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triple negative breast cancer cell line hcc1806  (ATCC)


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    Structured Review

    ATCC triple negative breast cancer cell line hcc1806
    Generation of PCDHGC3 knockout in breast cancer and melanoma cell lines. Western blot analysis of wild type (WT), control (C; transfected with the PCDH2 HDR Plasmid (h2) containing a puromycin resistance gene) and knockout (KO) <t>HCC1806</t> breast cancer cell line ( a ) and A2058 melanoma cell line ( b ). β-Actin served as an endogenous control.
    Triple Negative Breast Cancer Cell Line Hcc1806, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 973 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/triple+negative+breast+cancer+cell+line+hcc1806/pmc13118706-37-0-7?v=ATCC
    Average 97 stars, based on 973 article reviews
    triple negative breast cancer cell line hcc1806 - by Bioz Stars, 2026-07
    97/100 stars

    Images

    1) Product Images from "The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells"

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    Journal: NeuroSci

    doi: 10.3390/neurosci7020047

    Generation of PCDHGC3 knockout in breast cancer and melanoma cell lines. Western blot analysis of wild type (WT), control (C; transfected with the PCDH2 HDR Plasmid (h2) containing a puromycin resistance gene) and knockout (KO) HCC1806 breast cancer cell line ( a ) and A2058 melanoma cell line ( b ). β-Actin served as an endogenous control.
    Figure Legend Snippet: Generation of PCDHGC3 knockout in breast cancer and melanoma cell lines. Western blot analysis of wild type (WT), control (C; transfected with the PCDH2 HDR Plasmid (h2) containing a puromycin resistance gene) and knockout (KO) HCC1806 breast cancer cell line ( a ) and A2058 melanoma cell line ( b ). β-Actin served as an endogenous control.

    Techniques Used: Knock-Out, Western Blot, Control, Transfection, Plasmid Preparation

    Cell proliferation assay in control and PCDHGC3 knockout cells. Proliferation rate of control and PCDHGC3 knockout (KO) HCC1806 breast cancer cells ( a ) and of control and PCDHGC3 KO A2058 melanoma cells ( b ). **** = p < 0.0001, unpaired t test.
    Figure Legend Snippet: Cell proliferation assay in control and PCDHGC3 knockout cells. Proliferation rate of control and PCDHGC3 knockout (KO) HCC1806 breast cancer cells ( a ) and of control and PCDHGC3 KO A2058 melanoma cells ( b ). **** = p < 0.0001, unpaired t test.

    Techniques Used: Proliferation Assay, Control, Knock-Out

    Relative adhesion of PCDHGC3 knockout breast cancer and melanoma cells to human in vitro BBB models. Adhesion measurements of HCC1806 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( a ) and BLECs ( b ) after 30, 60, and 120 min. Adhesion measurements of A2058 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( c ) and BLECs ( d ) after 30, 60, and 120 min. Control cell adhesion was measured at each time point; however, for clarity, only the measurement after 30 min is shown. Data are presented as mean relative adhesion versus control with standard deviation, **** = p ≤ 0.0001, one-way ANOVA test.
    Figure Legend Snippet: Relative adhesion of PCDHGC3 knockout breast cancer and melanoma cells to human in vitro BBB models. Adhesion measurements of HCC1806 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( a ) and BLECs ( b ) after 30, 60, and 120 min. Adhesion measurements of A2058 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( c ) and BLECs ( d ) after 30, 60, and 120 min. Control cell adhesion was measured at each time point; however, for clarity, only the measurement after 30 min is shown. Data are presented as mean relative adhesion versus control with standard deviation, **** = p ≤ 0.0001, one-way ANOVA test.

