–6 mice/group). (D-E) Tumor cells (3 × 10 4 B16F10 cells in 100 μl phosphate-buffered saline) were subcutaneously injected into the flanks of WT mice on day 0. For pharmacological blockade of C5aR signaling, the C5aR antagonist (C5aRa) (PMX53, GL Biochem; 1 mg/kg daily) was subcutaneously injected into C57BL/6 mice on days 4 to 14. PD-L1 antibodies or the corresponding isotype control were injected on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 9–10 mice/group). (F-G) Tumor cells (3 × 10 4 B16F10 cells in 100 μl of phosphate-buffered saline) were subcutaneously injected into the flanks of WT mice on day 0. For pharmacological blockade of C5aR signaling, the C5aR antagonist (C5aRa) (PMX53, GL Biochem; 1 mg/kg daily) was subcutaneously injected into C57BL/6 mice on days 4 to 14. PD-1 antibodies or the corresponding isotype control were injected on days 4, 7, 10 and 13. Tumor growth was monitored every 2–3 d (n = 10 mice/group). Two-way ANOVA (B, C, E, G) was used to evaluate statistical significance (*p

    Article Snippet: B16F10 cells (mouse melanoma cell line) and MC38 cells (mouse colon cancer cell line) were obtained from American Type Culture Collection (ATCC).

    Techniques: Blocking Assay, Injection, Mouse Assay

    Anti-PD-L1 treatment leads to activation of the complement system. MC38 tumor-bearing mice (∼100 mm 3 ) were intraperitoneally injected with anti-PD-L1 antibodies. The tumors were removed at the indicated time points (n = 5–6 mice/group). (A) C3a and C5a levels in homogenates from tumors and spleens were quantified by ELISA. (B) C1q and C3b/iC3b/C3c staining of tumors and spleens were quantified by IHC. (C) C3b/iC3b/C3c levels of homogenates from tumors and spleens were quantified by ELISA. One-way ANOVA (A) and Multiple t-test (C) were used to evaluate statistical significance (*p

    Journal: Oncoimmunology

    Article Title: Blocking C5aR signaling promotes the anti-tumor efficacy of PD-1/PD-L1 blockade

    doi: 10.1080/2162402X.2017.1349587

    Figure Lengend Snippet: Anti-PD-L1 treatment leads to activation of the complement system. MC38 tumor-bearing mice (∼100 mm 3 ) were intraperitoneally injected with anti-PD-L1 antibodies. The tumors were removed at the indicated time points (n = 5–6 mice/group). (A) C3a and C5a levels in homogenates from tumors and spleens were quantified by ELISA. (B) C1q and C3b/iC3b/C3c staining of tumors and spleens were quantified by IHC. (C) C3b/iC3b/C3c levels of homogenates from tumors and spleens were quantified by ELISA. One-way ANOVA (A) and Multiple t-test (C) were used to evaluate statistical significance (*p

    Article Snippet: B16F10 cells (mouse melanoma cell line) and MC38 cells (mouse colon cancer cell line) were obtained from American Type Culture Collection (ATCC).

    Techniques: Activation Assay, Mouse Assay, Injection, Enzyme-linked Immunosorbent Assay, Staining, Immunohistochemistry

    Long-term anti-tumor immunity in TA99-treated mice relies on a specific T-cell memory response. C57BL/6N (A, B), athymic nude (C, D) and NSG (E, F) mice engrafted with 5.10 4 B16F10 melanoma cells received 6 injections (i.p.) of TA99 mAb (TA99), isotype control (IC) or PBS (PBS). The mean tumor sizes ± SEM (A, C, E) and Kaplan-Meier survival curves (B, D, F) are shown. Kaplan-Meier survival curves for tumor-free TA99-treated C57BL/6N (G) and athymic nude (H) mice after a second injection (s.c.) of 5.10 4 B16F10 cells on the opposite flank (challenge). (I) Tumor-free TA99-treated C57BL/6N mice were challenged (s.c.) with 5.10 5 MC38 colon adenocarcinoma cells (MC38). For G, H and I, a group of newly grafted C57BL/6N or athymic nude mice was used as control. *p

