kinase inhibitors sunitinib malate  (MedChemExpress)

Journal: Cell Death & Disease

Article Title: Novel engineered, membrane-localized variants of vascular endothelial growth factor (VEGF) protect retinal ganglion cells: a proof-of-concept study

doi: 10.1038/s41419-018-1049-0

Figure Lengend Snippet: a Representative immunocytochemistry showing VEGFR2 (red) expression and colocalization with eVEGF-38, eVEGF-53, VEGF189 (anti-Myc tag, green), or GFP (anti-GFP, green) on the cell bodies, neurites and axons of primary RGC at DIV 3. Note the lower levels of VEGFR2 expression and the lack of long neurites and axons in the RGC-expressing GFP. Scale bar = 20 µm. b Left, representative immunocytochemical localization of eVEGF-38, eVEGF-53, and VEGF189 (anti-Myc tag, green) outlining neurites and axons of RGC, in the presence or absence of the VEGFR2 inhibitor Sunitinib malate (1 μM) or the PI3K/AKT inhibitor LY294002 (LY, 10 μM), 3 days after AAV transduction. Scale bar = 20 µm, UT = untreated. Right, quantification of total neurite length per RGC in the presence or absence of Sunitnib malate or LY294002. *** P < 0.001 compared with the corresponding untreated (UT) control, unpaired two-tailed t test, n = 15; five different fields from three independent experiments. Data = mean ± SEM. All RGC were isolated from P3 mice

Article Snippet: To determine the roles of VEGFR2 activation and PI3K/Akt signaling in neurite outgrowth, RGC were treated with the VEGFR2-selective small-molecule receptor tyrosine kinase inhibitor sunitinib malate (1 μM, Selleck Chemicals, Houston, TX) or the PI3K small-molecule inhibitor LY294002 (1 μM, Cell Signaling Technology) at DIV 2 for 24 h. Apoptotic cells were detected using the In Situ Cell Death Detection Kit (TUNEL, Roche) according to manufacturer’s instructions.

Techniques: Immunocytochemistry, Expressing, Transduction, Control, Two Tailed Test, Isolation

Journal: Human molecular genetics

Article Title: High-throughput screening uncovers miRNAs enhancing glioblastoma cell susceptibility to tyrosine kinase inhibitors.

doi: 10.1093/hmg/ddx323

Figure Lengend Snippet: Figure 1. MiR-302/520 miRNA family increases susceptibility of GBM cells to sunitinib treatment. a) Overview

Article Snippet: Temozolomide and the multitargeted tyrosine kinase inhibitors sunitinib malate and axitinib were acquired from Selleckchem (Houston, USA) and stored at 20 C in DMSO.

Techniques:

Journal: Human molecular genetics

Article Title: High-throughput screening uncovers miRNAs enhancing glioblastoma cell susceptibility to tyrosine kinase inhibitors.

doi: 10.1093/hmg/ddx323

Figure Lengend Snippet: Figure 3. Combination of miRNA-302a/520b expression with multitargeted tyrosine kinase inhibitors decreases GBM cell viability. U87 and DBTRG cells were transfected with 50 nM of miRNA-302a, miR-520b or

Article Snippet: Temozolomide and the multitargeted tyrosine kinase inhibitors sunitinib malate and axitinib were acquired from Selleckchem (Houston, USA) and stored at 20 C in DMSO.

Techniques: Expressing, Transfection

Journal: Human molecular genetics

Article Title: High-throughput screening uncovers miRNAs enhancing glioblastoma cell susceptibility to tyrosine kinase inhibitors.

doi: 10.1093/hmg/ddx323

Figure Lengend Snippet: Figure 5. Cellular DNA content increases upon miR-302a transfection and treatment with multitargeted tyrosine kinase inhibitors. Cells were incubated with miR-302a or control miRNA (cel-miR-239b) mimics for

Article Snippet: Temozolomide and the multitargeted tyrosine kinase inhibitors sunitinib malate and axitinib were acquired from Selleckchem (Houston, USA) and stored at 20 C in DMSO.

