Journal: bioRxiv

Article Title: Slap restricts oncogenic Src-family kinase signaling to maintain colonic epithelial homeostasis

doi: 10.64898/2026.01.05.697659

Figure Lengend Snippet: (A) Slap-dependent colonic organoid development. Representative images of colon-derived organoids from Slap f/f and Slap f/f Villin-Cre ERT2 mice cultured in Matrigel for 2 days. Quantification of organoid number and area is shown as mean ± SEM from 100-200 organoids per mouse (n = 8 mice per group). ****p<0.0001 Mann–Whitney test. (B) Intestinal Slap deletion increases SFK activity and global protein tyrosine phosphorylation in colonic crypts. Representative immunoblots (right) and quantification (left) of phospho-SFK (pSRC) and total phospho-tyrosine levels in lysates from isolated colonic crypts of the indicated genotypes. Data are presented as mean ± SEM from n = 4-5 mice per group. *p<0.05; **p<0.001 t test. (C) Slap-dependent colonic organoid expansion requires SFK activity. Representative images and quantification of colon-derived organoids from Slap f/f and Slap f/f Villin-Cre ERT2 mice cultured for 2 days in the presence or absence of the SRC-family kinase inhibitor eCF506 (100 nM). Data are shown as mean ± SEM from 100-200 organoids per mouse, n = 4 mice per group. ***p<0.001, ****p<0.0001 Mann–Whitney test.

Article Snippet: After Matrigel polymerization, 500 μL of M2 medium (M1 media supplemented with EGF (50 ng/mL, Bio-techne), Noggin (100 ng/mL, Stem cell technologies), R-spondin1 (500 ng/mL, Stem cell technologies), Y27 (10 μM, Sigma-Aldrich), CHIR-99021 (3 μM, Tebu-Bio) and WNT3a (50 n/ mL, Thermo Fisher Scientific) was added to each well containing or not the SRC inhibitor eCF506 (100 nM, Medchem express) and in other cases the EphB inhibitors EPHB2i (ALW-II-49-7, 200 nM) and the pan-EPH inhibitor pan-EPHi (ALW-II-41-27, 100 nM, Medchem express).

Techniques: Derivative Assay, Cell Culture, MANN-WHITNEY, Activity Assay, Phospho-proteomics, Western Blot, Isolation

Journal: Molecular Oncology

Article Title: Proteome‐based molecular subtyping and therapeutic target prediction in gastric cancer

doi: 10.1002/1878-0261.13654

Figure Lengend Snippet: Assessing the vulnerability of the gastric cancer cell line panel to Src Family Kinase Inhibition. (A) The frequency and activity of Tyrosine kinases across the gastric cancer (GC) cell line panel inferred from Integrative Inferred Kinase Activity (INKA) scoring. See also Fig. . (B) The effect of the Src family kinase (SFK) inhibitor eCF506 on colony formation of KatoIII and N87 cell lines. (C) Quantification of the colony formation assay across the cell line panel. eCF506 (250 n m ) treatment data are expressed relative to vehicle control (DMSO) which was arbitrarily set at 1. Error bars represent the range of the mean from n = 2 independent experiments. (D) Predicted Src activity of each GC cell line. This was extracted from the Tyr kinase activity data, with error bars representing the range of the mean from n = 2 independent tyrosine phosphorylation profiling experiments. (E) Gene dependency scores of 7 individual SFKs in 34 GC cell lines, extracted from the DepMap database. The boxplot overlaid on the violin plot indicates the mean ± SD. The P values indicate results from a student's‐ t test comparing dependency on a particular SFK to all of the SFKs. EMT, epithelial‐mesenchyme transition.

Article Snippet: Inhibitors listed in Table , which include CSNK1D/E inhibitor SR3029, ErbB family inhibitor Lapatinib, pan‐PI3K inhibitor BKM120, AKT inhibitor MK2206, Src kinase family inhibitor eCF506, mTOR inhibitor Rapamycin, and MEK inhibitor Trametinib were purchased from Selleckchem and reconstituted in dimethyl sulfoxide (DMSO) (Merck).

Techniques: Inhibition, Activity Assay, Colony Assay, Control, Phospho-proteomics