    Journal: Oncoimmunology

    Article Title: PD-1 blockade at the time of tumor escape potentiates the immune-mediated antitumor effects of a melanoma-targeting monoclonal antibody

    doi: 10.1080/2162402X.2017.1353857

    Figure Lengend Snippet: Long-term anti-tumor immunity in TA99-treated mice relies on a specific T-cell memory response. C57BL/6N (A, B), athymic nude (C, D) and NSG (E, F) mice engrafted with 5.10 4 B16F10 melanoma cells received 6 injections (i.p.) of TA99 mAb (TA99), isotype control (IC) or PBS (PBS). The mean tumor sizes ± SEM (A, C, E) and Kaplan-Meier survival curves (B, D, F) are shown. Kaplan-Meier survival curves for tumor-free TA99-treated C57BL/6N (G) and athymic nude (H) mice after a second injection (s.c.) of 5.10 4 B16F10 cells on the opposite flank (challenge). (I) Tumor-free TA99-treated C57BL/6N mice were challenged (s.c.) with 5.10 5 MC38 colon adenocarcinoma cells (MC38). For G, H and I, a group of newly grafted C57BL/6N or athymic nude mice was used as control. *p

    Article Snippet: The C57BL/6 murine melanoma B16F10 and colon adenocarcinoma MC38 cell lines were from ATCC.

    Techniques: Mouse Assay, Injection

    Treatment of mouse CIK cells with CD3/CD28-coated beads results in increased CKR expression, enhanced trafficking and enhanced anti-tumour effect. ( A ) Levels of the CKR CXCR3 are increased after exposure to beads for 24 h in a day 14 culture (N.B. cellular cytotoxivity was unchanged, data not shown). ( B ) Transwell assay was used to follow movement of CIK cells (day 14, with or without bead treatment) towards lower wells containing recombinant IP-10 (Biolegend). Numbers of cells in the lower wells were determined by flow cytometry after 3 h. ( C ) Trafficking of bead-treated mCIK cells is significantly improved for in vivo delivery to subcutaneous MC38 tumours following tail-vein delivery of mCIK cells bound to NHS Cy5.5. CIK delivery to the tumour at 24 h after injection was determined by fluorescence imaging (using the FMT2500, Perkin Elmer) ( n =4). Significantly greater CIK cell fluorescence was found in the tumour for CIK cell preparations that had been pretreated with CD3/CD25-coated beads ( P =0.01). ( D ) Tumour volumes were also measured at the time of killing for these same groups (at day 7 post treatment), and an increased therapeutic effect was seen for bead-treated CIK cells ( n =8, P =0.003).

    Journal: British Journal of Cancer

    Article Title: Manipulating the expression of chemokine receptors enhances delivery and activity of cytokine-induced killer cells

    doi: 10.1038/bjc.2014.140

    Figure Lengend Snippet: Treatment of mouse CIK cells with CD3/CD28-coated beads results in increased CKR expression, enhanced trafficking and enhanced anti-tumour effect. ( A ) Levels of the CKR CXCR3 are increased after exposure to beads for 24 h in a day 14 culture (N.B. cellular cytotoxivity was unchanged, data not shown). ( B ) Transwell assay was used to follow movement of CIK cells (day 14, with or without bead treatment) towards lower wells containing recombinant IP-10 (Biolegend). Numbers of cells in the lower wells were determined by flow cytometry after 3 h. ( C ) Trafficking of bead-treated mCIK cells is significantly improved for in vivo delivery to subcutaneous MC38 tumours following tail-vein delivery of mCIK cells bound to NHS Cy5.5. CIK delivery to the tumour at 24 h after injection was determined by fluorescence imaging (using the FMT2500, Perkin Elmer) ( n =4). Significantly greater CIK cell fluorescence was found in the tumour for CIK cell preparations that had been pretreated with CD3/CD25-coated beads ( P =0.01). ( D ) Tumour volumes were also measured at the time of killing for these same groups (at day 7 post treatment), and an increased therapeutic effect was seen for bead-treated CIK cells ( n =8, P =0.003).

    Article Snippet: Murine colon adenocarcinoma cell line MC38 was purchased from ATCC, and the MC38-luc cell line was derived from MC38 through transfection with a luciferase expression plasmid.

