Journal: BMC Cancer

Article Title: No preclinical rationale for IGF1R directed therapy in chondrosarcoma of bone

doi: 10.1186/s12885-016-2522-8

Figure Lengend Snippet: a-b qRT-PCR and western blot analyses, respectively, reveal heterogeneous expression of IGF pathway members in chondrosarcoma cell lines. c Immunoprecipitation with IRS1 followed by a western blot for phospho-IRS1 reveals pathway activity in two out of three chondrosarcoma cell lines tested. d Evaluation of IGF1R downstream targets reveals an effect of OSI-906 on IGF1R and pAkt but not on pS6 and disphosphorylated ERK-1&2. Cell lines were treated for 72 hours with DMSO, 1 μM OSI-906 and/or 50 ng/ml IGF1

Article Snippet: The IGF1R inhibitors OSI-906, NVP-ADW742 and GSK1838705A were purchased from Selleck Chemicals LCC (see Additional file : Table S1 for properties) and dissolved in DMSO in a concentration of 10 mM.

Techniques: Quantitative RT-PCR, Western Blot, Expressing, Immunoprecipitation, Activity Assay

Journal: BMC Cancer

Article Title: No preclinical rationale for IGF1R directed therapy in chondrosarcoma of bone

doi: 10.1186/s12885-016-2522-8

Figure Lengend Snippet: Relative cell viability of 72 hours of treatment with IGF1R/IR inhibitors. a - b OSI-906 does not inhibit chondrosarcoma cell viability, even in the presence of IGF1. c - d IGF1R inhibitors NVP-ADW742 and GSK1838705A do not inhibit chondrosarcoma cell viability

Article Snippet: The IGF1R inhibitors OSI-906, NVP-ADW742 and GSK1838705A were purchased from Selleck Chemicals LCC (see Additional file : Table S1 for properties) and dissolved in DMSO in a concentration of 10 mM.

Techniques:

Journal: BMC Cancer

Article Title: No preclinical rationale for IGF1R directed therapy in chondrosarcoma of bone

doi: 10.1186/s12885-016-2522-8

Figure Lengend Snippet: IGF1R expression is high in chondrosarcoma cell lines but low in primary tumours. a IGF1R expression in chondrosarcoma cell line JJ012. b and d IGF1R expression in L835 cell line and primary tumour, respectively. c a conventional chondrosarcoma sample that was classified as weak IGF1R staining. Black bars represent 50 μm

Article Snippet: The IGF1R inhibitors OSI-906, NVP-ADW742 and GSK1838705A were purchased from Selleck Chemicals LCC (see Additional file : Table S1 for properties) and dissolved in DMSO in a concentration of 10 mM.

Techniques: Expressing, Staining

Journal: BMC Cancer

Article Title: No preclinical rationale for IGF1R directed therapy in chondrosarcoma of bone

doi: 10.1186/s12885-016-2522-8

Figure Lengend Snippet: Immunohistochemistry demonstrates only weak IGF1R expression in uncultured cartilage tumours

Article Snippet: The IGF1R inhibitors OSI-906, NVP-ADW742 and GSK1838705A were purchased from Selleck Chemicals LCC (see Additional file : Table S1 for properties) and dissolved in DMSO in a concentration of 10 mM.

Techniques: Immunohistochemistry, Expressing

Journal: Pharmacological research

Article Title: Ginsenoside F1 promotes angiogenesis by activating the IGF-1/IGF1R pathway.

doi: 10.1016/j.phrs.2019.04.021

Figure Lengend Snippet: Fig. 6. The pro-angiogenic effects of ginsenoside depend on IGF1R activation. (A–B) GF1 restored the OSI-906-induced decrease in the phosphorylation of IGF1R at Tyr1135 and Tyr980 in HUVECs. HUVECs were pretreated with OSI-906 (1 μM) for 3 h and then treated with or without GF1 (40 μM) for 8 h. The quantitative analysis of Western blots is shown. GAPDH served as the loading control. The quantitative data are presented as the p-IGF1R (Tyr1135)/ IGF1R and p- IGF1R (Tyr980)/IGF1R ratios. OSI-906 alleviated the GF1-stimulated mobility in HUVECs. (C-D) Scratch-wounded monolayers of HUVECs were treated with GF1 (40 μM) for 8 h in the presence or absence of OSI-906 (2 μM). Images were photographed at 0 and 8 h. Quantification of the wound width is shown. (E–F) HUVECs were suspended in serum-free ECM, added to the upper chamber of the Transwell, and the lower chamber was filled with ECM containing GF1 (40 μM) with or without OSI-906 (2 μM). The migrated cells were photographed at 12 h. Quantification of the number of migrated cells is shown. (G–H) The upper chamber was coated with diluted Matrigel and the subsequent procedures were to the same as the Transwell migration assay. Quantification of the number of invaded cells is shown. (I–J) GF1- induced endothelial tube formation was attenuated by the OSI-906 treatment. HUVECs were pretreated with OSI-906 (2 μM) for 3 h, trypsinized and seeded in Matrigel-coated 96-well plates, and treated with or without GF1 (40 μM) for 6 h. The tubes were observed and photographed 6 h after the GF1 treatment. Quantification of the number of tubes is shown. Representative images are shown; scale bars: 400 μm (C), 100 μm (E and G) and 200 μm (I); NS represents no significance. The data are presented mean ± SEM (n = 3). *P < 0.05, **P < 0.01, and ***P < 0.001 compared with the control group, and #P < 0.05, ##P < 0.01, and ###P < 0.001 compared with the GF1-treated group.

Article Snippet: The IGF1R inhibitor (OSI-906) was purchased from Medchemexpress (Monmouth Junction, NJ, USA).

Techniques: Activation Assay, Phospho-proteomics, Western Blot, Control, Transwell Migration Assay