    Techniques Used: Knock-Out, In Vitro, Control, Standard Deviation

    PCDHGC3 KO leads to stronger invasion of PCDHGC3 knockout breast cancer and melanoma cells. HCC1806 PCDHGC3 knockout (KO) and control cells ( a ) and A2058 PCDHGC3 knockout (KO) and control ( b ) invaded for 48 h through Transwells coated with Matrigel. The number of invaded cells is shown. Data are presented as mean cell number with standard deviation, * = p ≤ 0.05, unpaired t -test.
    Figure Legend Snippet: PCDHGC3 KO leads to stronger invasion of PCDHGC3 knockout breast cancer and melanoma cells. HCC1806 PCDHGC3 knockout (KO) and control cells ( a ) and A2058 PCDHGC3 knockout (KO) and control ( b ) invaded for 48 h through Transwells coated with Matrigel. The number of invaded cells is shown. Data are presented as mean cell number with standard deviation, * = p ≤ 0.05, unpaired t -test.

    Techniques Used: Knock-Out, Control, Standard Deviation

    Relative expression of target genes in PCDHGC3 KO breast cancer and melanoma cells. The relative expression (RQ value) of each target in PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells relative to control cells is shown. A RQ value < 1.0 indicates decreased expression, a RQ value > 1.0 indicates increased expression compared to the control cells. The means with standard deviation are shown as the fold of the control. * = p ≤ 0.05, ** = p ≤ 0.01, *** = p ≤ 0.001, **** = p ≤ 0.0001, unpaired t -test.
    Figure Legend Snippet: Relative expression of target genes in PCDHGC3 KO breast cancer and melanoma cells. The relative expression (RQ value) of each target in PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells relative to control cells is shown. A RQ value < 1.0 indicates decreased expression, a RQ value > 1.0 indicates increased expression compared to the control cells. The means with standard deviation are shown as the fold of the control. * = p ≤ 0.05, ** = p ≤ 0.01, *** = p ≤ 0.001, **** = p ≤ 0.0001, unpaired t -test.

    Techniques Used: Expressing, Control, Standard Deviation

    Matrix metalloproteinase (MMP) activity in cell culture medium of PCDHGC3 knockout (KO) breast cancer and melanoma cells. Fluorescence signal of MMP-substrate (SB) cleavage in the cell culture medium of PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells and control cells is expressed as relative fluorescence units (RFU) ± standard deviation. ** = p < 0.01, *** = p < 0.001, unpaired t test.
    Figure Legend Snippet: Matrix metalloproteinase (MMP) activity in cell culture medium of PCDHGC3 knockout (KO) breast cancer and melanoma cells. Fluorescence signal of MMP-substrate (SB) cleavage in the cell culture medium of PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells and control cells is expressed as relative fluorescence units (RFU) ± standard deviation. ** = p < 0.01, *** = p < 0.001, unpaired t test.

    Techniques Used: Activity Assay, Cell Culture, Knock-Out, Fluorescence, Control, Standard Deviation



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    Image Search Results


    Generation of PCDHGC3 knockout in breast cancer and melanoma cell lines. Western blot analysis of wild type (WT), control (C; transfected with the PCDH2 HDR Plasmid (h2) containing a puromycin resistance gene) and knockout (KO) HCC1806 breast cancer cell line ( a ) and A2058 melanoma cell line ( b ). β-Actin served as an endogenous control.

    Journal: NeuroSci

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    doi: 10.3390/neurosci7020047

    Figure Lengend Snippet: Generation of PCDHGC3 knockout in breast cancer and melanoma cell lines. Western blot analysis of wild type (WT), control (C; transfected with the PCDH2 HDR Plasmid (h2) containing a puromycin resistance gene) and knockout (KO) HCC1806 breast cancer cell line ( a ) and A2058 melanoma cell line ( b ). β-Actin served as an endogenous control.

    Article Snippet: Triple-negative breast cancer cell line HCC1806 (CRL-2335, ATCC, Manassas, VA, USA) was cultured in RPMI medium (R7509-500ML, Sigma-Aldrich, St. Louis, MO, USA) containing 10% FCS, L-glutamine and penicillin/streptomycin.

    Techniques: Knock-Out, Western Blot, Control, Transfection, Plasmid Preparation

    Cell proliferation assay in control and PCDHGC3 knockout cells. Proliferation rate of control and PCDHGC3 knockout (KO) HCC1806 breast cancer cells ( a ) and of control and PCDHGC3 KO A2058 melanoma cells ( b ). **** = p < 0.0001, unpaired t test.

