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Structured Review

Proteintech il1ra
(A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of <t>IL1RA</t> + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.
Il1ra, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 9 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Images

1) Product Images from "IL1RA + Myeloid-derived Suppressor Cells Activate Epithelial-mesenchymal Transition to Facilitate Lymphatic and Hepatic Metastasis in Pancreatic Ductal Carcinoma"

Article Title: IL1RA + Myeloid-derived Suppressor Cells Activate Epithelial-mesenchymal Transition to Facilitate Lymphatic and Hepatic Metastasis in Pancreatic Ductal Carcinoma

Journal: Journal of Clinical and Translational Hepatology

doi: 10.14218/JCTH.2025.00416

(A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of IL1RA + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.
Figure Legend Snippet: (A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of IL1RA + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.

Techniques Used: Derivative Assay, Flow Cytometry, Immunofluorescence, Staining, Gene Expression, Two Tailed Test

(A) Schematic illustration of IL1RN + MDSC–PDAC co-culture system. (B) Transwell migration assays in PANC-1 and ASPC-1 cells treated with normal medium (Control), IL1RA + MDSC-conditioned medium (IL1RA + MDSC CM), or IL1RA + MDSC CM + Axitinib. Scale bar = 50 µm. (C) Western blot analysis of EMT markers (N-cadherin, E-cadherin, ZO-1, Claudin-1) in PANC-1 cells under treatments identical to (B); β-actin was detected as a control. Grayscale was determined using ImageJ. (D) Relative expression of stemness-related mRNA after treatment with IL1RA + MDSC CM or IL1RA + MDSC CM + Axitinib. (E) Representative images of subcutaneous tumors in BALB/c nude mice from the PDX model: Group 1 (Control, tumor tissue only); Group 2 (tumor tissue co-implanted with IL1RN + MDSCs); Group 3 (tumor tissue co-implanted with IL1RN + MDSCs + Axitinib). (F) Excised tumor tissues from (E). (G, H) Tumor weights (G) and volumes (H) from the mouse model presented as bar graphs. (I) Representative H&E staining images of mouse pancreatic tumor tissues. Scale bar = 100 µm. Data are represented as mean ± SD of three independent biological replicates in (B) and four independent replicates in (F and G). Statistical significance was determined by one-way ANOVA with Dunnett’s post-hoc test: ns p ≥ 0.05; * p < 0.05; *** p < 0.001; **** p < 0.0001. PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.
Figure Legend Snippet: (A) Schematic illustration of IL1RN + MDSC–PDAC co-culture system. (B) Transwell migration assays in PANC-1 and ASPC-1 cells treated with normal medium (Control), IL1RA + MDSC-conditioned medium (IL1RA + MDSC CM), or IL1RA + MDSC CM + Axitinib. Scale bar = 50 µm. (C) Western blot analysis of EMT markers (N-cadherin, E-cadherin, ZO-1, Claudin-1) in PANC-1 cells under treatments identical to (B); β-actin was detected as a control. Grayscale was determined using ImageJ. (D) Relative expression of stemness-related mRNA after treatment with IL1RA + MDSC CM or IL1RA + MDSC CM + Axitinib. (E) Representative images of subcutaneous tumors in BALB/c nude mice from the PDX model: Group 1 (Control, tumor tissue only); Group 2 (tumor tissue co-implanted with IL1RN + MDSCs); Group 3 (tumor tissue co-implanted with IL1RN + MDSCs + Axitinib). (F) Excised tumor tissues from (E). (G, H) Tumor weights (G) and volumes (H) from the mouse model presented as bar graphs. (I) Representative H&E staining images of mouse pancreatic tumor tissues. Scale bar = 100 µm. Data are represented as mean ± SD of three independent biological replicates in (B) and four independent replicates in (F and G). Statistical significance was determined by one-way ANOVA with Dunnett’s post-hoc test: ns p ≥ 0.05; * p < 0.05; *** p < 0.001; **** p < 0.0001. PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.

