Journal: Cancer research

Article Title: Antagonizing integrin beta3 increases immune suppression in cancer

doi: 10.1158/0008-5472.CAN-15-2663

Figure Lengend Snippet: (A) Experimental schema. 1×105 PyMT-BO1-GFP-Luc cells were injected into MFP of 8-week-old female WT mice (n=5). Starting at day 10 after tumor cell injection, mice were treated daily with cilengitide for 5 days. At day 14, all mice were sacrificed. (B) Tumor growth was measured at the indicated time points by BLI. (C) Tumor weight at day 14. (D) TAM populations in tumor tissue were analyzed by FACS. Data represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: For the cilengitide treatment, mice were given cilengitide (5mg/kg, Selleckchem) by intraperitoneal injection for the indicated time point.

Techniques: Injection

Journal: Cancer research

Article Title: Antagonizing integrin beta3 increases immune suppression in cancer

doi: 10.1158/0008-5472.CAN-15-2663

Figure Lengend Snippet: (A) Western blots of p-SYK and SYK in LPS-stimulated WT and Itgb3−/− BMMs. (B) Western blots of p-STAT1 and STAT1 in LPS-stimulated WT and Itgb3−/− BMMs. (C) Western blots of p-STAT1 and STAT1 in LPS-stimulated WT BMMs with or without cilengitide pretreatment. (D) Western blots of p-STAT1 and total STAT1 in WT BMMs overexpressing integrin beta3. M+pMX: macrophage treated with empty pMX vector. M+hβ3: macrophage treated with human integrin beta3 constructed pMX vector. (E) Western blots of p-STAT6 and total STAT6 in IL-4 stimulated WT and Itgb3−/− BMMs. (F) Ym1 mRNA expression after IL-4 treatment of WT and Itgb3−/− BMMs. (G) Itgb3 mRNA expression level after IL-4 treatment in Stat6−/− macrophages. (H) Western blot analysis of integrin beta3 expression in WT, Itgb3−/−, and Stat6−/− BMMs after 5ng/ml IL-4 treatment for 48 hours.

Article Snippet: For the cilengitide treatment, mice were given cilengitide (5mg/kg, Selleckchem) by intraperitoneal injection for the indicated time point.

Techniques: Western Blot, Plasmid Preparation, Construct, Expressing

Journal: Cancer research

Article Title: Antagonizing integrin beta3 increases immune suppression in cancer

doi: 10.1158/0008-5472.CAN-15-2663

Figure Lengend Snippet: (A) PyMT-BO1-GFP-Luc MFP tumor established on β3KOM mice (n=5). From day 10 after tumor cell injection, mice were treated daily with cilengitide for 5 days. Tumor growth was measured at the indicated time points. (B) Experimental schema. 1×105 PyMT-BO1-GFP-Luc cells were injected into MFP of 8-week-old female WT mice at day 0. Anti-CSF1 antibody treatment started on day 6 by i.p. injection of 1mg of antibody per mouse, followed by 0.5mg of antibody on day 9 and day 12. Cilengitide treatment started on day 9 for 5 days with a dosage of 5mg/kg per mouse by i.p. injection (n=7 or 8 per group). (C) Tumor burden was measured by BLI at day 15. (D-G) Tumor-infiltrating myeloid cells and T-cells were measured by FACS at day 15. Data represent mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: For the cilengitide treatment, mice were given cilengitide (5mg/kg, Selleckchem) by intraperitoneal injection for the indicated time point.

Techniques: Injection

Journal: Neoplasia (New York, N.Y.)

Article Title: The Challenges and the Promise of Molecular Targeted Therapy in Malignant Gliomas 1

doi: 10.1016/j.neo.2015.02.002

Figure Lengend Snippet: Select Molecular Targeted Drugs of Malignant Glioma in Clinical Trials

Article Snippet: However, the result of the primary endpoint of the phase III trial (NCT00689221) was reported this year and it did not achieve the expected outcome; newly diagnosed GBM patients with MGMT gene promoter methylation did not live significantly longer when treated with cilengitide plus chemo-radiotherapy (www.merckserono.com).

Techniques:

Journal: Bioengineered

Article Title: Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model

doi: 10.1080/21655979.2022.2029236

Figure Lengend Snippet: Cilengitide decreases cell viability and induces apoptosis of B16 and A375 cells in vitro . (a) RNA sequencing results of normal B16 cells and cilengitide treated B16 cells. (b) Eleven enriched pathways with cilengitide treatment identified by GO analysis. (c) Ten enriched pathways with cilengitide treatment identified using KEGG classification. (d) Viability of B16 and A375 cells treated with cilengitide detected by CCK-8 assay. (e) The IC50 values for cilengitide in B16 and A375 cells. (f) Cell colony numbers of B16 and A375 cells treated with 0, 5, and 10 µg/ml cilengitide. (g) Flow cytometry was used to detect B16 and A375 cells apoptosis after treatment with 5 µg/ml and 10 µg/ml cilengitide. Data were represented as mean ± standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, NS, not significance (Student’s t test). Each experiment was repeated three times.

