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epha2 function  (MedChemExpress)
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MedChemExpress epha2 function
Expression of <t>EphA2</t> and its association with VM formation induced by CAF-CM in gastric cancer cells. (A) Explant cultures of CAFs and NF after two weeks. (B) Cultured CAFs at passage 5 were confirmed by positive staining for vimentin and α-SMA. The capability of VM formation in (C) SNU216 and (D) AGS gastric cancer cells was observed following a 24 h-incubation with CAF-CM (50%). (E) Magnified view of the white box in (D). Asterisks indicate micro vessel-like channel structures lined by AGS cells. Scale bars, 100 µm. (F) Western blot images for EphA2 and phosphorylated EphA2 (serine-residue) in five different gastric adenocarcinoma cell lines. EphA2, erythropoietin-producing human hepatocellular receptor A2; VM, vasculogenic mimicry; CAF, cancer-associated fibroblast; CM, conditioned-medium; NF, normal gastric fibroblast; α-SMA, α smooth muscle actin.
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Expression of EphA2 and its association with VM formation induced by CAF-CM in gastric cancer cells. (A) Explant cultures of CAFs and NF after two weeks. (B) Cultured CAFs at passage 5 were confirmed by positive staining for vimentin and α-SMA. The capability of VM formation in (C) SNU216 and (D) AGS gastric cancer cells was observed following a 24 h-incubation with CAF-CM (50%). (E) Magnified view of the white box in (D). Asterisks indicate micro vessel-like channel structures lined by AGS cells. Scale bars, 100 µm. (F) Western blot images for EphA2 and phosphorylated EphA2 (serine-residue) in five different gastric adenocarcinoma cell lines. EphA2, erythropoietin-producing human hepatocellular receptor A2; VM, vasculogenic mimicry; CAF, cancer-associated fibroblast; CM, conditioned-medium; NF, normal gastric fibroblast; α-SMA, α smooth muscle actin.

Journal: Oncology Letters

Article Title: Role of EphA2-PI3K signaling in vasculogenic mimicry induced by cancer-associated fibroblasts in gastric cancer cells

doi: 10.3892/ol.2019.10677

Figure Lengend Snippet: Expression of EphA2 and its association with VM formation induced by CAF-CM in gastric cancer cells. (A) Explant cultures of CAFs and NF after two weeks. (B) Cultured CAFs at passage 5 were confirmed by positive staining for vimentin and α-SMA. The capability of VM formation in (C) SNU216 and (D) AGS gastric cancer cells was observed following a 24 h-incubation with CAF-CM (50%). (E) Magnified view of the white box in (D). Asterisks indicate micro vessel-like channel structures lined by AGS cells. Scale bars, 100 µm. (F) Western blot images for EphA2 and phosphorylated EphA2 (serine-residue) in five different gastric adenocarcinoma cell lines. EphA2, erythropoietin-producing human hepatocellular receptor A2; VM, vasculogenic mimicry; CAF, cancer-associated fibroblast; CM, conditioned-medium; NF, normal gastric fibroblast; α-SMA, α smooth muscle actin.

Article Snippet: To block the EphA2 function of gastric cancer cells, a novel EphA2 receptor inhibitor ALW-II-41-27 (MedChem Express) was used.

Techniques: Expressing, Cell Culture, Staining, Incubation, Western Blot, Residue

EphA2-inhibition abrogates VM formation promoted by CAF-CM in gastric cancer cells. AGS gastric cancer cells were treated with (A) CAF-CM (50%) and (C) CAF-CM (100%) with or without ALW-II-41-27 (1 µM) on a Matrigel matrix for 24 h. Representative images of VM formation in each experimental group. Scale bars, 100 µm. Statistical analysis of the number of tubules and intersections among the (B) CAF-CM (50%) and (D) CAF-CM (100%) groups. Data are presented as the mean ± standard deviation of ≥3 independent experiments. *P<0.001 vs. control; # P<0.001 vs. CAF-CM. EphA2, erythropoietin-producing human hepatocellular receptor A2; CON, DMEM-treated AGS cells; NF, normal gastric fibroblast; CAF, cancer-associated fibroblast; CM, conditioned-medium; VM, vasculogenic mimicry; ALW, ALW-II-41-27.

