sk mel 103  (ATCC)

Journal: Cancer Cell International

Article Title: PHI-501, a dual inhibitor of RAF and DDR1/2, overcomes MAPK drug resistance in Melanoma

doi: 10.1186/s12935-026-04271-w

Figure Lengend Snippet: PHI-501 inhibits MAPK signaling in both BRAF- and NRAS-mutant melanoma. ( A ) Western blot analysis of four BRAF-mutant and two NRAS-mutant melanoma cell lines treated with PHI-501 (1 and 10 µM) for 24 h. ( B ) SK-MEL-2 and SK-MEL-3 cells were treated with PHI-501 (10 µM) for 48 h, and GSEA was performed using the KEGG MAPK signaling pathway gene set. ( C ) Western blot analysis of the dose-dependent effect of PHI-501 on SK-MEL-3 cells under type I collagen (40 µg/ml) stimulation for 48 h. ( D ) Quantification of pAKT and pERK levels normalized to β-actin from the western blot analysis shown in ( C ). Data are presented as mean ± SEM from three independent experiments. ( E ) Time-dependent inhibitory effects of PHI-501 (1 µM) compared to vemurafenib (1 µM) in SK-MEL-2 cells. ( F ) Quantification of pERK normalized to total ERK and pAKT normalized to total AKT from the western blot analysis shown in (E). Data are presented as mean ± SEM from three independent experiments. ( G ) Dose-dependent inhibitory effects of PHI-501 compared to vemurafenib in SK-MEL-2 cells. ( H ) Quantification of pERK normalized to total ERK and pAKT normalized to total AKT from the western blot analysis shown in (G). Data are presented as mean ± SEM from three independent experiments

Article Snippet: SK-MEL-2, SK-MEL-3, A375P, and A375M cells were purchased from the Korean cell line bank.

Techniques: Mutagenesis, Western Blot

Journal: Cancer Cell International

Article Title: PHI-501, a dual inhibitor of RAF and DDR1/2, overcomes MAPK drug resistance in Melanoma

doi: 10.1186/s12935-026-04271-w

Figure Lengend Snippet: PHI-501 Effectively Inhibits Growth and Suppresses MAPK and DDR Signaling in Drug-Resistant Melanoma Cells. ( A ) Clonogenic assay comparing the inhibitory effects of PHI-501 against belvarafenib, dabrafenib, trametinib, and the combination of dabrafenib plus trametinib (DAB + TRA) in drug-resistant melanoma cells. ( B ) Dose–response curves and GI₅₀ values of belvarafenib, dabrafenib, dabrafenib + trametinib, and PHI-501 in resistant melanoma cells. Cells were treated with inhibitors (0.001–10 µM) or DMSO (vehicle) for 48 h. Data are presented as mean ± SEM. (C ) Table summarizing the GI₅₀ values shown in Fig. 5B. ( D ) Immunoblot analysis of pDDR1/2, pERK, pAKT and β-actin in resistant melanoma cell lines (SK-MEL-2BR, SK-MEL-2CR, SK-MEL-3DR, SK-MEL-3TR, and SK-MEL-3DTR) following 48-h treatment with the indicated inhibitors (1 or 10 µM). ( E ) Principal component analysis (PCA) of RNA-seq data from six melanoma cell lines (SK-MEL-2, SK-MEL-3, SK-MEL-2BR, SK-MEL-3DR, SK-MEL-3TR, and SK-MEL-3DTR) treated with 10 µM PHI-501 for 48 h. ( F ) Hierarchical clustering heatmap displaying the top 1000 most variable genes across all five cell lines treated with or without PHI-501. ( G ) GSEA enrichment plots for the MAPK signaling pathway in drug-resistant cells following PHI-501 treatment

Article Snippet: SK-MEL-2, SK-MEL-3, A375P, and A375M cells were purchased from the Korean cell line bank.

Techniques: Clonogenic Assay, Western Blot, RNA Sequencing