Techniques Used: Co-Culture Assay, Migration, Control, Western Blot, Expressing, Staining, Derivative Assay



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(A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of <t>IL1RA</t> + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.
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(A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of <t>IL1RA</t> + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.
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Fig. 2. Low expression of <t>IL1RA</t> in OSCC and validation of IL1RA overexpression efficiency. A. Expression levels of IL1RA in HNSCC and normal specimens available from the GEPIA database. B. H&E and IHC staining of OSCC and paracancerous specimens in vitro (n=50, scale bar=100 μm). The percentage of low and high IL1RA expressions in OSCC and paracancerous specimens is visualized. C-D. Efficiency of IL1RA overexpression by lentivirus transfection is validated in CAL27 and HN6 cells by RT-qPCR (C) and Western blot (D) in vitro. *P<0.05, and **P<0.01 vs. NC group.
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Fig. 2. Low expression of <t>IL1RA</t> in OSCC and validation of IL1RA overexpression efficiency. A. Expression levels of IL1RA in HNSCC and normal specimens available from the GEPIA database. B. H&E and IHC staining of OSCC and paracancerous specimens in vitro (n=50, scale bar=100 μm). The percentage of low and high IL1RA expressions in OSCC and paracancerous specimens is visualized. C-D. Efficiency of IL1RA overexpression by lentivirus transfection is validated in CAL27 and HN6 cells by RT-qPCR (C) and Western blot (D) in vitro. *P<0.05, and **P<0.01 vs. NC group.
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Image Search Results


(A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of IL1RA + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.

Journal: Journal of Clinical and Translational Hepatology

Article Title: IL1RA + Myeloid-derived Suppressor Cells Activate Epithelial-mesenchymal Transition to Facilitate Lymphatic and Hepatic Metastasis in Pancreatic Ductal Carcinoma

doi: 10.14218/JCTH.2025.00416

Figure Lengend Snippet: (A) tSNE plot showing the four neutrophil-derived MDSC subtypes. (B) The top five expressed genes of IL1RN + MDSCs in the four neutrophil-derived MDSC subsets. (C, D) Representative flow cytometry data and quantification graphs showing the proportion of IL1RA + MDSCs in LNN and LNP PDAC tissues. (E) Representative images of immunofluorescence staining of IL1RA + MDSCs in LNN and LNP PDAC tissues. Scale bar = 100 µm. (F) Trajectory of neutrophil-derived MDSCs along pseudotime in two-dimensional space. (G) Heatmap showing dynamic changes in gene expression along pseudotime. (H) Prognostic analysis of PDAC patients with low or high IL1RA + MDSC recruitment (stratified by the median IL1RA + MDSC proportion in all samples). Kaplan–Meier survival plots of 16 patients are shown. Data are presented as mean ± SD in (D). Statistical differences were assessed using a two-tailed Student’s t -test. LNN, lymph node-negative; LNP, lymph node-positive; PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.

Article Snippet: Primary antibodies included CD11b (Abcam, Cambridge, UK), CD68 (Proteintech, Wuhan, China), MPO (Abcam), IL1RA (Proteintech), and VEGFA (Proteintech).

Techniques: Derivative Assay, Flow Cytometry, Immunofluorescence, Staining, Gene Expression, Two Tailed Test