Techniques: Transfection, Incubation, Control

Journal: Cancer Biology & Therapy

Article Title: Anti-angiogenic treatment promotes triple-negative breast cancer invasion via vasculogenic mimicry

doi: 10.1080/15384047.2017.1294288

Figure Lengend Snippet: Discontinuation of sunitinib promotes TNBC tumor regrowth and invasion. (A) Effects of sunitinib on the tumor volume of TNBC and non-TNBC cells. There wa sno significant difference in tumor volume when the treatment started. After mice were treated with sunitinib for one week, both the TNBC MDA-MB-231 tumors and the non-TNBC MCF-7 tumors in the treatment groups were smaller than those in the control groups. The sunitinib-treated TNBC MDA-MB-231 tumors regrew after treatment discontinuation, while the discontinuation had no significant effect on the tumor volume of the non-TNBC MCF-7 tumors. (B) H&E staining indicated that the TNBC MDA-MB-231 tumor cells invaded into adipose tissue (arrows) and skeletal muscle tissue (arrow heads) after treatment discontinuation. There was no aggressive behavior in the non-TNBC MCF-7 tumors. (C) IHC for MMP2 staining shows that TNBC MDA-MB-231 tumors after treatment was stopped expressed a higher level of MMP2 than tumors during the sunitinib treatment. There was nodifferenceinMMP2 expression in the non-TNBC MCF-7 tumors between the sunitinib treatment and after sunitinib was discontinued. (D) Quantification of MMP2 expression in the different groups. The scale bar represents 100 μm, and the error bar indicates the standard deviation (SD). *P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The VEGF receptor tyrosine kinase inhibitor sunitinib malate (S-8803) was purchased from LC Laboratories (Boston, USA).

Techniques: Control, Staining, Expressing, Standard Deviation

Journal: Cancer Biology & Therapy

Article Title: Anti-angiogenic treatment promotes triple-negative breast cancer invasion via vasculogenic mimicry

doi: 10.1080/15384047.2017.1294288

Figure Lengend Snippet: Effects of sunitinib treatment on the expression of EMT-associated transcription factors in TNBC tumors. (A) IHC staining for VE-cadherin, Twist1, Snail and Slug. VE-cadherin is upregulated in the sunitinib-treated MDA-MB-231 tumors compared with the placebo-treated MDA-MB-231 tumors. Sunitinib increased Twist1 expression in the MDA-MB-231 tumors, and Twist1 localized to the nucleus in the treatment group. There was no change observed in the MCF-7 groups. Sunitinib did not affect the expression of Snail and Slug in the TNBC MDA-MB-231 tumors and the non-TNBC MCF-7 tumors. (B) Quantification of VE-cadherin expression in the different groups. (C)Quantification of Twist1 expression in the different groups. (D) Quantification of Slug expression in the different groups. The scale bar indicates 100 μm, and the error bar indicates the standard deviation (SD). * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: The VEGF receptor tyrosine kinase inhibitor sunitinib malate (S-8803) was purchased from LC Laboratories (Boston, USA).

Techniques: Expressing, Immunohistochemistry, Standard Deviation

Journal: Cancer Biology & Therapy

Article Title: Anti-angiogenic treatment promotes triple-negative breast cancer invasion via vasculogenic mimicry

doi: 10.1080/15384047.2017.1294288

Figure Lengend Snippet: Effects of sunitinib treatment on the microcirculation patterns in TNBC tumors. (A) PAS and endomucin double staining in TNBCMDA-MB-231 and non-TNBC MCF-7 tumors. There were VM channels formed by PAS-positive molecules and tumor cells in the human TNBCMDA-MB-231 tumors, whereas no VM channels were observed in the human non-TNBC MCF-7 tumors. Growth of endothelium-dependent vessels in the TNBC MDA-MB-231 tumors was blocked by sunitinib, during which the number of VM channels significantly increased. Endothelium-dependent vessel growth rebounded in MDA-MB-231 tumors after treatment discontinuation, but there was no significant difference in the number of endothelium-dependent vessels between sunitinib-treated and post-treatment non-TNBC MCF-7 tumors. (B)Quantification of VM channels in the different groups. (C)Quantification of endothelium-dependent vessels in the different groups. (D)Hypoxia and endomucin double staining inTNBCMDA-MB-231 and non-TNBC MCF-7 tumors. There were more hypoxic regions in the sunitinib-treatedMDA-MB-231 tumors compared with those in the other groups when the endothelium-dependent vessels are inhibited. After treatment discontinuation, the hypoxic area in the MDA-MB-231 tumors decreased after the endothelium-dependent vessels rebounded. The hypoxic area in the MCF-7 tumors was similar in the sunitinib-treated and discontinued groups. (E)Quantification of the hypoxic area in the different groups. The scale bar indicates 100 μm, and the error bar indicates the standard deviation (SD). * P < 0.05, **P < 0.01, ***P < 0.001.

Article Snippet: The VEGF receptor tyrosine kinase inhibitor sunitinib malate (S-8803) was purchased from LC Laboratories (Boston, USA).

Techniques: Double Staining, Standard Deviation