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ATCC pc3 cat crl 1435 cell lines

Native NPM1 and YAP1 proteins form complexes in prostate cancer cell models (A) The Venn diagram illustrates proteins associated with YAP1 in LNCaP cells treated with dihydrotestosterone (DHT, 10 nM) or enzalutamide (ENZ, 20 μM) under dextran-coated charcoal-stripped (DCC) serum conditions. Unique and shared proteins for each treatment are indicated. (B) A protein interaction network generated using the GeneMania web portal positions NPM1 within the YAP1 network. (C) Western blot analysis of NPM1 protein levels in AR-positive (LNCaP, C4-2, C4-2B, and 22Rv1) and AR-negative <t>(PC3</t> and ARCaP) cell lines . β-actin served as a loading control. (D) Quantitative PCR analysis showing correlation between NPM1 transcript and protein levels across the same cell lines. (E) Co-immunofluorescence staining of NPM1 (green) and YAP1 (red) in LNCaP and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (F) Western blot showing NPM1 in YAP1 immune complexes in nuclear extracts from LNCaP, C4-2, C4-2B, and PC3 cells. IgG served as a negative control . (G) Reciprocal co-IP using an NPM1 antibody demonstrates YAP1 presence in NPM1 immune complexes exclusively in PC3 cells. β-actin was used as a loading control. (H) Representative confocal images showing PLA foci (red) indicating YAP1-NPM1 interactions in LNCaP, C4-2, and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (I) Enlarged images of boxed regions from panel H highlight nuclear localization of PLA foci. (J) Quantification of PLA foci per cell across the indicated cell lines. Statistical significance was determined using a two-tailed t test (∗ p < 0.01). Data are represented as mean ± SEM.

Pc3 Cat Crl 1435 Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 14283 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node"

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

Journal: iScience

doi: 10.1016/j.isci.2026.115588

Figure Legend Snippet: Native NPM1 and YAP1 proteins form complexes in prostate cancer cell models (A) The Venn diagram illustrates proteins associated with YAP1 in LNCaP cells treated with dihydrotestosterone (DHT, 10 nM) or enzalutamide (ENZ, 20 μM) under dextran-coated charcoal-stripped (DCC) serum conditions. Unique and shared proteins for each treatment are indicated. (B) A protein interaction network generated using the GeneMania web portal positions NPM1 within the YAP1 network. (C) Western blot analysis of NPM1 protein levels in AR-positive (LNCaP, C4-2, C4-2B, and 22Rv1) and AR-negative (PC3 and ARCaP) cell lines . β-actin served as a loading control. (D) Quantitative PCR analysis showing correlation between NPM1 transcript and protein levels across the same cell lines. (E) Co-immunofluorescence staining of NPM1 (green) and YAP1 (red) in LNCaP and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (F) Western blot showing NPM1 in YAP1 immune complexes in nuclear extracts from LNCaP, C4-2, C4-2B, and PC3 cells. IgG served as a negative control . (G) Reciprocal co-IP using an NPM1 antibody demonstrates YAP1 presence in NPM1 immune complexes exclusively in PC3 cells. β-actin was used as a loading control. (H) Representative confocal images showing PLA foci (red) indicating YAP1-NPM1 interactions in LNCaP, C4-2, and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (I) Enlarged images of boxed regions from panel H highlight nuclear localization of PLA foci. (J) Quantification of PLA foci per cell across the indicated cell lines. Statistical significance was determined using a two-tailed t test (∗ p < 0.01). Data are represented as mean ± SEM.

Techniques Used: Generated, Western Blot, Control, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Negative Control, Co-Immunoprecipitation Assay, Two Tailed Test

NPM1 influences YAP1 activity and the regulation of its target genes in cellular contexts (A–C) Quantitative PCR analysis of NPM1, YAP1, and MYC mRNA levels in LNCaP and PC3 cells after transient transfection with scrambled or NPM1-specific siRNA. (D and E) Western blot analysis showing YAP1 and MYC protein levels in LNCaP and PC3 cells with or without NPM1 knockdown. (F–G) Quantitative PCR analysis of YAP1 target gene expression in LNCaP and PC3 cells transfected with scramble control or NPM1-specific siRNA (∗ p < 0.001; ∗∗ p < 0.01). Data are represented as mean ± SEM. (I–K) Quantitative PCR analysis of YAP1 target genes (CCN1, CCN2, and ANKRD1) in LNCaP cells after transfection with scramble control or NPM1-specific siRNA, followed by overnight treatment with EtOH (vehicle) or DHT under 5% CSS-fed conditions . Statistical significance was assessed using a two-tailed t test (∗ p < 0.05; ∗∗ p < 0.01). Data are presented as mean ± SEM.

