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cell carcinoma cell lines  (ATCC)


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    ATCC cell carcinoma cell lines
    Cell Carcinoma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 247 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cell carcinoma cell lines/product/ATCC
    Average 96 stars, based on 247 article reviews
    cell carcinoma cell lines - by Bioz Stars, 2026-03
    96/100 stars

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    Growth‑inhibitory effect of cabozantinib. (A) Dose-response cell viability after 48 h cabozantinib treatment in 786-O <t>and</t> <t>Caki-1</t> cells. Values represent mean ± standard deviation (SD) (n=4); *p<0.01 vs. vehicle. (B) Immunoblot analysis of total MET and phospho-MET (Y1234/1235) in parental (Par) and chronically treated (Chr) cells, with or without cabozantinib treatment. Cabozantinib robustly suppressed phospho-MET in both Par and Chr states of both cell lines. β-actin serves as a loading control. (C) Time-course viability (24-72 h) of Par and Chr 786-O cells. (D) Time-course viability (24-72 h) of Par and Chr Caki-1 cells. Cab: acute cabozantinib-treated; Par: parental; Chr: chronically cabozantinib-treated cells (>4 months). *p<0.05; **p<0.01. Statistical significance was determined using an unpaired two-tailed Student’s t-test.
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    Growth‑inhibitory effect of cabozantinib. (A) Dose-response cell viability after 48 h cabozantinib treatment in 786-O <t>and</t> <t>Caki-1</t> cells. Values represent mean ± standard deviation (SD) (n=4); *p<0.01 vs. vehicle. (B) Immunoblot analysis of total MET and phospho-MET (Y1234/1235) in parental (Par) and chronically treated (Chr) cells, with or without cabozantinib treatment. Cabozantinib robustly suppressed phospho-MET in both Par and Chr states of both cell lines. β-actin serves as a loading control. (C) Time-course viability (24-72 h) of Par and Chr 786-O cells. (D) Time-course viability (24-72 h) of Par and Chr Caki-1 cells. Cab: acute cabozantinib-treated; Par: parental; Chr: chronically cabozantinib-treated cells (>4 months). *p<0.05; **p<0.01. Statistical significance was determined using an unpaired two-tailed Student’s t-test.
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    Growth‑inhibitory effect of cabozantinib. (A) Dose-response cell viability after 48 h cabozantinib treatment in 786-O <t>and</t> <t>Caki-1</t> cells. Values represent mean ± standard deviation (SD) (n=4); *p<0.01 vs. vehicle. (B) Immunoblot analysis of total MET and phospho-MET (Y1234/1235) in parental (Par) and chronically treated (Chr) cells, with or without cabozantinib treatment. Cabozantinib robustly suppressed phospho-MET in both Par and Chr states of both cell lines. β-actin serves as a loading control. (C) Time-course viability (24-72 h) of Par and Chr 786-O cells. (D) Time-course viability (24-72 h) of Par and Chr Caki-1 cells. Cab: acute cabozantinib-treated; Par: parental; Chr: chronically cabozantinib-treated cells (>4 months). *p<0.05; **p<0.01. Statistical significance was determined using an unpaired two-tailed Student’s t-test.
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    Growth‑inhibitory effect of cabozantinib. (A) Dose-response cell viability after 48 h cabozantinib treatment in 786-O <t>and</t> <t>Caki-1</t> cells. Values represent mean ± standard deviation (SD) (n=4); *p<0.01 vs. vehicle. (B) Immunoblot analysis of total MET and phospho-MET (Y1234/1235) in parental (Par) and chronically treated (Chr) cells, with or without cabozantinib treatment. Cabozantinib robustly suppressed phospho-MET in both Par and Chr states of both cell lines. β-actin serves as a loading control. (C) Time-course viability (24-72 h) of Par and Chr 786-O cells. (D) Time-course viability (24-72 h) of Par and Chr Caki-1 cells. Cab: acute cabozantinib-treated; Par: parental; Chr: chronically cabozantinib-treated cells (>4 months). *p<0.05; **p<0.01. Statistical significance was determined using an unpaired two-tailed Student’s t-test.
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    ( A ) Epigenomic datasets generated from 4 tRCC (s-TFE, FU-UR-1, UOK109, and UOK146) and 6 ccRCC (Caki-1, A-498, RFX393, 786-O, 769-P, and <t>KMRC-1)</t> cell lines, either in-house or in a previously published study ( , ). ( B ) Unsupervised hierarchical clustering of the H3K4me3 ChIP-seq, H3K27ac ChIP-seq, and MeDIP-seq consensus peaks across tRCC and ccRCC cell lines analyzed in this study. ( C ) Volcano plots showing differentially marked peaks between tRCC and ccRCC cell lines for H3K4me3 ChIP-Seq, H3K27ac ChIP-seq, and MeDIP-seq. Thresholds for significance were set at FDR-q < 0.01 and log 2 FC > 1 for H3K27ac and MeDIP and > 2 for H3K4me3.
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    Image Search Results