    Techniques: Expressing, Transwell Assay, Recombinant, Flow Cytometry, Cytometry, In Vivo, Injection, Fluorescence, Imaging

    CKR profiles and kinetics in mouse models. ( A ) Mouse CIK cells also displayed a reduction in CKR levels, only over a shorter time in culture (day 10 to day 14), and for a smaller range of CKR (CXCR3 appears critical); data shown are for percentages of CXCR3-positive cells in mCIK cultures expanded from C57/BL6 mice at days 7 and 14 ( n =7, reduction is significant, P =0.0018). CTL assay-determined cellular cytotoxicity also increased over the same time period (MC38-luc cells used as target) (data is average from n =3 preparations). ( B ) Loss of CXCR3 reduces trafficking of CIK cells to their tumour targets and reduced anti-tumour effects in vivo . Mice (C57/BL6) bearing subcutaneous tumours (MC38-luc of 50–100 mm 3 ) were treated with intravenous (tail vein) injection of CIK cells (1 × 10 7 cells) expanded from a C57BL6 CXCR3−/− and GFP+ transgenic mouse or from a GFP+ strain ( n =4 per group). Subsequent tumour trafficking was determined both by flow cytometry on dissociated tumours (left) and through examination of GFP staining in tumour sections post mortem. Significantly less CXCR3−/− CIK cells were found in the tumours, P =0.0014); ( C ) Anti-tumour effects as determined by bioluminescence imaging of MC38-luc cells were determined in the same model ( n =6 per group). *CIK cells produced significantly enhanced therapeutic effects relative to all other groups on days 11, 14 and 18 ( P

    Journal: British Journal of Cancer

    Article Title: Manipulating the expression of chemokine receptors enhances delivery and activity of cytokine-induced killer cells

    doi: 10.1038/bjc.2014.140

    Figure Lengend Snippet: CKR profiles and kinetics in mouse models. ( A ) Mouse CIK cells also displayed a reduction in CKR levels, only over a shorter time in culture (day 10 to day 14), and for a smaller range of CKR (CXCR3 appears critical); data shown are for percentages of CXCR3-positive cells in mCIK cultures expanded from C57/BL6 mice at days 7 and 14 ( n =7, reduction is significant, P =0.0018). CTL assay-determined cellular cytotoxicity also increased over the same time period (MC38-luc cells used as target) (data is average from n =3 preparations). ( B ) Loss of CXCR3 reduces trafficking of CIK cells to their tumour targets and reduced anti-tumour effects in vivo . Mice (C57/BL6) bearing subcutaneous tumours (MC38-luc of 50–100 mm 3 ) were treated with intravenous (tail vein) injection of CIK cells (1 × 10 7 cells) expanded from a C57BL6 CXCR3−/− and GFP+ transgenic mouse or from a GFP+ strain ( n =4 per group). Subsequent tumour trafficking was determined both by flow cytometry on dissociated tumours (left) and through examination of GFP staining in tumour sections post mortem. Significantly less CXCR3−/− CIK cells were found in the tumours, P =0.0014); ( C ) Anti-tumour effects as determined by bioluminescence imaging of MC38-luc cells were determined in the same model ( n =6 per group). *CIK cells produced significantly enhanced therapeutic effects relative to all other groups on days 11, 14 and 18 ( P

    Article Snippet: Murine colon adenocarcinoma cell line MC38 was purchased from ATCC, and the MC38-luc cell line was derived from MC38 through transfection with a luciferase expression plasmid.

    Techniques: Mouse Assay, CTL Assay, In Vivo, Injection, Transgenic Assay, Flow Cytometry, Cytometry, Staining, Imaging, Produced

    S100P integrates to SLC2A5 promoter and reduces its methylation levels to promote SLC2A5 transcription. a Representative IHC images of tissue microarray (TMA), showing the positive expression of S100P in the nucleus. Scale bar, 20 μm (40×). The histogram shows the proportion of nuclear S100P-positive or nuclear S100P negative samples in S100P-positive CRC tissues. b IF analysis of subcellular localisation of S100P in SW480 and Caco2 cells. Scale bar, 10 μm (100×). c Heatmap shows methylation mass spectrometry sequencing of the SLC2A5 promoter in SW480-LV-S100P or SW480-LV-NC cells. d Schematic representation of the SLC2A5 promoter, showing the translational start site. The five regions used for chromatin immunoprecipitation (ChIP) are also indicated. e ChIP analysis showing the occupancy of S100P on the SLC2A5 promoter in SW480 or Caco2 cells with S100P overexpression or control vector. Data are shown as fold enrichment relative to input and mean ± SEM ( n = 3). *** P

