Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effects of ActRIIA and its downstream signaling proteins on the survival of LUAD. Cox regression was used to analyze the data (n=530). The Kaplan-Meier survival curves represented the impacts of different proteins on the survival of LUAD: (A) ActRIIA, (B) SMAD3, (C) MAPK1 and (D) MAPK3. (E) Sample distribution differences of LUAD data from GSE116959 were analyzed through principal component analysis. (F) Volcano plot of GSE116959 was analyzed using log 2 FC>1 and adjusted P-value <0.05. Upregulated DEGs were shown in red and downregulated DEGs were shown in blue. (G) Statistical analysis results of microarray-based data analysis from GSE116959. LUAD, lung adenocarcinoma; DEGs, differentially expressed genes.

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Microarray

Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effect of activin A on viability and proliferation of A549 cells. (A) The viability of A549 cells was examined by Cell Counting Kit-8 assay after treated with activin A. (B and C) The proliferation of A549 cells was determined by real-time cell analysis in the presence or absence of activin A. (D) The proliferation of A549 cells treated with activin A for 24 was examined by BrdU incorporation. *P<0.05 and **P<0.01 compared with control group (n=3).

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Cell Counting, Cell Analysis, BrdU Incorporation Assay, Control

Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effect of activin A on the apoptosis of A549 cells. (A) The apoptosis of A549 cells treated with activin A for 24 h was assayed by Hoechst fluorescent staining. Typical cells were marked by white arrows. Scale bar, 100 µm. (B) The apoptotic ratio of A549 cells was examined by flow cytometry with YF ® 488-Annexin V and PI staining after treated with activin A for 24 h. *P<0.05 and **P<0.01 compared with control group.

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Staining, Flow Cytometry, Control

Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effect of activin A on expression of endoplasmic reticulum stress pathway-related proteins in A549 cells. Levels of proteins were examined by western blotting in A549 cells after treated with activin A for 24 h. The graph represented the relative levels of proteins in three separate experiments. The levels of proteins were normalized against GAPDH expression, and the results were shown as the fold-increase of the control. **P<0.01 compared with control group.

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Expressing, Western Blot, Control

Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effects of calcium signaling on apoptosis of A549 cells. (A and B) The calcium levels in A549 cells treated with activin A were measured by Fluo-4 fluorescence signal intensity. F0, fluorescence baseline. F, fluorescence intensity after treated with 20 ng/ml activin A. The graph represented the comparison of the peak value of calcium signal normalized to the baseline (F/F0). Typical cells were marked by white arrows. Scale bar, 1,000 µm. (C) BAPTA-AM and ionomycin affected apoptosis of activin A-induced A549 cells. The apoptosis of cells labeled with YF ® 488-Annexin V and PI was tested by flow cytometry. The graph revealed the percentage of apoptotic cells in three separate experiments. **P<0.01 compared with 0.025% DMSO control group; ## P<0.01 compared with 0.025% DMSO + Activin A group.

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Fluorescence, Comparison, Labeling, Flow Cytometry, Control

Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effects of activin A on expression of activin receptors, Smad3 and MAPK signaling proteins in A549 cells. (A) Levels of ActRIA, ActRIB, ActRIIA, ActRIIB and Smad3 mRNAs were determined by reverse transcription-quantitative PCR in A549 cells treated with activin A for 4 h. The graph represented the relative levels of mRNA in three separate experiments. The levels of mRNA were normalized against GAPDH expression, and the results were shown as the fold-increase of the control. (B) Level of ActRIIA protein was examined by western blotting in A549 cells treated with activin A for 4 h. The graph represented the relative levels of proteins in three separate experiments. The levels of ActRIIA protein were normalized against GAPDH, and the results were presented as the fold-increase of the control. (C) Levels of Smad3, p-Smad3, ERK1/2, p-ERK1/2, JNK and p-JNK proteins were determined by western blotting in A549 cells subject to 0–40 ng/ml of activin A for 4 h. The graph represented the relative levels of protein in three separate experiments. The levels of protein were normalized against GAPDH expression, and the results were presented as the fold-increase of the control. **P<0.01 compared with control group. p-, phosphorylated.