    Journal: NeuroSci

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    doi: 10.3390/neurosci7020047

    Figure Lengend Snippet: Cell proliferation assay in control and PCDHGC3 knockout cells. Proliferation rate of control and PCDHGC3 knockout (KO) HCC1806 breast cancer cells ( a ) and of control and PCDHGC3 KO A2058 melanoma cells ( b ). **** = p < 0.0001, unpaired t test.

    Article Snippet: Triple-negative breast cancer cell line HCC1806 (CRL-2335, ATCC, Manassas, VA, USA) was cultured in RPMI medium (R7509-500ML, Sigma-Aldrich, St. Louis, MO, USA) containing 10% FCS, L-glutamine and penicillin/streptomycin.

    Techniques: Proliferation Assay, Control, Knock-Out

    Relative adhesion of PCDHGC3 knockout breast cancer and melanoma cells to human in vitro BBB models. Adhesion measurements of HCC1806 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( a ) and BLECs ( b ) after 30, 60, and 120 min. Adhesion measurements of A2058 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( c ) and BLECs ( d ) after 30, 60, and 120 min. Control cell adhesion was measured at each time point; however, for clarity, only the measurement after 30 min is shown. Data are presented as mean relative adhesion versus control with standard deviation, **** = p ≤ 0.0001, one-way ANOVA test.

    Journal: NeuroSci

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    doi: 10.3390/neurosci7020047

    Figure Lengend Snippet: Relative adhesion of PCDHGC3 knockout breast cancer and melanoma cells to human in vitro BBB models. Adhesion measurements of HCC1806 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( a ) and BLECs ( b ) after 30, 60, and 120 min. Adhesion measurements of A2058 PCDHGC3 knockout (KO) and control cells to hCMEC/D3 ( c ) and BLECs ( d ) after 30, 60, and 120 min. Control cell adhesion was measured at each time point; however, for clarity, only the measurement after 30 min is shown. Data are presented as mean relative adhesion versus control with standard deviation, **** = p ≤ 0.0001, one-way ANOVA test.

    Article Snippet: Triple-negative breast cancer cell line HCC1806 (CRL-2335, ATCC, Manassas, VA, USA) was cultured in RPMI medium (R7509-500ML, Sigma-Aldrich, St. Louis, MO, USA) containing 10% FCS, L-glutamine and penicillin/streptomycin.

    Techniques: Knock-Out, In Vitro, Control, Standard Deviation

    PCDHGC3 KO leads to stronger invasion of PCDHGC3 knockout breast cancer and melanoma cells. HCC1806 PCDHGC3 knockout (KO) and control cells ( a ) and A2058 PCDHGC3 knockout (KO) and control ( b ) invaded for 48 h through Transwells coated with Matrigel. The number of invaded cells is shown. Data are presented as mean cell number with standard deviation, * = p ≤ 0.05, unpaired t -test.

    Journal: NeuroSci

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    doi: 10.3390/neurosci7020047

    Figure Lengend Snippet: PCDHGC3 KO leads to stronger invasion of PCDHGC3 knockout breast cancer and melanoma cells. HCC1806 PCDHGC3 knockout (KO) and control cells ( a ) and A2058 PCDHGC3 knockout (KO) and control ( b ) invaded for 48 h through Transwells coated with Matrigel. The number of invaded cells is shown. Data are presented as mean cell number with standard deviation, * = p ≤ 0.05, unpaired t -test.

    Article Snippet: Triple-negative breast cancer cell line HCC1806 (CRL-2335, ATCC, Manassas, VA, USA) was cultured in RPMI medium (R7509-500ML, Sigma-Aldrich, St. Louis, MO, USA) containing 10% FCS, L-glutamine and penicillin/streptomycin.