    Journal: British Journal of Cancer

    Article Title: S100P contributes to promoter demethylation and transcriptional activation of SLC2A5 to promote metastasis in colorectal cancer

    doi: 10.1038/s41416-021-01306-z

    Figure Lengend Snippet: S100P integrates to SLC2A5 promoter and reduces its methylation levels to promote SLC2A5 transcription. a Representative IHC images of tissue microarray (TMA), showing the positive expression of S100P in the nucleus. Scale bar, 20 μm (40×). The histogram shows the proportion of nuclear S100P-positive or nuclear S100P negative samples in S100P-positive CRC tissues. b IF analysis of subcellular localisation of S100P in SW480 and Caco2 cells. Scale bar, 10 μm (100×). c Heatmap shows methylation mass spectrometry sequencing of the SLC2A5 promoter in SW480-LV-S100P or SW480-LV-NC cells. d Schematic representation of the SLC2A5 promoter, showing the translational start site. The five regions used for chromatin immunoprecipitation (ChIP) are also indicated. e ChIP analysis showing the occupancy of S100P on the SLC2A5 promoter in SW480 or Caco2 cells with S100P overexpression or control vector. Data are shown as fold enrichment relative to input and mean ± SEM ( n = 3). *** P

    Article Snippet: Human CRC cell lines (LoVo, HCT116, RKO, Caco2, HT-29, LS-174-T, SW480 and SW620) and mouse CRC cell lines (MC38 and CT26) were obtained from the American Type Culture Collection (ATCC).

    Techniques: Methylation, Immunohistochemistry, Microarray, Expressing, Mass Spectrometry, Sequencing, Chromatin Immunoprecipitation, Over Expression, Plasmid Preparation

    SLC2A5 promotes CRC cells metastasis in vivo. a The endogenous expression levels of SLC2A5 in MC38 and CT26 cells were detected by western blotting. b Protein expression levels of SLC2A5 in MC38 and CT26 cells that expressed LV-SLC2A5 or LV-NC were detected using western blotting. c Intrasplenic injection model was used to evaluate the in vivo effects of SLC2A5 on tumour metastasis. Representative images of livers derived from C57BL/6 and BALB/c mice injected with LV-SLC2A5 or LV-NC transfected MC38 or CT26 cells are shown. Formation of metastatic nodules at the liver surfaces are summarised in the right panels. Results are presented as mean ± SEM ( n = 6). *** P

    Journal: British Journal of Cancer

    Article Title: S100P contributes to promoter demethylation and transcriptional activation of SLC2A5 to promote metastasis in colorectal cancer

    doi: 10.1038/s41416-021-01306-z

    Figure Lengend Snippet: SLC2A5 promotes CRC cells metastasis in vivo. a The endogenous expression levels of SLC2A5 in MC38 and CT26 cells were detected by western blotting. b Protein expression levels of SLC2A5 in MC38 and CT26 cells that expressed LV-SLC2A5 or LV-NC were detected using western blotting. c Intrasplenic injection model was used to evaluate the in vivo effects of SLC2A5 on tumour metastasis. Representative images of livers derived from C57BL/6 and BALB/c mice injected with LV-SLC2A5 or LV-NC transfected MC38 or CT26 cells are shown. Formation of metastatic nodules at the liver surfaces are summarised in the right panels. Results are presented as mean ± SEM ( n = 6). *** P

    Article Snippet: Human CRC cell lines (LoVo, HCT116, RKO, Caco2, HT-29, LS-174-T, SW480 and SW620) and mouse CRC cell lines (MC38 and CT26) were obtained from the American Type Culture Collection (ATCC).

    Techniques: In Vivo, Expressing, Western Blot, Injection, Derivative Assay, Mouse Assay, Transfection