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Control, Western Blot

Journal: Oncology Reports

Article Title: Activin A induces apoptosis of human lung adenocarcinoma A549 cells through endoplasmic reticulum stress pathway

doi: 10.3892/or.2023.8688

Figure Lengend Snippet: Effects of ERK inhibitor FR180204 on activin A-induced A549 cell apoptosis. (A) A549 cells were pretreated for 2 h with 1% DMSO or 10 µM FR180204 in 1% DMSO, then treated with 20 ng/ml activin A for 4 h. Levels of p-ERK and ERK protein were examined by western blotting. The graph represented the relative levels of proteins in three separate experiments. The levels of p-ERK and ERK protein were normalized against GAPDH, and the results were shown as the fold-increase of the control. (B) A549 cells were pretreated for 2 h with 1% DMSO or 10 µM FR180204, then treated for 12 h with or without 20 ng/ml activin A. The apoptosis of cells labeled with YF ® 488-Annexin V and PI was assayed by flow cytometry. The graph revealed the percentage of apoptotic cells in three separate experiments. (C) A549 cells were pretreated for 2 h with 1% DMSO or 10 µM FR180204, then treated for 12 h with or without 20 ng/ml activin A. Levels of CHOP and caspase-12 protein were examined by western blotting. The graph represented the relative levels of proteins in three separate experiments. *P<0.05 and **P<0.01 compared with 1% DMSO control group; ## P<0.01 compared with activin A + 1% DMSO control group. p-, phosphorylated.

Article Snippet: The human LUAD cell line A549 ( https://www.cellosaurus.org/CVCL_0023 ; cat. no. CCL-185; American Type Culture Collection) was cultured in RPMI-1640 (cat. no. 11875093; Thermo Fisher Scientific, Inc.) supplemented with 10% fetal bovine serum (FBS) (cat. no. C04001; Shanghai VivaCell Biosciences, Ltd.) and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO 2 .

Techniques: Western Blot, Control, Labeling, Flow Cytometry

Journal: Cancer Cell

Article Title: Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia

doi: 10.1016/j.ccell.2017.03.001

Figure Lengend Snippet: Meis1 Increases Syk Protein Levels in Hoxa9-Driven Leukemia (A) Kaplan-Meier survival curves of mice transplanted with either H- or H/M-transformed myeloid progenitor cells (n = 11). The p value is from a Mantel-Cox test. (B) Volcano plot relating q values for differential protein expression to average normalized SILAC ratios from six biological replicates. Blue (higher expression in H cells) and orange (higher expression in H/M cells) dots indicate significantly regulated proteins (q < 0.01). (C) Heatmap of SILAC ratios for significantly differentially expressed proteins in H and H/M cells across the six biological replicates. (D) Syk protein expression in H and H/M cells by immunoblotting. Actin was used as loading control for relative protein quantification. (E) Relative Syk mRNA expression as measured by qPCR, normalized to GAPDH expression (mean ± SD, n = 3); ns, not significant (two-sided unpaired t test). (F and G) Immunohistochemical staining of HOXA9, MEIS1, and SYK in bone marrow biopsies from patients with AML. SYK expression levels were analyzed in 21 AML cases with high HOXA9 expression (F) and 28 cases with high HOXA9/MEIS1 expression (G). Proportions of SYK expression levels as determined by two independent pathologists using a three-stage staining score are shown. See also Figure S1 , , and .

Article Snippet: CD34+ BM-MNCs were isolated using the human CD34 MultiSort Kit (Miltenyi Biotec) following the manufacturer's instructions.

Techniques: Transformation Assay, Expressing, Multiplex sample analysis, Western Blot, Control, Immunohistochemical staining, Staining