(A) Schematic illustration of IL1RN + MDSC–PDAC co-culture system. (B) Transwell migration assays in PANC-1 and ASPC-1 cells treated with normal medium (Control), IL1RA + MDSC-conditioned medium (IL1RA + MDSC CM), or IL1RA + MDSC CM + Axitinib. Scale bar = 50 µm. (C) Western blot analysis of EMT markers (N-cadherin, E-cadherin, ZO-1, Claudin-1) in PANC-1 cells under treatments identical to (B); β-actin was detected as a control. Grayscale was determined using ImageJ. (D) Relative expression of stemness-related mRNA after treatment with IL1RA + MDSC CM or IL1RA + MDSC CM + Axitinib. (E) Representative images of subcutaneous tumors in BALB/c nude mice from the PDX model: Group 1 (Control, tumor tissue only); Group 2 (tumor tissue co-implanted with IL1RN + MDSCs); Group 3 (tumor tissue co-implanted with IL1RN + MDSCs + Axitinib). (F) Excised tumor tissues from (E). (G, H) Tumor weights (G) and volumes (H) from the mouse model presented as bar graphs. (I) Representative H&E staining images of mouse pancreatic tumor tissues. Scale bar = 100 µm. Data are represented as mean ± SD of three independent biological replicates in (B) and four independent replicates in (F and G). Statistical significance was determined by one-way ANOVA with Dunnett’s post-hoc test: ns p ≥ 0.05; * p < 0.05; *** p < 0.001; **** p < 0.0001. PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.

Journal: Journal of Clinical and Translational Hepatology

Article Title: IL1RA + Myeloid-derived Suppressor Cells Activate Epithelial-mesenchymal Transition to Facilitate Lymphatic and Hepatic Metastasis in Pancreatic Ductal Carcinoma

doi: 10.14218/JCTH.2025.00416

Figure Lengend Snippet: (A) Schematic illustration of IL1RN + MDSC–PDAC co-culture system. (B) Transwell migration assays in PANC-1 and ASPC-1 cells treated with normal medium (Control), IL1RA + MDSC-conditioned medium (IL1RA + MDSC CM), or IL1RA + MDSC CM + Axitinib. Scale bar = 50 µm. (C) Western blot analysis of EMT markers (N-cadherin, E-cadherin, ZO-1, Claudin-1) in PANC-1 cells under treatments identical to (B); β-actin was detected as a control. Grayscale was determined using ImageJ. (D) Relative expression of stemness-related mRNA after treatment with IL1RA + MDSC CM or IL1RA + MDSC CM + Axitinib. (E) Representative images of subcutaneous tumors in BALB/c nude mice from the PDX model: Group 1 (Control, tumor tissue only); Group 2 (tumor tissue co-implanted with IL1RN + MDSCs); Group 3 (tumor tissue co-implanted with IL1RN + MDSCs + Axitinib). (F) Excised tumor tissues from (E). (G, H) Tumor weights (G) and volumes (H) from the mouse model presented as bar graphs. (I) Representative H&E staining images of mouse pancreatic tumor tissues. Scale bar = 100 µm. Data are represented as mean ± SD of three independent biological replicates in (B) and four independent replicates in (F and G). Statistical significance was determined by one-way ANOVA with Dunnett’s post-hoc test: ns p ≥ 0.05; * p < 0.05; *** p < 0.001; **** p < 0.0001. PDAC, pancreatic ductal adenocarcinoma; MDSCs, myeloid-derived suppressor cells.

Article Snippet: Primary antibodies included CD11b (Abcam, Cambridge, UK), CD68 (Proteintech, Wuhan, China), MPO (Abcam), IL1RA (Proteintech), and VEGFA (Proteintech).

Techniques: Co-Culture Assay, Migration, Control, Western Blot, Expressing, Staining, Derivative Assay

Fig. 2. Low expression of IL1RA in OSCC and validation of IL1RA overexpression efficiency. A. Expression levels of IL1RA in HNSCC and normal specimens available from the GEPIA database. B. H&E and IHC staining of OSCC and paracancerous specimens in vitro (n=50, scale bar=100 μm). The percentage of low and high IL1RA expressions in OSCC and paracancerous specimens is visualized. C-D. Efficiency of IL1RA overexpression by lentivirus transfection is validated in CAL27 and HN6 cells by RT-qPCR (C) and Western blot (D) in vitro. *P<0.05, and **P<0.01 vs. NC group.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 2. Low expression of IL1RA in OSCC and validation of IL1RA overexpression efficiency. A. Expression levels of IL1RA in HNSCC and normal specimens available from the GEPIA database. B. H&E and IHC staining of OSCC and paracancerous specimens in vitro (n=50, scale bar=100 μm). The percentage of low and high IL1RA expressions in OSCC and paracancerous specimens is visualized. C-D. Efficiency of IL1RA overexpression by lentivirus transfection is validated in CAL27 and HN6 cells by RT-qPCR (C) and Western blot (D) in vitro. *P<0.05, and **P<0.01 vs. NC group.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: Expressing, Biomarker Discovery, Over Expression, Immunohistochemistry, In Vitro, Transfection, Quantitative RT-PCR, Western Blot