Article Snippet: Dong and colleagues reported that cilengitide reversed erlotinib resistance by inhibiting the Galectin-3/KRAS/RALB/TBK1/NF-κB signaling pathway in non-small cell lung cancer [ ].

Techniques: In Vitro, RNA Sequencing, CCK-8 Assay, Flow Cytometry, Standard Deviation

Journal: Bioengineered

Article Title: Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model

doi: 10.1080/21655979.2022.2029236

Figure Lengend Snippet: Cilengitide decreases the expression of PD-L1 in B16 and A375 cells . (a and b) Fluorescence microscopic images showing the expression of PD-L1 in B16 and A375 cells treated with or without 5 µg/ml cilengitide for 12 hours. Scale bar: 50 µm. (c and d) The proportion of PD-L1 positive B16 and A375 cells detected by flow cytometry after treatment with 5 µg/ml cilengitide for 12 hours. (e and f) The expressions of STAT3, p-STAT3, and PD-L1 detected by Western blotting in B16 and A375 cells after treatment with 0, 5, 10, and 20 µg/ml cilengitide for 12 hours. Data were represented as mean ± standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, NS, not significance (Student’s t test). Each experiment was repeated three times.

Article Snippet: Dong and colleagues reported that cilengitide reversed erlotinib resistance by inhibiting the Galectin-3/KRAS/RALB/TBK1/NF-κB signaling pathway in non-small cell lung cancer [ ].

Techniques: Expressing, Fluorescence, Flow Cytometry, Western Blot, Standard Deviation

Journal: Bioengineered

Article Title: Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model

doi: 10.1080/21655979.2022.2029236

Figure Lengend Snippet: Cilengitide downregulates the expression of PD-L1 via STAT3 pathway and decreases the expression of PD-L1 in B16 murine melanoma model . (a and b) B16 and A375 cells were treated with blank control, 20 ng/ml IL-6, 5 µg/ml cilengitide, or 20 ng/ml IL-6 plus 5 µg/ml cilengitide for 12 hours. The expressions of STAT3, p-STAT3, and PD-L1 was detected by Western blotting. (c) B16 cells were inoculated subcutaneously into the C57BL/6 mice, and the mice were treated with 50 mg/kg cilengitide for 7 days. Tumor tissues were then isolated and the expression of PD-L1 was detected by Western blotting. (d) The PD-L1 expression of tumor tissues was detected by immunohistochemical staining. Scale bar: 100 µm. Data were represented as mean ± standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, NS, not significance (Student’s t test). Western blotting was repeated three times.

Article Snippet: Dong and colleagues reported that cilengitide reversed erlotinib resistance by inhibiting the Galectin-3/KRAS/RALB/TBK1/NF-κB signaling pathway in non-small cell lung cancer [ ].

Techniques: Expressing, Control, Western Blot, Isolation, Immunohistochemical staining, Staining, Standard Deviation

Journal: Bioengineered

Article Title: Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model

doi: 10.1080/21655979.2022.2029236

Figure Lengend Snippet: Cilengitide enhances the in vivo antitumor effect of anti-PD1 antibody in B16 murine melanoma model . (A, B, and D) Tumor volumes of C57BL/6 mice in different treatment groups (n = 6). (c) Quantified results of tumor weights at day 21 (n = 6). (e) Survival time of mice in different treatment groups (n = 6). (f) Quantified results of mice’s body weight (n = 6). (g) Tumors were detected by bioluminescence assay at 8 and 20 days after tumor implantation (n = 2). Data were represented as mean ± standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, NS, not significance (Student’s t test) and *p < 0.0332, **p < 0.0021, ***p < 0.0002, NS, not significance (Kaplan-Meier survival analysis). The in vivo experiments were repeated three times.

Article Snippet: Dong and colleagues reported that cilengitide reversed erlotinib resistance by inhibiting the Galectin-3/KRAS/RALB/TBK1/NF-κB signaling pathway in non-small cell lung cancer [ ].

Techniques: In Vivo, ATP Bioluminescent Assay, Tumor Implantation, Standard Deviation

Journal: Bioengineered

Article Title: Cilengitide, an αvβ3-integrin inhibitor, enhances the efficacy of anti-programmed cell death-1 therapy in a murine melanoma model

doi: 10.1080/21655979.2022.2029236

Figure Lengend Snippet: Cilengitide potentiates anti-PD1 antibody efficacy by activating CD8 + T cell response . (a) Representative images of immunofluorescence staining of CD3, CD4 and CD8 in tumors (n = 3). Scale bar: 100 µm. (b and c) Quantified results of CD4 + and CD8 + cells in tumors. (d) The contents of granzyme B in tumors determined by ELISA (n = 4). (e) The contents of IFN-γ in tumors determined by ELISA (n = 4). Data were represented as mean ± standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, NS, not significance (Student’s t test).

Article Snippet: Dong and colleagues reported that cilengitide reversed erlotinib resistance by inhibiting the Galectin-3/KRAS/RALB/TBK1/NF-κB signaling pathway in non-small cell lung cancer [ ].

Techniques: Immunofluorescence, Staining, Enzyme-linked Immunosorbent Assay, Standard Deviation