Figure Legend Snippet: NPM1 influences YAP1 activity and the regulation of its target genes in cellular contexts (A–C) Quantitative PCR analysis of NPM1, YAP1, and MYC mRNA levels in LNCaP and PC3 cells after transient transfection with scrambled or NPM1-specific siRNA. (D and E) Western blot analysis showing YAP1 and MYC protein levels in LNCaP and PC3 cells with or without NPM1 knockdown. (F–G) Quantitative PCR analysis of YAP1 target gene expression in LNCaP and PC3 cells transfected with scramble control or NPM1-specific siRNA (∗ p < 0.001; ∗∗ p < 0.01). Data are represented as mean ± SEM. (I–K) Quantitative PCR analysis of YAP1 target genes (CCN1, CCN2, and ANKRD1) in LNCaP cells after transfection with scramble control or NPM1-specific siRNA, followed by overnight treatment with EtOH (vehicle) or DHT under 5% CSS-fed conditions . Statistical significance was assessed using a two-tailed t test (∗ p < 0.05; ∗∗ p < 0.01). Data are presented as mean ± SEM.

Techniques Used: Activity Assay, Real-time Polymerase Chain Reaction, Transfection, Western Blot, Knockdown, Targeted Gene Expression, Control, Two Tailed Test

Synergistic interactions between NPM1 and YAP1 regulate cell growth (A) Western blot analysis of NPM1 protein levels in LNCaP cells with or without NPM1 silencing by siRNA; β-actin served as a loading control. (B) Colony-forming ability of LNCaP cells with or without NPM1 knockdown, visualized by crystal violet staining. The accompanying graph presents quantification of colony numbers (∗ p < 0.01, two-tailed t test). (C and D) Dose-response curves for LNCaP, C4-2, C4-2B, and PC3 cells treated with NPM1 inhibitors NSC348884 or nucleozin. Graphs show log values of drug concentration versus percent cell growth; IC50 values were calculated for each cell line. (E–G) Cell-cycle distribution in LNCaP, C4-2, and PC3 cells treated with DMSO (mock), NSC348884, or nucleozin, as evaluated by flow cytometry. Graphs display the percentages of cells in the G1, S, and G2/M phases. (H) Confocal images showing YAP1–NPM1 interactions in LNCaP cells treated with DMSO, NSC348884, or nucleozin under serum-fed conditions. PLA was used to detect YAP1-NPM1 interactions (red foci); nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. The accompanying graph quantifies PLA foci. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are presented as mean ± SEM. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are represented as mean ± SEM.

Figure Legend Snippet: Synergistic interactions between NPM1 and YAP1 regulate cell growth (A) Western blot analysis of NPM1 protein levels in LNCaP cells with or without NPM1 silencing by siRNA; β-actin served as a loading control. (B) Colony-forming ability of LNCaP cells with or without NPM1 knockdown, visualized by crystal violet staining. The accompanying graph presents quantification of colony numbers (∗ p < 0.01, two-tailed t test). (C and D) Dose-response curves for LNCaP, C4-2, C4-2B, and PC3 cells treated with NPM1 inhibitors NSC348884 or nucleozin. Graphs show log values of drug concentration versus percent cell growth; IC50 values were calculated for each cell line. (E–G) Cell-cycle distribution in LNCaP, C4-2, and PC3 cells treated with DMSO (mock), NSC348884, or nucleozin, as evaluated by flow cytometry. Graphs display the percentages of cells in the G1, S, and G2/M phases. (H) Confocal images showing YAP1–NPM1 interactions in LNCaP cells treated with DMSO, NSC348884, or nucleozin under serum-fed conditions. PLA was used to detect YAP1-NPM1 interactions (red foci); nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. The accompanying graph quantifies PLA foci. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are presented as mean ± SEM. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are represented as mean ± SEM.