Fig. 3. IL1RA inhibits the proliferation and migration of OSCC cells in vitro. CAL27 and HN6 cells were transfected with NC and oeIL1RA. A. Cell viability at 0, 24, 48, and 72 h was detected by CCK-8 assay. B. Clone number detected by colony formation assay. C. Cell migration was detected by the cell scratch assay at 0 and 24 h (scale bar=100 μm). *P<0.05, and **P<0.01 vs. NC group.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 3. IL1RA inhibits the proliferation and migration of OSCC cells in vitro. CAL27 and HN6 cells were transfected with NC and oeIL1RA. A. Cell viability at 0, 24, 48, and 72 h was detected by CCK-8 assay. B. Clone number detected by colony formation assay. C. Cell migration was detected by the cell scratch assay at 0 and 24 h (scale bar=100 μm). *P<0.05, and **P<0.01 vs. NC group.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: Migration, In Vitro, Transfection, CCK-8 Assay, Colony Assay, Wound Healing Assay

Fig. 4. IL1RA inhibits tumor growth in OSCC in vivo. Nude mice were subcutaneously implanted with 1 × 106 CAL27 cells transfected with NC and oeIL1RA. A. Gross view of OSCC xenografts at 21 days, and the mean tumor weight and volume. B. The mRNA level of IL1RA in OSCC xenografts of NC group and oeIL1RA group. C. H&E and IHC staining of OSCC xenografts in the NC group and oeIL1RA group (scale bar=100 μm). n=6. *P<0.05, and **P<0.01 vs. NC group.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 4. IL1RA inhibits tumor growth in OSCC in vivo. Nude mice were subcutaneously implanted with 1 × 106 CAL27 cells transfected with NC and oeIL1RA. A. Gross view of OSCC xenografts at 21 days, and the mean tumor weight and volume. B. The mRNA level of IL1RA in OSCC xenografts of NC group and oeIL1RA group. C. H&E and IHC staining of OSCC xenografts in the NC group and oeIL1RA group (scale bar=100 μm). n=6. *P<0.05, and **P<0.01 vs. NC group.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: In Vivo, Transfection, Immunohistochemistry

Fig. 5. IL1RA is associated with oncogenic signaling pathways and type I interferon response in OSCC in vitro. A. Volcano plots visualizing 132 DEGs between CAL27 cells transfected with NC and oeIL1RA. Down-regulated, up-regulated and non-regulated genes were labeled in blue, red, and grey colors, respectively. B. GSEA showed less enriched cancer-related features or processes in CAL27 cells overexpressing IL1RA. C. GSEA showed that IL1RA overexpression was significantly associated with the type I interferon response. D. A Venn diagram visualizing 45 (61.6 %) OSCC patients simultaneously carrying mutations in the IL1RA, IFNA, and IFNB genes in the TCGA dataset.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 5. IL1RA is associated with oncogenic signaling pathways and type I interferon response in OSCC in vitro. A. Volcano plots visualizing 132 DEGs between CAL27 cells transfected with NC and oeIL1RA. Down-regulated, up-regulated and non-regulated genes were labeled in blue, red, and grey colors, respectively. B. GSEA showed less enriched cancer-related features or processes in CAL27 cells overexpressing IL1RA. C. GSEA showed that IL1RA overexpression was significantly associated with the type I interferon response. D. A Venn diagram visualizing 45 (61.6 %) OSCC patients simultaneously carrying mutations in the IL1RA, IFNA, and IFNB genes in the TCGA dataset.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: Protein-Protein interactions, In Vitro, Transfection, Labeling, Over Expression

