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Image Search Results
Journal: Cell Reports Methods
Article Title: Cortical organoid-derived models of the melanoma brain metastatic niche enable prioritization of cancer-targeting drugs
doi: 10.1016/j.crmeth.2025.101236
Figure Lengend Snippet: Selinexor selectively causes metastasis regression in A375- and MelDCC8-MBMs (A) Dose-dependent effect of DEBIO-0932 on ATP-based cellular viability of 2D and tumoroid (3D) MelDCC8 cell cultures after 5 days ( n = 2 experiments per condition). Data are presented as mean ± SEM. IC 50 (2D): 0.65 μM; IC 50 (3D): 0.23 μM. (B) Dose- and time-dependent effect of DEBIO-0932 on fluorescence-based cellular viability of A375-MBMs ( n = 3 technical replicates per condition). Data are presented as mean ± SD. IC 50 : 0.25 μM. (C) Dose- and time-dependent effect of selinexor on fluorescence-based cellular viability of A375-MBMs ( n = 3 technical replicates per condition). Data are presented as mean ± SD. IC 50 : 0.13 μM. (D) Concentration response of selinexor in A375-MBMs and hCOs. Viability is assessed based on the fluorescence intensity or ATP-based 3D CellTiter-Glo assay after 6 days of treatment ( n = 2 experiments per condition). Data are presented as mean ± SEM. (E) Concentration-dependent caspase-3/7 activity in A375-MBM after 6 days of selinexor exposure ( n = 2 experiments). Data are presented as mean ± SEM. (F) Immunohistochemical confocal images of A375-MBMs treated with 0.25 μM for 72 h of cancer cells (RFP), proliferation marker Ki-67, and XPO1 target TP53. Scale bars represent 50 μm. (G) Time-course analysis of MelDCC3- and MelDCC8-MBMs compared to A375-MBMs during 7 days of colonization ( n = 6 independent batches each). Data are presented as mean ± SEM. (H) Ultrastructural analysis of A375-, MelDCC8-, MelDCC3-MBMs demonstrates close proximity of colonized cancer and neuronal cells. Scale bars represent 10 μm. (I) Fluorescence-based cellular viability readout of MBMs treated with 0.25 and 0.5 μM selinexor for 144 h ( n = 10–33 from at least 2 independent experiments). Data are presented as mean ± SEM. See also .
Article Snippet:
Techniques: Fluorescence, Concentration Assay, Glo Assay, Activity Assay, Immunohistochemical staining, Marker
Journal: Cell Reports Methods
Article Title: Cortical organoid-derived models of the melanoma brain metastatic niche enable prioritization of cancer-targeting drugs
doi: 10.1016/j.crmeth.2025.101236
Figure Lengend Snippet: Blood-brain barrier permeation of selinexor and DEBIO-0932 tested in an hiPSC-derived brain capillary endothelial cell model (A) Schematic overview of small-molecule permeation and transport assay between apical (A) and basolateral (B) compartment using hiPSC-derived brain capillary endothelial cells (BCECs). Impedance (Z)-based measurements of transendothelial electrical resistance (TEER) and capacitance (C cl ) as well as fluorescein permeability underlining blood-brain barrier (BBB) integrity. (B) Monitoring of TEER (left axis) and C cl (right axis) to analyze BBB integrity over time after replating onto insert membranes ( n = 3 independent differentiations). Data are presented as mean ± SEM. Labels indicate the time point of medium change (MC) and 1 h window for compound testing. (C) Analysis of fluorescein permeability coefficient during compound administration ( n = 6–9 independent experiments). Data are presented as mean ± SEM. Carbamazepine (quick), verapamil (medium), and atenolol (slow permeation) serve as reference compounds. (D) Apparent permeability coefficient ( P app ) in both directions (apical to basolateral [A-B] and basolateral to apical [B-A]) after 1 h of selinexor or DEBIO-0932 exposure in comparison to reference compounds carbamazepine (quick), verapamil (medium), and atenolol (slow permeation) analyzed by mass spectrometry ( n = 3–6 experiments). Data are presented as mean ± SEM. (E) Overview of calculated P app values and efflux ratios (ERs) of selinexor, DEBIO-0932, and reference compounds.
Article Snippet:
Techniques: Derivative Assay, Transport Assay, Permeability, Comparison, Mass Spectrometry