egfr v  (MedChemExpress)

Journal: Archives of Dermatological Research

Article Title: EGFR influences the resistance to targeted therapy in BRAF V600E melanomas by regulating the ferroptosis process

doi: 10.1007/s00403-025-03895-8

Figure Lengend Snippet: Construction of A375 cells with high EGFR expression and validation of their drug resistance in vitro. A, B,C . High expression of EGFR was confirmed by fluorescence detection (green is GFP), PCR and Western blot (WB) in A375 EGFR+ stable cell line, * indicates P < 0.05; D, E, F .Comparison of drug resistance of A375 cells (NC group) and A375 EGFR + cells (EGFR + group) to vemurafenib, trametinib and SCH772984. * P < 0.05.Drug response curves are shown as mean ± SEM of three replicates and are representative of at least three independent experiments. NC group (A375): human BRAFV600E melanoma A375 cells; EGFR + group (A375EGFR+): A375 cells overexpressing EGFR; treated groups NC-V and EGFR+-V with the BRAF inhibitor Vemurafenib (MCE, HY-12057); NC-T and EGFR+-T treated with the MEK inhibitor Trametinib (MCE, HY-10999); and NC-S and EGFR+-S treated with the ERK inhibitor SCH772984 (MCE, HY-50846)

Article Snippet: NC group (A375): human BRAFV600E melanoma A375 cells; EGFR + group (A375EGFR+): A375 cells overexpressing EGFR; treated groups NC-V and EGFR+-V with the BRAF inhibitor Vemurafenib (MCE, HY-12057); NC-T and EGFR+-T treated with the MEK inhibitor Trametinib (MCE, HY-10999); and NC-S and EGFR+-S treated with the ERK inhibitor SCH772984 (MCE, HY-50846) Fig. 5 Measurement of the IC50 of ferroptosis-induced BRAFV600E melanoma cells for vemurafenib.

Techniques: Expressing, Biomarker Discovery, In Vitro, Fluorescence, Western Blot, Stable Transfection, Comparison

Journal: Archives of Dermatological Research

Article Title: EGFR influences the resistance to targeted therapy in BRAF V600E melanomas by regulating the ferroptosis process

doi: 10.1007/s00403-025-03895-8

Figure Lengend Snippet: Measurement of the IC50 of ferroptosis-induced BRAFV600E melanoma cells for vemurafenib. A375 and A375EGFR + cells were pretreated with DMSO and 5 μm artesunate for 8 h, respectively, to calculate the IC50 values of vemurafenib. A , C. IC50 determination for A375 cells induced with vemurafenib; B. D. IC50 determination for A375 EGFR+ cells induced with vemurafenib; E.F. Percentages of viable cells calculated relative to DMSO. Drug response curves are shown as mean ± SEM of three replicates and are representative of at least three independent experiments

Article Snippet: NC group (A375): human BRAFV600E melanoma A375 cells; EGFR + group (A375EGFR+): A375 cells overexpressing EGFR; treated groups NC-V and EGFR+-V with the BRAF inhibitor Vemurafenib (MCE, HY-12057); NC-T and EGFR+-T treated with the MEK inhibitor Trametinib (MCE, HY-10999); and NC-S and EGFR+-S treated with the ERK inhibitor SCH772984 (MCE, HY-50846) Fig. 5 Measurement of the IC50 of ferroptosis-induced BRAFV600E melanoma cells for vemurafenib.

Techniques:

Journal: International Journal of Nanomedicine

Article Title: Therapeutic Potential of Nanomedicine in Management of Alzheimer’s Disease and Glioma

doi: 10.2147/IJN.S405454

Figure Lengend Snippet: Summary of In Vivo and In Vitro with Drug Nano Formulation Demonstrating the Encapsulation Efficiency in Treatment of Glioma and AD

Article Snippet: Integrins and ApoE are targeted by Dox due to common EGFR by EGFR(V) antibody conjugated to an EnGeneIC delivery vehicle (EDV), loaded with DOX (EGFR(V)-EDV-Dox).

Techniques: In Vivo, In Vitro, Formulation, Encapsulation, Liposomes, Transgenic Assay, Derivative Assay, Capsules, Polymer, Injection, Expressing, Disruption, Activation Assay

Journal: Technology in Cancer Research & Treatment

Article Title: Nanocarriers Call the Last Shot in the Treatment of Brain Cancers

doi: 10.1177/15330338221080974

Figure Lengend Snippet: Nanocarrier-based Clinical Trials.

Article Snippet: The EnGeneIC EDVTM technology-based EGFR (V)-EDV-Dox is a 400 nm Dox-loaded bacterial minicell that utilizes bispecific antibodies to function as a targeted therapy in cancer treatment ( ).

Techniques: Concentration Assay, Expressing, Cell Surface Receptor Assay, Derivative Assay