Journal: Cancer Cell

Article Title: Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia

doi: 10.1016/j.ccell.2017.03.001

Figure Lengend Snippet: Meis1 Sensitizes Hoxa9-Driven Leukemia to Syk Inhibition (A) Syk protein expression in H/M cells transfected with either a control shRNA (GL2) or two shRNAs targeting Syk. Actin was used as loading control for relative protein quantification. (B) Percentage of BFP-positive shRNA-expressing cells relative to BFP-negative shRNA-negative cells at the times indicated (mean ± SD, normalized to day 0, n = 3). (C) Same as (A), before and after 5 days of doxycycline (dox) treatment in vivo. (D) Kaplan-Meier survival curves of mice transplanted with H/M cells and treated with doxycycline for 43 days to express non-specific control and Syk-specific shRNA (n = 8). The p value is from a Mantel-Cox test. (E) Percentage of YFP-positive cells from peripheral blood of mice transplanted with H (left) or H/M (right) cells after treating for 7 days with R788 or placebo. Measurements were taken at the indicated time points. The black line connects median values. (F) Kaplan-Meier survival curves of mice transplanted with either H or H/M cells and treated for 20 days with R788 or placebo (n = 11). The p value is from a Mantel-Cox test. (G) Relative HOXA9 and MEIS1 mRNA expression in MV4-11 and KG1 cell lines, and in patient-derived AML cells as measured by qPCR, normalized to GAPDH expression (mean ± SD, n = 3). (H) (p)SYK expression in the patient-derived AML cells in (G). Actin was used as loading control for relative protein quantification. avg, average. (I) Half maximal inhibitory concentration (IC 50 ) for R406 (left) and PRT062607 (right) in patient-derived AML cells as determined by an Annexin V/7-AAD apoptosis assay. Cells were treated for 24 hr and DMSO was used as a control (n = 3). Representative dose-response curves for AML no. 1 (HOXA9 high, MEIS1 low) and AML no. 5 (HOXA9 high, MEIS1 high) are shown at the top. Ticks correspond to estimated IC 50 values. (J) Relative viability of CD34 + bone marrow cells from healthy donors. Cells were treated with either R406 or PRT062607. Blue lines indicate the IC 50 for both SYK inhibitors in H cells. (K) Kaplan-Meier survival curves of NSG mice transplanted with patient-derived AML cells indicated in (G) and treated for 14 days with R788 or vehicle (n = 6 for AML no. 1 and 5; n = 5 for AML no. 2 and 6). The p values are from a Mantel-Cox test. See also Figure S6 .

Article Snippet: CD34+ BM-MNCs were isolated using the human CD34 MultiSort Kit (Miltenyi Biotec) following the manufacturer's instructions.

Techniques: Inhibition, Expressing, Transfection, Control, shRNA, In Vivo, Derivative Assay, Concentration Assay, Apoptosis Assay

Journal: Cancer Cell

Article Title: Hoxa9 and Meis1 Cooperatively Induce Addiction to Syk Signaling by Suppressing miR-146a in Acute Myeloid Leukemia

doi: 10.1016/j.ccell.2017.03.001

Figure Lengend Snippet:

Article Snippet: CD34+ BM-MNCs were isolated using the human CD34 MultiSort Kit (Miltenyi Biotec) following the manufacturer's instructions.

Techniques: Recombinant, Blocking Assay, Lysis, SYBR Green Assay, Reporter Assay, Extraction, Bicinchoninic Acid Protein Assay, cDNA Synthesis, Reverse Transcription, TaqMan microRNA Assay, Mass Spectrometry, Microarray, Gene Expression, Retroviral, Negative Control, Plasmid Preparation, Software, Multiplex sample analysis

Journal: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

Article Title: Reparameterization of PAM50 expression identifies novel breast tumor dimensions and leads to discovery of a genomewide significant breast cancer locus at 12q15

doi: 10.1158/1055-9965.EPI-17-0887

Figure Lengend Snippet: Example Utah high-risk breast cancer pedigree 1817. a. Confirmed and sampled breast cancer cases are indicated in black (55 sampled out of 138 total confirmed UCR cases). Star, triangle and hexagon symbols indicate pedigree branches. b. shows only those cases from (a) with tumor expression data available and indicates PAM50 intrinsic subtype by color. Cases whose tumors are extreme for PC3 are indicated by ‘3’; extreme for PC5 are indicated by ‘5’. c. shows only the PC3-extreme cases from (b). A ‘+’ indicates those cases that share the genomewide significant region at 12q15.

Article Snippet: Gene expression data was generated using the PAM50 RT-qPCR research assay( 12 ) in the Bernard Lab at the Huntsman Cancer Institute( 15 ).

Techniques: Expressing

Journal: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

Article Title: Reparameterization of PAM50 expression identifies novel breast tumor dimensions and leads to discovery of a genomewide significant breast cancer locus at 12q15

doi: 10.1158/1055-9965.EPI-17-0887

Figure Lengend Snippet: Summary of the 11 high-risk Utah pedigrees Tumor count by intrinsic subtype per pedigree.

Article Snippet: Gene expression data was generated using the PAM50 RT-qPCR research assay( 12 ) in the Bernard Lab at the Huntsman Cancer Institute( 15 ).

