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ABclonal Biotechnology vimentin
TPM2 depletion suppresses EMT/ECM-related programs and Notch signaling in intrahepatic cholangiocarcinoma organoids. (A) Representative immunofluorescence staining <t>of</t> <t>CK19,</t> TPM2, and <t>Vimentin</t> 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.
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Image Search Results


Primer Sequences Used for Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) and Quantitative Polymerase Chain Reaction (qPCR).

Journal: Annals of Neurosciences

Article Title: Cyclodextrin-enabled δ-Tocotrienol for Treating Stress and Memory Dysfunction: Molecular Insights, Biotechnological Applications and Biomanufacturing Implications

doi: 10.1177/09727531261479841

Figure Lengend Snippet: Primer Sequences Used for Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) and Quantitative Polymerase Chain Reaction (qPCR).

Article Snippet: Protein samples (20 μM) were resolved by SDS-PAGE, transferred to nitrocellulose membrane (Millipore) by electroblotting using a semidry transfer blotter and probed with antibodies including MAP2 (M3696; Sigma-Aldrich), PSD (MA1-046; Thermo Fisher Scientific), NeuF-H/NF-200 (N4142; Sigma-Aldrich), GFAP (G9269; Sigma-Aldrich), GAP43 (sc-17790; Santa Cruz), NCAM (sc-106; Santa Cruz), Vimentin (sc-6260; Santa Cruz), Survivin (71G4B7; Cell Signalling), Nestin (sc-23927; Santa Cruz) and Mortalin.

Techniques: Reverse Transcription, Polymerase Chain Reaction, Real-time Polymerase Chain Reaction, Sequencing

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.

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: Primary antibodies included AFP (#14550-1-AP; Proteintech; 1:200), CK19 (#GB15198; Servicebio; 1:600), ALB (# GB152080 ; Servicebio; 1:50), and Vimentin (#A11952SP; Abclonal; 1:100).

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