Journal: Advanced Science

Article Title: AI‐Designed TREM1‐Targeted LYTAC Nanoparticles Reprogram the Neuroimmune Microenvironment in Traumatic Brain Injury

doi: 10.1002/advs.77972

Figure Lengend Snippet: Key resources table.

Article Snippet: βIII‐Tubulin Rabbit mAb , ABclonal , A17913.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, Software

Journal: Cancer Biology & Therapy

Article Title: Fibroblast-associated TPM2 links cell-matrix remodeling to EMT-Notch signaling and gemcitabine resistance in intrahepatic cholangiocarcinoma

doi: 10.1080/15384047.2026.2725344

Figure Lengend Snippet: Functional validation of TPM2-associated gemcitabine response in patient-derived intrahepatic cholangiocarcinoma organoids. (A) Representative brightfield images of patient-derived intrahepatic cholangiocarcinoma organoids and hematoxylin and eosin (H&E) staining of organoids and matched primary tumor tissues from two cases. Scale bars, 100 μm. (B) Representative immunofluorescence staining showing AFP (red) and CK19 (green) in organoids (left panels), and ALB (red) in corresponding organoid samples (right panels). Nuclei are counterstained with DAPI (blue). Scale bars, 100 μm. (C) Dose-response curves showing gemcitabine sensitivity of two intrahepatic cholangiocarcinoma organoid models. Cell viability was assessed after treatment with serial concentrations of gemcitabine. Data are representative of three independent biological experiments. (D) Representative radiologic images obtained before treatment and after two cycles of hepatic arterial infusion chemotherapy (HAIC) with gemcitabine plus oxaliplatin (GEMOX) from the patients corresponding to ICCO1 and ICCO2 organoids. Yellow dashed outlines delineate the radiologically visible intrahepatic tumor lesions, and yellow arrows highlight the corresponding lesions to facilitate comparison of tumor changes before and after treatment. (E) Representative western blot validation of TPM2 knockout in the relatively gemcitabine-resistant ICCO2 organoid model using two independent sgRNAs targeting TPM2. β -Tubulin was used as a loading control. Data are representative of three independent biological experiments. (F) Representative brightfield images and corresponding Calcein-AM/PI fluorescence images of control and TPM2-knockout ICCO2 organoids following 5-day treatment with DMSO or 10 μM gemcitabine. Calcein-AM marks viable cells, whereas PI marks dead cells. Scale bars, 50 μm. (G) Quantification of Calcein-AM-positive and PI-positive areas in ICCO2 organoids following 5-day treatment with DMSO or 10 μM gemcitabine. At least 10 organoids per group were quantified in each independent biological experiment. Data are presented as mean ± SEM from three independent biological experiments. (H) Quantification of Calcein-AM-positive organoid area following 5-day treatment with DMSO or 10 μM gemcitabine. At least 20 organoids per group were quantified in each independent biological experiment. Data are presented as mean ± SEM from three independent biological experiments. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: Equal volumes of lysates were separated by SDS-PAGE, transferred onto nitrocellulose membranes, and probed with antibodies against TPM2 (#A3096; ABclonal; 1:1000), Notch1 (#A19090; ABclonal; 1:1000), HES1 (#A0925; ABclonal; 1:1000) and β -Tubulin (#A12289; ABclonal; 1:5000).

Techniques: Functional Assay, Biomarker Discovery, Derivative Assay, Organoids, Brightfield, Staining, Immunofluorescence, Sensitivity, Comparison, Western Blot, Knock-Out, Control, Fluorescence

Journal: Cancer Biology & Therapy

Article Title: Fibroblast-associated TPM2 links cell-matrix remodeling to EMT-Notch signaling and gemcitabine resistance in intrahepatic cholangiocarcinoma

doi: 10.1080/15384047.2026.2725344

Figure Lengend Snippet: TPM2 depletion suppresses EMT/ECM-related programs and Notch signaling in intrahepatic cholangiocarcinoma organoids. (A) Representative immunofluorescence staining of CK19, TPM2, and Vimentin in control and TPM2-knockout ICCO2 organoids. CK19 marks cholangiocytic epithelial tumor cells, TPM2 denotes the knockout target, and Vimentin serves as an EMT-associated marker. Nuclei were counterstained with DAPI. Scale bar, 20 μm. (B, C) Quantification of TPM2-positive area (B) and Vimentin-positive area (C) in control and TPM2-knockout ICCO2 organoids. At least 20 fields of view per group were quantified in each independent biological experiment. Positive areas were quantified within organoid regions using ImageJ under identical imaging and thresholding settings. Data are presented as mean ± SEM. *** P < 0.001. (D) RT-qPCR analysis of Notch pathway genes, EMT-associated markers, and ECM-related genes in control and TPM2-knockout ICCO2 organoids. Relative mRNA expression was normalized to GAPDH and is shown relative to the control group. Experiments were performed using three independent biological replicates, with three technical replicates per biological replicate. (E) Representative western blot analysis showing reduced Notch1 and HES1 expression after TPM2 knockout in ICCO2 organoids. β -Tubulin was used as a loading control. Data are representative of three independent biological experiments. (F) Proposed model illustrating the convergence of fibroblast-associated and tumor-cell-intrinsic TPM2 programs on cell-matrix/cytoskeletal remodeling, Notch-EMT signaling, and gemcitabine tolerance. Solid arrows indicate relationships directly supported by the experimental data in the corresponding context, whereas dashed arrows indicate inferred, indirect, or biologically plausible relationships that require further validation.

Article Snippet: Equal volumes of lysates were separated by SDS-PAGE, transferred onto nitrocellulose membranes, and probed with antibodies against TPM2 (#A3096; ABclonal; 1:1000), Notch1 (#A19090; ABclonal; 1:1000), HES1 (#A0925; ABclonal; 1:1000) and β -Tubulin (#A12289; ABclonal; 1:5000).

Techniques: Organoids, Immunofluorescence, Staining, Control, Knock-Out, Marker, Imaging, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Cytoskeletal, Biomarker Discovery