Techniques:

Journal: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology

Article Title: Reparameterization of PAM50 expression identifies novel breast tumor dimensions and leads to discovery of a genomewide significant breast cancer locus at 12q15

doi: 10.1158/1055-9965.EPI-17-0887

Figure Lengend Snippet: A slice from a three-dimensional scatterplot of PC1, PC2, and PC4 shows that they recapitulate the PAM50 intrinsic subtypes. Reinforcing the constrasts illustrated in Figure 2, PC1 here clearly distinguishes Basal-like from Luminal A tumors. PC2 and PC4 aid in distinguishing HER2-enriched from Luminal B tumors. Combined, these three components define clusters corresponding to the intrinsic subtypes.

Article Snippet: Gene expression data was generated using the PAM50 RT-qPCR research assay( 12 ) in the Bernard Lab at the Huntsman Cancer Institute( 15 ).

Techniques:

Journal: Cell Reports

Article Title: Chromatin accessibility governs the differential response of cancer and T cells to arginine starvation

doi: 10.1016/j.celrep.2021.109101

Figure Lengend Snippet:

Article Snippet: For microarray analysis, RNA was extracted from THP1 or stimulated human CD4+ T cells using the RNeasy Mini kit (QIAGEN).

Techniques: Recombinant, Multiplex sample analysis, Cell Isolation, Activation Assay, Staining, Flow Cytometry, Expressing, Reverse Transcription, Transfection, TA Cloning, Plasmid Preparation, Methylation, Immunoprecipitation, Purification, DNA Library Preparation, Library Quantification, Control, Sequencing, Methylation Sequencing, Amplification, Software

Journal: Cell Reports Medicine

Article Title: Lymph node and tumor-associated PD-L1 + macrophages antagonize dendritic cell vaccines by suppressing CD8 + T cells

doi: 10.1016/j.xcrm.2023.101377

Figure Lengend Snippet: T cell-depleted tumors and maturation trajectories of human DC vaccines (A) CIBERSORT deconvolution across TCGA cancer types. Population abundances were row normalized (C1, n = 1,313; C2, n = 1,210, C3, n = 688; C4, n = 222, C5, n = 2; C6, n = 111). (B) Overall survival of cancer patients’ transcriptome profiled before ICBs treatment (anti-PD-1/CTLA4/PD-L1 ICBs, or combinations thereof) sub-grouped in T cell-depleted C4/C5 tumors (n = 667) and immunogenic C2/C3/C6 tumors (n = 474). Statistics: log rank test. (C) GISTIC 2.0 analysis with indicated 12 genes. Statistical significance: false discovery rate (FDR) < 0.05 (random permutations to background score distribution, BH adjusted). Bladder cancer, n = 136; breast cancer, n = 880; colorectal adenocarcinomas, n = 585; glioblastoma multiforme, n = 580; head and neck cancer, n = 310; kidney cancer, n = 497; acute myeloid leukemia, n = 200; lung adenocarcinoma, n = 357; lung squamous cell carcinoma, n = 344; ovarian cancer, n = 563; endometrial cancer, n = 496. (D–J) Single-cell trajectory reconstruction exploration and mapping (STREAM) DC vaccine trajectory of 93 DC vaccines from 18 prostate adenocarcinoma patients vaccinated with five to eight vaccines. (D) Overview of STREAM DC vaccine trajectory. (E and F) Pseudo-time inferred from DC vaccines’ transcriptome based on variable genes. Principal graph initiated with epg_alpha = 0.01, epg_mu = 0.2, epg_lambda = 0.03, and epg_n_nodes = 5. Dots depict individual DC vaccines and dot color represents (E) patient number or (F) DC vaccine batch/cycle (chi-squared test of independence of variables). (G and H) Signature scores overlaid on the graph as streamplots. Type I IFN/ISG-response signature (G) or mature regulatory DC signature (H) were used as color intensity. (I and J) Patient outcomes were overlaid on the graph as streamplots. PSA doubling time at week 48 (I) and intensity of IFNγ production of peripheral blood mononuclear cell after antigen restimulation (J) were used as color intensity. Here, “n” represents different patients (biological replicates). See also Figure S1 .

Article Snippet: For DC vaccine creation, bone marrow derived DCs were stimulated with dying cancer cells in a 1:1 ratio or with TC1 antigens (i.e., Human Papillomavirus (HPV) e6/e7 epitopes: VYDFAFRDL/DKKQRFHNI, RAHYNIVTF/LCVQSTHVD)), with or without 2.5 ng/mL interferon beta (IFNβ) (R&D systems #8234-MB-010) for 48h.