Fig. 6. DEGs in OSCC cells overexpressing IL1RA are involved in multiple interferon response processes. A. GO enrichment analysis showed that over expression of IL1RA was associated with the type I interferon response in OSCC, with a positive correlation. B. The analysis in the Reactome Pathway Database showed that overexpression of IL1RA was associated with interferon signaling pathways, including the interferon α/βand interferon γ signaling pathways.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 6. DEGs in OSCC cells overexpressing IL1RA are involved in multiple interferon response processes. A. GO enrichment analysis showed that over expression of IL1RA was associated with the type I interferon response in OSCC, with a positive correlation. B. The analysis in the Reactome Pathway Database showed that overexpression of IL1RA was associated with interferon signaling pathways, including the interferon α/βand interferon γ signaling pathways.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: Over Expression, Protein-Protein interactions

Fig. 7. Overexpression of IL1RA up-regulates type I interferon proteins in OSCC in vitro. A. H&E (the first lane) and IHC staining (the latter three lanes) of IFNA and IFNB in OSCC specimens of the high and low IL1RA expression groups (n=30, scale bar=100 μm). B-C. The mRNA (B) and protein expressions (C) of IFNA and IFNB in OSCC specimens of the high and low IL1RA expression groups. *P<0.05, and **P<0.01 vs. NC group.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 7. Overexpression of IL1RA up-regulates type I interferon proteins in OSCC in vitro. A. H&E (the first lane) and IHC staining (the latter three lanes) of IFNA and IFNB in OSCC specimens of the high and low IL1RA expression groups (n=30, scale bar=100 μm). B-C. The mRNA (B) and protein expressions (C) of IFNA and IFNB in OSCC specimens of the high and low IL1RA expression groups. *P<0.05, and **P<0.01 vs. NC group.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: Over Expression, In Vitro, Immunohistochemistry, Expressing

Fig. 8. IL1RA promotes the expressions of IFNA and IFNB in the OSCC xenografts and their release in OSCC cells. A. IHC staining of positive expressions of IFNA and IFNB in OSCC xenografts of oeIL1RA group and NC group in vivo (scale bar=100 μm). B. The mRNA levels of IFNA and IFNB in OSCC xenografts of the oeIL1RA group and NC group in vivo. C. ELISA showed contents of IFNA and IFNB in the cell supernatant of the oeIL1RA group and NC group in vitro. *P<0.05, and **P<0.01 vs. NC group.

Journal: Translational oncology

Article Title: IL1RA inhibits the progression of oral squamous cell carcinoma by mediating type Ⅰ interferon response.

doi: 10.1016/j.tranon.2025.102428

Figure Lengend Snippet: Fig. 8. IL1RA promotes the expressions of IFNA and IFNB in the OSCC xenografts and their release in OSCC cells. A. IHC staining of positive expressions of IFNA and IFNB in OSCC xenografts of oeIL1RA group and NC group in vivo (scale bar=100 μm). B. The mRNA levels of IFNA and IFNB in OSCC xenografts of the oeIL1RA group and NC group in vivo. C. ELISA showed contents of IFNA and IFNB in the cell supernatant of the oeIL1RA group and NC group in vitro. *P<0.05, and **P<0.01 vs. NC group.

Article Snippet: Slices were then incubated with diluted primary antibodies against IL1RA (NBP1-32568, Novusbio, 1:600), E-Cadherin (#13116, CST, 1:400), N-Cadherin (#3195, CST, 1:100), Vimentin (#5741, CST, 1:100), IFNA (18013-AP, Proteintech, 1:400), and IFNB (27506-AP, Proteintech, 1:400) overnight at 4◦ C, and the secondary antibody (horseradish peroxidase-labeled goat antirabbit) at room temperature for 2 h. Cell nuclei were dyed with a DAB staining solution.

Techniques: Immunohistochemistry, In Vivo, Enzyme-linked Immunosorbent Assay, In Vitro