    Techniques: Knock-Out, Control, Standard Deviation

    Relative expression of target genes in PCDHGC3 KO breast cancer and melanoma cells. The relative expression (RQ value) of each target in PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells relative to control cells is shown. A RQ value < 1.0 indicates decreased expression, a RQ value > 1.0 indicates increased expression compared to the control cells. The means with standard deviation are shown as the fold of the control. * = p ≤ 0.05, ** = p ≤ 0.01, *** = p ≤ 0.001, **** = p ≤ 0.0001, unpaired t -test.

    Journal: NeuroSci

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    doi: 10.3390/neurosci7020047

    Figure Lengend Snippet: Relative expression of target genes in PCDHGC3 KO breast cancer and melanoma cells. The relative expression (RQ value) of each target in PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells relative to control cells is shown. A RQ value < 1.0 indicates decreased expression, a RQ value > 1.0 indicates increased expression compared to the control cells. The means with standard deviation are shown as the fold of the control. * = p ≤ 0.05, ** = p ≤ 0.01, *** = p ≤ 0.001, **** = p ≤ 0.0001, unpaired t -test.

    Article Snippet: Triple-negative breast cancer cell line HCC1806 (CRL-2335, ATCC, Manassas, VA, USA) was cultured in RPMI medium (R7509-500ML, Sigma-Aldrich, St. Louis, MO, USA) containing 10% FCS, L-glutamine and penicillin/streptomycin.

    Techniques: Expressing, Control, Standard Deviation

    Matrix metalloproteinase (MMP) activity in cell culture medium of PCDHGC3 knockout (KO) breast cancer and melanoma cells. Fluorescence signal of MMP-substrate (SB) cleavage in the cell culture medium of PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells and control cells is expressed as relative fluorescence units (RFU) ± standard deviation. ** = p < 0.01, *** = p < 0.001, unpaired t test.

    Journal: NeuroSci

    Article Title: The Knockout of Protocadherin Gamma C3 (PCDHGC3) in Breast Cancer and Melanoma Cell Lines Leads to Increased Adhesion of Knockout Cells to Brain Microvascular Endothelial Cells

    doi: 10.3390/neurosci7020047

    Figure Lengend Snippet: Matrix metalloproteinase (MMP) activity in cell culture medium of PCDHGC3 knockout (KO) breast cancer and melanoma cells. Fluorescence signal of MMP-substrate (SB) cleavage in the cell culture medium of PCDHGC3 KO HCC1806 ( a ) and PCDHGC3 KO A2058 ( b ) cells and control cells is expressed as relative fluorescence units (RFU) ± standard deviation. ** = p < 0.01, *** = p < 0.001, unpaired t test.

    Article Snippet: Triple-negative breast cancer cell line HCC1806 (CRL-2335, ATCC, Manassas, VA, USA) was cultured in RPMI medium (R7509-500ML, Sigma-Aldrich, St. Louis, MO, USA) containing 10% FCS, L-glutamine and penicillin/streptomycin.

    Techniques: Activity Assay, Cell Culture, Knock-Out, Fluorescence, Control, Standard Deviation

    Effect of ERβ on sncRNA expression profiles and miRNA-regulated functions in TNBC. ( A ) Western blot analysis of ERβ expression in the HCC1806, MDA-MB-468, and Hs 578T cell lines upon induction of exogenous receptor expression by doxycycline (Doxy+) or in its absence (Doxy−). ( B ) Venn diagram of specific and commonly up-regulated (left panel) or down-regulated (right panel) sncRNAs in ERβ-expressing TNBC cells (|Fold-Change|(|FC|) ≥ 1.5, p < 0.05). Only sncRNAs characterized by the same behavior (up- or down-regulated) were included. ( C ) Heatmap showing ERβ-regulated miRNAs in the indicated cell lines (|FC| ≥ 1.5, p < 0.05) ( D ) Ingenuity Pathway Software (IPA) functional annotation analysis performed on ERβ-modulated genes predicted to be targets of differentially expressed miRNAs (|FC| ≥ 1.5, p < 0.05) in the corresponding cell lines. Commonly influenced functions in the three cell lines are indicated in orange. The vertical orange line indicates the p threshold ( p < 0.05).