Techniques: Vaccines

Journal: Cell Reports Medicine

Article Title: Lymph node and tumor-associated PD-L1 + macrophages antagonize dendritic cell vaccines by suppressing CD8 + T cells

doi: 10.1016/j.xcrm.2023.101377

Figure Lengend Snippet: Optimization of DCvax-IT for T cell-depleted tumors (A) Metagene expression for indicated signatures in different subcutaneous tumors (from GEO: GSE85509 ). (B) Flow cytometry analysis of CD45 + fraction from subcutaneous MC38/TC1 tumors on day 23 after injection (percentage of CD8 + of CD3 + cells, n = 6; two-tailed Student’s t test). (C) Tumor volume of TC1-tumor-bearing mice treated with anti-PD-1/CTLA4 on day 9/16 after injection (n = 6; area under curve; one-way ANOVA, Kruskal-Wallis test). (D) Survival of WT, Ripk3 −/− , and Mlkl −/− TC1 cells 24/48 h after treatment (three or four repeats). (E) Cell death of WT and Mlkl −/− TC1 cells 48 h after treatment. p values depict comparison WT vs. Mlkl −/− TC1 cells (n = 3; two-way ANOVA, Sidak’s multiple comparisons test). (F) Schematic overview of the vaccine formulation process. (G and H) Functional analysis of DCs untreated or stimulated with LPS, IFNβ, or with untreated or dying TC1s (with/without IFNβ). (G) Flow cytometry of DC maturation (MHCII + CD86 + frequency of CD11c + ). p values depict comparison vs. UT DCs (n = 3; one-way ANOVA, Dunnett’s multiple comparisons test). (H) IFN-signature expression (qPCR). p values depict comparison vs. UT DCs (n = 3; one sample t test). (I) Flow cytometry of frequency of PD-L1 + PD-L2 + CD200 + of CD11c + cells (moDCs alone/cocultured with untreated/dying WT/ Mlkl −/− TC1 cells). p values depict comparison vs. UT moDCs (n = 4, LPS/IFNβ n = 3; one-way ANOVA, Fischer least significant difference [LSD]). (J) Flow cytometry of frequency of CD11b + F4/80 + in moDCs (alone/cocultured with untreated/dying WT/ Mlkl −/− TC1 cells) or bone-marrow-derived macrophages (BMDMs). p values depict comparison vs. BMDMs (n = 3; one-way ANOVA, Dunnett’s multiple comparisons test). (K) Cytokine secretion via cytokine array. From all values, the background was subtracted. Normalization was done using moDCs + untreated cancer cells (n = 3). Here, “n” represents biological replicates and error bars represent SEM. See also Figures S2 and .

Article Snippet: For DC vaccine creation, bone marrow derived DCs were stimulated with dying cancer cells in a 1:1 ratio or with TC1 antigens (i.e., Human Papillomavirus (HPV) e6/e7 epitopes: VYDFAFRDL/DKKQRFHNI, RAHYNIVTF/LCVQSTHVD)), with or without 2.5 ng/mL interferon beta (IFNβ) (R&D systems #8234-MB-010) for 48h.

Techniques: Expressing, Flow Cytometry, Injection, Two Tailed Test, Comparison, Formulation, Functional Assay, Derivative Assay

Journal: Cell Reports Medicine

Article Title: Lymph node and tumor-associated PD-L1 + macrophages antagonize dendritic cell vaccines by suppressing CD8 + T cells

doi: 10.1016/j.xcrm.2023.101377

Figure Lengend Snippet:

Article Snippet: For DC vaccine creation, bone marrow derived DCs were stimulated with dying cancer cells in a 1:1 ratio or with TC1 antigens (i.e., Human Papillomavirus (HPV) e6/e7 epitopes: VYDFAFRDL/DKKQRFHNI, RAHYNIVTF/LCVQSTHVD)), with or without 2.5 ng/mL interferon beta (IFNβ) (R&D systems #8234-MB-010) for 48h.

Techniques: Control, Recombinant, Lysis, Protease Inhibitor, Western Blot, Staining, Stripping, Liposomes, CRISPR, MTS Assay, ATP Assay, Reverse Transcription, Cell Isolation, Enzyme-linked Immunosorbent Assay, Conjugation Assay, Selection, Drug discovery, Vaccines, Single-cell Analysis, RNA Sequencing, Mutagenesis, Microarray, Purification, Software