c met inhibitor su11274  (MedChemExpress)

Journal: Cancer Cell International

Article Title: The anti-tumor effects of AZD4547 on ovarian cancer cells: differential responses based on c-Met and FGF19/FGFR4 expression

doi: 10.1186/s12935-024-03235-2

Figure Lengend Snippet: Combination of c-Met inhibitor with AZD4547 induced cell death of AZD4547-resistant cells overexpressing c-Met. ( A ) To determine the pathway signature activity, Gene Set Enrichment Analysis (GSEA) was performed in AZD4547-resistant and -sensitive patient-derived cells. ( B ) Expression of p-c-Met and c-Met was analyzed by western blotting in EOC cells. ( C ) Cell viability was measured in cells treated with SU11274, a c-Met-specific inhibitor, AZD4547, and the combination of SU11274 with AZD4547 in HayA8-MDR and SKOV3-TR cells for 48 h (* p < 0.05, ** p < 0.001). ( D ) Expression of p-c-Met and c-Met was analyzed by western blot in lysates from the same experimental conditions as in ( C ). Expression of p-c-Met was normalized by total c-Met expression using Image J, and the result is shown in the right panel

Article Snippet: The selective FGFR1-3 inhibitor AZD4547, (N-[5-[2-(3,5-dimethoxyphenyl)ethyl]-2 H-pyrazol-3-yl]-4-(3,5-diemthylpiperazin-1-yl) benzamide) (AstraZeneca), the selective potent FGFR4 inhibitor FGF401 (roblitinib) (MedChemExpress), c-Met inhibitor SU11274 (SelleckChem) were resuspended in dimethyl sulfoxide (DMSO) at a concentration of 10 mmol/ml and diluted in culture media.

Techniques: Activity Assay, Derivative Assay, Expressing, Western Blot

Journal: Heliyon

Article Title: Human telomerase reverse transcriptase promotes the epithelial to mesenchymal transition in lung cancer cells by enhancing c-MET upregulation

doi: 10.1016/j.heliyon.2021.e08673

Figure Lengend Snippet: c-MET induced EMT is positively associated with hTERT expression. (A) Western blot showing increased E-cadherin expression and decreased vimentin expression following c-MET knockdown A549 cells. (B) c-MET knocked down A549 cells were starved for 12 h and treated with HGF (20 ng/ml) for 24 h. Western blots show inverse relationship between expression of c-MET and epithelial marker E-cadherin and a direct relationship with mesenchymal marker vimentin. C) hTERT knockdown A549 cells were treated with HGF and analyzed for expression of E-cadherin and vimentin. shRNA targeting hTERT. Western blots show that knocking down hTERT expression promoted the expression of epithelial marker E-cadherin and decreased the mesenchymal protein vimentin in cells. D) Immunofluorescence staining of cytokeratin-18a was done in hTERT knockdown A549 cells treated with HGF. HGF treatment reduced the cytokeratin level, while hTERT-shRNA treatment restored the cytokeratin expression. E) Stably hTERT over-expressing A549 cells were starved and then stimulated by HGF (20 ng/ml), leading to increased expression of vimentin and suppression of E-cadherin synergistically. F) hTERT downregulated A549 cells were treated with the 8 μM SU11274 (c-MET inhibitor), and expression of E-cadherin and vimentin were detected by western blotting. G) Immunoblot analysis of epithelial marker E-cadherin and vimentin following SU11274 (8 μM) treatment in hTERT over-expressing A549 cells showed lower expression of this mesenchymal marker. Full and non-adjusted images of immunoblots were shown in the supplementary material (Figure SM 4)

Article Snippet: HGF was procured from Peprotech and c-MET inhibitor (SU11274) from Santa Cruz.

Techniques: Expressing, Western Blot, Knockdown, Marker, shRNA, Immunofluorescence, Staining, Stable Transfection

Journal: Journal of Cellular and Molecular Medicine

Article Title: Inhibition of c‐MET increases the antitumour activity of PARP inhibitors in gastric cancer models

doi: 10.1111/jcmm.15655

Figure Lengend Snippet: Steady‐state levels of gastric cancer cell lines. Using Western blot assay, steady protein levels of BRCA1, BRCA2 and c‐MET are analysed in primary gastric cancer cell lines HS746T and AGS. Protein levels were normalized against actin

Article Snippet: The c‐MET inhibitor SU11274 (#S9820) and PARP inhibitor NU1025 (#N7287) were obtained from Sigma‐Aldrich.

Techniques: Western Blot

Journal: Journal of Cellular and Molecular Medicine

Article Title: Inhibition of c‐MET increases the antitumour activity of PARP inhibitors in gastric cancer models

doi: 10.1111/jcmm.15655

Figure Lengend Snippet: Low levels of c‐MET partially sensitize GC cell lines in PARP inhibition. A, HS746T/AGS cells, control‐siRNA‐Hs746T/AGS cells and si‐c‐MET Hs746T/AGS cells were exposed to increasing doses (0‐40 µmol/L) of NU1025 for 48 h for determination of cell viability (MTT metabolic activity assay). The protein levels of c‐MET expression (by Western blot analysis) revealed down‐regulation of the c‐MET receptor in both cell lines (HS746T and AGS); (B) HS746T cells, control‐siRNA‐Hs746T cells and si‐BRCA1/2 Hs746T cells were exposed to increasing doses (0‐40 µmol/L) of NU1025 for 48 h for determination of cell viability (MTT metabolic activity assay). The protein levels of BRCA1 and BRCA2 expression (by Western blot analysis) revealed down‐regulation of the BRCA1/2 in HS746T cell line; (C) HS746T cells, control‐siRNA‐Hs746T, siBRCA1/2‐Hs746T and siMET/BRCA1/2‐Hs746T cells were cultured with the indicated concentrations of NU1025 (5, 10 and 20 μmol/L) for 48 h for determination of cell viability (MTT metabolic activity assay). Error bars represent SD