Techniques Used: Western Blot, Control, Knockdown, Staining, Two Tailed Test, Concentration Assay, Flow Cytometry, CCK-8 Assay, Transfection

NPM1 regulates cell migration and shows increased interaction with YAP1 in high-grade prostate cancer tissues (A) Wound-healing assay images demonstrate a time-dependent delay in wound closure in LNCaP cells following NPM1 knockdown compared to scramble (Scram) siRNA control ( p < 1.14E−13). Scale bar: 10 μm. (B and C) Migration assays in LNCaP and PC3 cells show reduced motility upon NPM1 depletion in collagen-coated Boyden chambers, with or without EGF stimulation (∗ p < 0.01). Scale bar: 10 μm. Data are from two independent experiments performed in duplicate. (D) Representative PLA micrographs reveal increased YAP1-NPM1 interaction in high-grade tumors (GS > 7) versus low-grade (GS < 7) prostate cancer tissues ( n = 8). Scale bars: 10 and 5 μm, respectively. (E) Quantification of PLA foci in red (corresponding to D) ( n = 8). Data are expressed as mean ± SEM. (F) Schematic summary of findings created using BioRender.

Figure Legend Snippet: NPM1 regulates cell migration and shows increased interaction with YAP1 in high-grade prostate cancer tissues (A) Wound-healing assay images demonstrate a time-dependent delay in wound closure in LNCaP cells following NPM1 knockdown compared to scramble (Scram) siRNA control ( p < 1.14E−13). Scale bar: 10 μm. (B and C) Migration assays in LNCaP and PC3 cells show reduced motility upon NPM1 depletion in collagen-coated Boyden chambers, with or without EGF stimulation (∗ p < 0.01). Scale bar: 10 μm. Data are from two independent experiments performed in duplicate. (D) Representative PLA micrographs reveal increased YAP1-NPM1 interaction in high-grade tumors (GS > 7) versus low-grade (GS < 7) prostate cancer tissues ( n = 8). Scale bars: 10 and 5 μm, respectively. (E) Quantification of PLA foci in red (corresponding to D) ( n = 8). Data are expressed as mean ± SEM. (F) Schematic summary of findings created using BioRender.

Techniques Used: Migration, Wound Healing Assay, Knockdown, Control

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Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: Native NPM1 and YAP1 proteins form complexes in prostate cancer cell models (A) The Venn diagram illustrates proteins associated with YAP1 in LNCaP cells treated with dihydrotestosterone (DHT, 10 nM) or enzalutamide (ENZ, 20 μM) under dextran-coated charcoal-stripped (DCC) serum conditions. Unique and shared proteins for each treatment are indicated. (B) A protein interaction network generated using the GeneMania web portal positions NPM1 within the YAP1 network. (C) Western blot analysis of NPM1 protein levels in AR-positive (LNCaP, C4-2, C4-2B, and 22Rv1) and AR-negative (PC3 and ARCaP) cell lines . β-actin served as a loading control. (D) Quantitative PCR analysis showing correlation between NPM1 transcript and protein levels across the same cell lines. (E) Co-immunofluorescence staining of NPM1 (green) and YAP1 (red) in LNCaP and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (F) Western blot showing NPM1 in YAP1 immune complexes in nuclear extracts from LNCaP, C4-2, C4-2B, and PC3 cells. IgG served as a negative control . (G) Reciprocal co-IP using an NPM1 antibody demonstrates YAP1 presence in NPM1 immune complexes exclusively in PC3 cells. β-actin was used as a loading control. (H) Representative confocal images showing PLA foci (red) indicating YAP1-NPM1 interactions in LNCaP, C4-2, and PC3 cells; nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. (I) Enlarged images of boxed regions from panel H highlight nuclear localization of PLA foci. (J) Quantification of PLA foci per cell across the indicated cell lines. Statistical significance was determined using a two-tailed t test (∗ p < 0.01). Data are represented as mean ± SEM.

Article Snippet: LNCaP (Cat# CRL-1740), C4-2 (Cat# CRL-3314), C4-2B (Cat# CRL-3315), 22Rv1 (Cat# CRL-2505), and PC3 (Cat# CRL-1435) cell lines were obtained from the American Type Culture Collection (ATCC).