Journal: Oncology Letters

Article Title: Role of EphA2-PI3K signaling in vasculogenic mimicry induced by cancer-associated fibroblasts in gastric cancer cells

doi: 10.3892/ol.2019.10677

Figure Lengend Snippet: EphA2-inhibition abrogates VM formation promoted by CAF-CM in gastric cancer cells. AGS gastric cancer cells were treated with (A) CAF-CM (50%) and (C) CAF-CM (100%) with or without ALW-II-41-27 (1 µM) on a Matrigel matrix for 24 h. Representative images of VM formation in each experimental group. Scale bars, 100 µm. Statistical analysis of the number of tubules and intersections among the (B) CAF-CM (50%) and (D) CAF-CM (100%) groups. Data are presented as the mean ± standard deviation of ≥3 independent experiments. *P<0.001 vs. control; # P<0.001 vs. CAF-CM. EphA2, erythropoietin-producing human hepatocellular receptor A2; CON, DMEM-treated AGS cells; NF, normal gastric fibroblast; CAF, cancer-associated fibroblast; CM, conditioned-medium; VM, vasculogenic mimicry; ALW, ALW-II-41-27.

Article Snippet: To block the EphA2 function of gastric cancer cells, a novel EphA2 receptor inhibitor ALW-II-41-27 (MedChem Express) was used.

Techniques: Inhibition, Standard Deviation, Control

Silencing of the EphA2 gene suppresses the VM forming ability of gastric cancer cells. (A) Representative images of VM formation in AGS cells transfected with siCON or siEphA2 for 24 and 48 h, in either NF-CM or CAF-CM (50%). Scale bars, 100 µm. (B) Graphs present the number of tubules and intersections in each experimental group. (C) Western blot images of EphA2, MMP2, VEGF-A and VE-cadherin expression in siCON and siEphA2 AGS cells. (D) Graphs presenting the protein expression levels of EphA2, MMP2, VEGF-A and VE-cadherin. Mean ± standard deviation from three independent experiments. *P<0.001 vs. siCON. EphA2, erythropoietin-producing human hepatocellular receptor A2; VM, vasculogenic mimicry; CON, non-treated AGS cells; siRNA, small interfering RNA; siCON, non-silencing siRNA; siEphA2, siRNA-EphA2; VE-cad, VE-cadherin; NF, normal gastric fibroblasts; CM, conditioned medium; CAF, cancer-associated fibroblasts; MMP2, matrix metalloproteinase 2; VEGF-A, vascular endothelial growth factor A.

Journal: Oncology Letters

Article Title: Role of EphA2-PI3K signaling in vasculogenic mimicry induced by cancer-associated fibroblasts in gastric cancer cells

doi: 10.3892/ol.2019.10677

Figure Lengend Snippet: Silencing of the EphA2 gene suppresses the VM forming ability of gastric cancer cells. (A) Representative images of VM formation in AGS cells transfected with siCON or siEphA2 for 24 and 48 h, in either NF-CM or CAF-CM (50%). Scale bars, 100 µm. (B) Graphs present the number of tubules and intersections in each experimental group. (C) Western blot images of EphA2, MMP2, VEGF-A and VE-cadherin expression in siCON and siEphA2 AGS cells. (D) Graphs presenting the protein expression levels of EphA2, MMP2, VEGF-A and VE-cadherin. Mean ± standard deviation from three independent experiments. *P<0.001 vs. siCON. EphA2, erythropoietin-producing human hepatocellular receptor A2; VM, vasculogenic mimicry; CON, non-treated AGS cells; siRNA, small interfering RNA; siCON, non-silencing siRNA; siEphA2, siRNA-EphA2; VE-cad, VE-cadherin; NF, normal gastric fibroblasts; CM, conditioned medium; CAF, cancer-associated fibroblasts; MMP2, matrix metalloproteinase 2; VEGF-A, vascular endothelial growth factor A.

Article Snippet: To block the EphA2 function of gastric cancer cells, a novel EphA2 receptor inhibitor ALW-II-41-27 (MedChem Express) was used.

Techniques: Transfection, Western Blot, Expressing, Standard Deviation, Small Interfering RNA