Article Snippet: The c‐MET inhibitor SU11274 (#S9820) and PARP inhibitor NU1025 (#N7287) were obtained from Sigma‐Aldrich.

Techniques: Inhibition, Metabolic Assay, Expressing, Western Blot, Cell Culture

Journal: Journal of Cellular and Molecular Medicine

Article Title: Inhibition of c‐MET increases the antitumour activity of PARP inhibitors in gastric cancer models

doi: 10.1111/jcmm.15655

Figure Lengend Snippet: Co‐inhibition of c‐MET (SU11274) and PARP (NU1025) sensitizes GC cells after knockdown BRCA1/2. Knocking down BRCA1 or BRCA2 sensitizes cells to PARP and c‐MET inhibition in HS746T cells expressing low levels of c‐MET (AGS cells, c‐MET knockdown Hs746T cells) to PARP inhibition. A, HS746T cells, control‐siRNA‐Hs746T cells and siBRCA1/2‐Hs746T (upper panel) and AGS (lower panel) cells were exposed to 5 µmol/L of NU1025 and/or 5 µmol/L of SU11274 for 48 h for determination of cell viability (MTT metabolic activity assay). Results are expressed as percentages. Average values of three experiments ± SD are shown; (B) Western blot analysis of PARP and cl.caspase‐3 in Hs746T‐control‐siRNA, siBRCA1/2‐Hs746T (upper panel) and AGS (lower panel) cell lines. Cells were cultured with the indicated drugs (5 μmol/L NU1025, 5 μmol/L SU11274 alone or in combination for 24 h of treatment). Protein levels were normalized against actin

Article Snippet: The c‐MET inhibitor SU11274 (#S9820) and PARP inhibitor NU1025 (#N7287) were obtained from Sigma‐Aldrich.

Techniques: Inhibition, Expressing, Metabolic Assay, Western Blot, Cell Culture

Journal: Journal of Cellular and Molecular Medicine

Article Title: Inhibition of c‐MET increases the antitumour activity of PARP inhibitors in gastric cancer models

doi: 10.1111/jcmm.15655

Figure Lengend Snippet: NU1025 plus SU11274 increases DNA damage in GC cell line. A, Western blot analysis of γ‐H2AX in Hs746T‐control‐siRNA, siBRCA1/2‐Hs746T and AGS cell lines. Cells were cultured with the indicated drugs (5 μmol/L NU1025, 5 μmol/L SU11274 alone or in combination after 24 h of treatment). Protein levels were normalized against actin; (B) confocal microscope images of two‐dimensional culture of HS746T (left panel) and AGS (right panel) cell lines. Hs746T‐control‐siRNA, siBRCA1/2‐Hs746T and AGS cells were cultured with the indicated drugs and concentrations for 24 h. Representative images of Hs746T and AGS nuclei (DAPI‐blue staining) and of γ‐H2AX (green) are shown in the figure

Article Snippet: The c‐MET inhibitor SU11274 (#S9820) and PARP inhibitor NU1025 (#N7287) were obtained from Sigma‐Aldrich.

Techniques: Western Blot, Cell Culture, Microscopy, Staining

Journal: Journal of Cellular and Molecular Medicine

Article Title: Inhibition of c‐MET increases the antitumour activity of PARP inhibitors in gastric cancer models

doi: 10.1111/jcmm.15655

Figure Lengend Snippet: Effect of combinatorial treatment of c‐MET and PARP inhibition in tumour xenograft (AGS) model. AGS cells were inoculated into SCID mice (5 mice per group) on day 0. Mice were inoculated subcutaneously in the right flank with 0.1 mL PBS containing 3 × 106 AGS human gastric cancer cells. When the tumour volume reached ~ 100 mm3, mice were administered with NU1025 (1 mg/mouse) or SU11274 (1 mg/kg), alone or in combination every 4 d for 20 d. Tumour growth was calculated at the indicated time points. Tumour volume was measured 5 d using a calliper and calculated as (width) 2 × length/2. Photographs of excised AGS tumours after receiving different treatments (control, NU1025, SU11274 and NU1025 + SU11274) were captured at the end of 20 d of therapy (A‐left panel) and AGS tumour size progression as a function of time after administration (A‐right panel). Western blot showing the levels of PARP and cleaved caspase‐3 in the subcutaneous tumour tissues isolated from the mice after 20 d of therapy (B)

Article Snippet: The c‐MET inhibitor SU11274 (#S9820) and PARP inhibitor NU1025 (#N7287) were obtained from Sigma‐Aldrich.

Techniques: Inhibition, Western Blot, Isolation