Techniques: Generated, Western Blot, Control, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Negative Control, Co-Immunoprecipitation Assay, Two Tailed Test

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: NPM1 influences YAP1 activity and the regulation of its target genes in cellular contexts (A–C) Quantitative PCR analysis of NPM1, YAP1, and MYC mRNA levels in LNCaP and PC3 cells after transient transfection with scrambled or NPM1-specific siRNA. (D and E) Western blot analysis showing YAP1 and MYC protein levels in LNCaP and PC3 cells with or without NPM1 knockdown. (F–G) Quantitative PCR analysis of YAP1 target gene expression in LNCaP and PC3 cells transfected with scramble control or NPM1-specific siRNA (∗ p < 0.001; ∗∗ p < 0.01). Data are represented as mean ± SEM. (I–K) Quantitative PCR analysis of YAP1 target genes (CCN1, CCN2, and ANKRD1) in LNCaP cells after transfection with scramble control or NPM1-specific siRNA, followed by overnight treatment with EtOH (vehicle) or DHT under 5% CSS-fed conditions . Statistical significance was assessed using a two-tailed t test (∗ p < 0.05; ∗∗ p < 0.01). Data are presented as mean ± SEM.

Techniques: Activity Assay, Real-time Polymerase Chain Reaction, Transfection, Western Blot, Knockdown, Targeted Gene Expression, Control, Two Tailed Test

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: Synergistic interactions between NPM1 and YAP1 regulate cell growth (A) Western blot analysis of NPM1 protein levels in LNCaP cells with or without NPM1 silencing by siRNA; β-actin served as a loading control. (B) Colony-forming ability of LNCaP cells with or without NPM1 knockdown, visualized by crystal violet staining. The accompanying graph presents quantification of colony numbers (∗ p < 0.01, two-tailed t test). (C and D) Dose-response curves for LNCaP, C4-2, C4-2B, and PC3 cells treated with NPM1 inhibitors NSC348884 or nucleozin. Graphs show log values of drug concentration versus percent cell growth; IC50 values were calculated for each cell line. (E–G) Cell-cycle distribution in LNCaP, C4-2, and PC3 cells treated with DMSO (mock), NSC348884, or nucleozin, as evaluated by flow cytometry. Graphs display the percentages of cells in the G1, S, and G2/M phases. (H) Confocal images showing YAP1–NPM1 interactions in LNCaP cells treated with DMSO, NSC348884, or nucleozin under serum-fed conditions. PLA was used to detect YAP1-NPM1 interactions (red foci); nuclei were counterstained with DAPI (blue). Scale bar: 10 μm. The accompanying graph quantifies PLA foci. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are presented as mean ± SEM. (I) Cell growth with or without YAP1 induction under NPM1 knockdown conditions, assessed by CCK-8 assay at 72 h post-transfection (∗ p < 0.001; ∗∗ p < 0.01, two-tailed t test). Data are represented as mean ± SEM.

Techniques: Western Blot, Control, Knockdown, Staining, Two Tailed Test, Concentration Assay, Flow Cytometry, CCK-8 Assay, Transfection

Journal: iScience

Article Title: The YAP1-NPM1 nuclear complex regulates MYC and reveals a targetable oncogenic node

doi: 10.1016/j.isci.2026.115588

Figure Lengend Snippet: NPM1 regulates cell migration and shows increased interaction with YAP1 in high-grade prostate cancer tissues (A) Wound-healing assay images demonstrate a time-dependent delay in wound closure in LNCaP cells following NPM1 knockdown compared to scramble (Scram) siRNA control ( p < 1.14E−13). Scale bar: 10 μm. (B and C) Migration assays in LNCaP and PC3 cells show reduced motility upon NPM1 depletion in collagen-coated Boyden chambers, with or without EGF stimulation (∗ p < 0.01). Scale bar: 10 μm. Data are from two independent experiments performed in duplicate. (D) Representative PLA micrographs reveal increased YAP1-NPM1 interaction in high-grade tumors (GS > 7) versus low-grade (GS < 7) prostate cancer tissues ( n = 8). Scale bars: 10 and 5 μm, respectively. (E) Quantification of PLA foci in red (corresponding to D) ( n = 8). Data are expressed as mean ± SEM. (F) Schematic summary of findings created using BioRender.

Techniques: Migration, Wound Healing Assay, Knockdown, Control

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