    Growth‑inhibitory effect of cabozantinib. (A) Dose-response cell viability after 48 h cabozantinib treatment in 786-O and Caki-1 cells. Values represent mean ± standard deviation (SD) (n=4); *p<0.01 vs. vehicle. (B) Immunoblot analysis of total MET and phospho-MET (Y1234/1235) in parental (Par) and chronically treated (Chr) cells, with or without cabozantinib treatment. Cabozantinib robustly suppressed phospho-MET in both Par and Chr states of both cell lines. β-actin serves as a loading control. (C) Time-course viability (24-72 h) of Par and Chr 786-O cells. (D) Time-course viability (24-72 h) of Par and Chr Caki-1 cells. Cab: acute cabozantinib-treated; Par: parental; Chr: chronically cabozantinib-treated cells (>4 months). *p<0.05; **p<0.01. Statistical significance was determined using an unpaired two-tailed Student’s t-test.

    Journal: Cancer Genomics & Proteomics

    Article Title: Timescale-dependent Phosphoproteomic Remodeling and Motility-associated Adaptation under Chronic Cabozantinib Exposure in Renal Cell Carcinoma

    doi: 10.21873/cgp.20576

    Figure Lengend Snippet: Growth‑inhibitory effect of cabozantinib. (A) Dose-response cell viability after 48 h cabozantinib treatment in 786-O and Caki-1 cells. Values represent mean ± standard deviation (SD) (n=4); *p<0.01 vs. vehicle. (B) Immunoblot analysis of total MET and phospho-MET (Y1234/1235) in parental (Par) and chronically treated (Chr) cells, with or without cabozantinib treatment. Cabozantinib robustly suppressed phospho-MET in both Par and Chr states of both cell lines. β-actin serves as a loading control. (C) Time-course viability (24-72 h) of Par and Chr 786-O cells. (D) Time-course viability (24-72 h) of Par and Chr Caki-1 cells. Cab: acute cabozantinib-treated; Par: parental; Chr: chronically cabozantinib-treated cells (>4 months). *p<0.05; **p<0.01. Statistical significance was determined using an unpaired two-tailed Student’s t-test.

    Article Snippet: Parental 786-O and Caki-1 renal cell carcinoma cell lines were obtained from ATCC (Manassas, VA, USA) and cultured in RPMI-1640 medium supplemented with 10% fetal bovine serum at 37°C in a humidified atmosphere containing 5% CO 2 .

    Techniques: Standard Deviation, Western Blot, Control, Two Tailed Test

    ( A ) Epigenomic datasets generated from 4 tRCC (s-TFE, FU-UR-1, UOK109, and UOK146) and 6 ccRCC (Caki-1, A-498, RFX393, 786-O, 769-P, and KMRC-1) cell lines, either in-house or in a previously published study ( , ). ( B ) Unsupervised hierarchical clustering of the H3K4me3 ChIP-seq, H3K27ac ChIP-seq, and MeDIP-seq consensus peaks across tRCC and ccRCC cell lines analyzed in this study. ( C ) Volcano plots showing differentially marked peaks between tRCC and ccRCC cell lines for H3K4me3 ChIP-Seq, H3K27ac ChIP-seq, and MeDIP-seq. Thresholds for significance were set at FDR-q < 0.01 and log 2 FC > 1 for H3K27ac and MeDIP and > 2 for H3K4me3.

    Journal: The Journal of Clinical Investigation

    Article Title: Cell-free DNA epigenomic profiling enables noninvasive detection and monitoring of translocation renal cell carcinoma

    doi: 10.1172/JCI195725

    Figure Lengend Snippet: ( A ) Epigenomic datasets generated from 4 tRCC (s-TFE, FU-UR-1, UOK109, and UOK146) and 6 ccRCC (Caki-1, A-498, RFX393, 786-O, 769-P, and KMRC-1) cell lines, either in-house or in a previously published study ( , ). ( B ) Unsupervised hierarchical clustering of the H3K4me3 ChIP-seq, H3K27ac ChIP-seq, and MeDIP-seq consensus peaks across tRCC and ccRCC cell lines analyzed in this study. ( C ) Volcano plots showing differentially marked peaks between tRCC and ccRCC cell lines for H3K4me3 ChIP-Seq, H3K27ac ChIP-seq, and MeDIP-seq. Thresholds for significance were set at FDR-q < 0.01 and log 2 FC > 1 for H3K27ac and MeDIP and > 2 for H3K4me3.

    Article Snippet: The cell lines 786-O (ATCC, CRL-1932; RRID: CVCL_1051), 293T (ATCC, CRL-11268; RRID: CVCL_0063), A-498 (ATCC, HTB-44; RRID: CVCL_1056), 769-P (ATCC, CRL-1933; RRID: CVCL_1050), KMRC-1 (JCRB1010; RRID: CVCL_2983), Caki-1 (ATCC, HTB-46; RRID: CVCL_0234), UOK109 (RRID: CVCL_B123), and UOK146 (RRID: CVCL_B123) were obtained from W. Marston Linehan’s laboratory (National Cancer Institute).

    Techniques: Generated, ChIP-sequencing, Methylated DNA Immunoprecipitation