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pc3 prostate cancer cell lines  (ATCC)


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    ATCC pc3 prostate cancer cell lines
    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
    Pc3 Prostate Cancer Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 15916 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 15916 article reviews
    pc3 prostate cancer cell lines - by Bioz Stars, 2026-04
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    1) Product Images from "Dynamic optimization of extrachromosomal DNA copy number drives tumour evolution"

    Article Title: Dynamic optimization of extrachromosomal DNA copy number drives tumour evolution

    Journal: bioRxiv

    doi: 10.64898/2026.03.20.713026

    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and PC3 DM.
    Figure Legend Snippet: (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and PC3 DM.

    Techniques Used: Marker



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    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
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    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
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    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
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    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
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    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
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    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and <t>PC3</t> DM.
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    Image Search Results


    (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and PC3 DM.

    Journal: bioRxiv

    Article Title: Dynamic optimization of extrachromosomal DNA copy number drives tumour evolution

    doi: 10.64898/2026.03.20.713026

    Figure Lengend Snippet: (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and PC3 DM.

    Article Snippet: COLO 320DM and COLO 320HSR (colorectal cancer) and the parental PC3 (prostate cancer) cell lines were obtained from ATCC.

    Techniques: Marker

    Engineering hPSMA-CARs with mbIL12 rescues CAR T cell functionality a Schema of hPSMA-CAR variants with mbIL12 expression. b Flow cytometric analysis of ET260-1 CAR and ET260-1(58) CAR with or without mbIL12 as detected by extracellular Fc and intracellular IL-12. c Tumor cell killing of hPSMA-CARs at an E:T of 1:4 over 72 hrs. d Expression of 4-1BB over 72 hrs on hPSMA-CARs. e Expression of CD25 on hPSMA-CARs after 72 hrs. f Secretion of IFNγ of hPSMA-CARs with mbIL12 after 72 hrs as determined by ELISA. g Tumor cell killing of hPSMA-CARs with mbIL12 and J591 against PC-3 PIP at E:T of 1:10 over 5 days at varying concentrations of anti-IFNγR1 blocking antibody and isotype control. Data are presented as mean values ± SEM. P values indicate differences between ET260-1-dCH2(28tm)BBz and ET260-1-dCH2(28tm)BBz/mbIL12 and between ET260-1-dCH2(28tm)BBz/mbIL12 and J591-dCH2(4tm)BBz using a two-tailed Student’s t-test.

    Journal: bioRxiv

    Article Title: IL12-engineered human PSMA-CAR T cells for the treatment of advanced prostate cancer

    doi: 10.64898/2026.03.05.709907

    Figure Lengend Snippet: Engineering hPSMA-CARs with mbIL12 rescues CAR T cell functionality a Schema of hPSMA-CAR variants with mbIL12 expression. b Flow cytometric analysis of ET260-1 CAR and ET260-1(58) CAR with or without mbIL12 as detected by extracellular Fc and intracellular IL-12. c Tumor cell killing of hPSMA-CARs at an E:T of 1:4 over 72 hrs. d Expression of 4-1BB over 72 hrs on hPSMA-CARs. e Expression of CD25 on hPSMA-CARs after 72 hrs. f Secretion of IFNγ of hPSMA-CARs with mbIL12 after 72 hrs as determined by ELISA. g Tumor cell killing of hPSMA-CARs with mbIL12 and J591 against PC-3 PIP at E:T of 1:10 over 5 days at varying concentrations of anti-IFNγR1 blocking antibody and isotype control. Data are presented as mean values ± SEM. P values indicate differences between ET260-1-dCH2(28tm)BBz and ET260-1-dCH2(28tm)BBz/mbIL12 and between ET260-1-dCH2(28tm)BBz/mbIL12 and J591-dCH2(4tm)BBz using a two-tailed Student’s t-test.

    Article Snippet: Human metastatic prostate cancer cell line PC-3 (ATCC CRL-1435) was cultured in RPMI-1640 (Corning) containing 10% fetal bovine serum (FBS, Hyclone), and 1X antibiotic-antimycotic (AA, Gibco) (complete RPMI).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Blocking Assay, Control, Two Tailed Test

    mbIL12-engineered hPSMA-CAR T cells demonstrate improved activity in a recursive tumor cell assay in vitro a Tumor cell killing of hPSMA-CARs over 8 days when co-cultured with PSMA-expressing cell lines at E:T of 1:20. b Fold expansion of hPSMA-CARs compared to J591-CAR after 8-day co-culture. c Production of IFNγ at 8 days as determined by ELISA. d Schema of rechallenge with PSMA-CARs co-cultured with PC-3 PSMA lo , PC-3 PSMA hi , or PC-3 PIP and rechallenged with tumor cells every 3 days. e PC-3 PSMA lo (left), PC-3 PSMA hi (center), or PC-3 PIP (right) cell counts were quantified by flow cytometry. b Fold expansion of T cells after each rechallenge were quantified by flow cytometry. c Production of IFNγ by T cells following each rechallenge as determined by ELISA. Data are presented as mean values ± SEM. P values indicate differences between ET260-1-dCH2(28tm)BBz and ET260-1-dCH2(28tm)BBz/mbIL12 and between ET260-1-dCH2(28tm)BBz/mbIL12 and J591-dCH2(4tm)BBz using a two-tailed Student’s t-test.

    Journal: bioRxiv

    Article Title: IL12-engineered human PSMA-CAR T cells for the treatment of advanced prostate cancer

    doi: 10.64898/2026.03.05.709907

    Figure Lengend Snippet: mbIL12-engineered hPSMA-CAR T cells demonstrate improved activity in a recursive tumor cell assay in vitro a Tumor cell killing of hPSMA-CARs over 8 days when co-cultured with PSMA-expressing cell lines at E:T of 1:20. b Fold expansion of hPSMA-CARs compared to J591-CAR after 8-day co-culture. c Production of IFNγ at 8 days as determined by ELISA. d Schema of rechallenge with PSMA-CARs co-cultured with PC-3 PSMA lo , PC-3 PSMA hi , or PC-3 PIP and rechallenged with tumor cells every 3 days. e PC-3 PSMA lo (left), PC-3 PSMA hi (center), or PC-3 PIP (right) cell counts were quantified by flow cytometry. b Fold expansion of T cells after each rechallenge were quantified by flow cytometry. c Production of IFNγ by T cells following each rechallenge as determined by ELISA. Data are presented as mean values ± SEM. P values indicate differences between ET260-1-dCH2(28tm)BBz and ET260-1-dCH2(28tm)BBz/mbIL12 and between ET260-1-dCH2(28tm)BBz/mbIL12 and J591-dCH2(4tm)BBz using a two-tailed Student’s t-test.

    Article Snippet: Human metastatic prostate cancer cell line PC-3 (ATCC CRL-1435) was cultured in RPMI-1640 (Corning) containing 10% fetal bovine serum (FBS, Hyclone), and 1X antibiotic-antimycotic (AA, Gibco) (complete RPMI).

    Techniques: Activity Assay, In Vitro, Cell Culture, Expressing, Co-Culture Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Two Tailed Test