    Journal: Cells

    Article Title: Small Non-Coding RNA Profiling Identifies miR-181a-5p as a Mediator of Estrogen Receptor Beta-Induced Inhibition of Cholesterol Biosynthesis in Triple-Negative Breast Cancer

    doi: 10.3390/cells9040874

    Figure Lengend Snippet: Effect of ERβ on sncRNA expression profiles and miRNA-regulated functions in TNBC. ( A ) Western blot analysis of ERβ expression in the HCC1806, MDA-MB-468, and Hs 578T cell lines upon induction of exogenous receptor expression by doxycycline (Doxy+) or in its absence (Doxy−). ( B ) Venn diagram of specific and commonly up-regulated (left panel) or down-regulated (right panel) sncRNAs in ERβ-expressing TNBC cells (|Fold-Change|(|FC|) ≥ 1.5, p < 0.05). Only sncRNAs characterized by the same behavior (up- or down-regulated) were included. ( C ) Heatmap showing ERβ-regulated miRNAs in the indicated cell lines (|FC| ≥ 1.5, p < 0.05) ( D ) Ingenuity Pathway Software (IPA) functional annotation analysis performed on ERβ-modulated genes predicted to be targets of differentially expressed miRNAs (|FC| ≥ 1.5, p < 0.05) in the corresponding cell lines. Commonly influenced functions in the three cell lines are indicated in orange. The vertical orange line indicates the p threshold ( p < 0.05).

    Article Snippet: Triple-negative breast cancer cell lines HCC1806 (CRL-2335), MDA-MB-468 (HTB-132), and Hs 578T (HTB-126) were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA) and maintained in culture as previously described [ ].

    Techniques: Expressing, Western Blot, Software, Functional Assay

    ( a ) HCC1806 cells were cultured and harvested for PRO-seq and ChIP-exo. PRO-seq measures nascent transcription. ChIP-exo identifies the exonuclease left and right borders that flank protein-DNA interactions. ( b ) Illustration of the genomic context for ChIP targets: Pol II, H2A.Z, H3K4me3, H3K4me2, H3K4me1, H3K27ac, H3K9ac, H3K27me3, H4K20me1, and CTCF.

    Journal: Scientific Data

    Article Title: Epigenetic and transcriptional profiling of triple negative breast cancer

    doi: 10.1038/sdata.2019.33

    Figure Lengend Snippet: ( a ) HCC1806 cells were cultured and harvested for PRO-seq and ChIP-exo. PRO-seq measures nascent transcription. ChIP-exo identifies the exonuclease left and right borders that flank protein-DNA interactions. ( b ) Illustration of the genomic context for ChIP targets: Pol II, H2A.Z, H3K4me3, H3K4me2, H3K4me1, H3K27ac, H3K9ac, H3K27me3, H4K20me1, and CTCF.

    Article Snippet: The human HCC1806 triple negative breast cancer cell line, basal-like 2 subtype (ATCC) was maintained at 37 ° C in 5% CO 2 between 20–80% confluency in RPMI 1640 (Roswell Park Memorial Institute, Gibco 11875-093) containing 10% bovine calf serum (Gibco 16170-078), 1% L-glutamine (Gibco 25030-081), and 1% Penicillin/Streptomycin (Gibco-15146-122).

    Techniques: Cell Culture

    ( a ) Row-linked heatmaps show RPKM normalized number of reads across a 4 kb genomic interval in 40 bp bins relative to the TSS. Heatmaps were generated from merged biological replicate pairs for each data set. Regions are sorted in descending order based on average row tag density for Pol II. Each row represents a gene, with 18,793 genes displayed. Red and blue reflect high and low read densities, respectively. ( b ) Composite plots below each heatmap quantify the normalized tag density. The central trace denotes the average tag density for each 40 bp bin and the orange fill reflects the standard deviation. ( c ) Genome browser view of PRO-seq and ChIP-exo signal for the indicated targets in HCC1806 cells shown at the MYC gene. Tag distributions were smoothed and RPKM normalized using deepTOOLS. Traces were generated from merged biological replicate pairs.

    Journal: Scientific Data

    Article Title: Epigenetic and transcriptional profiling of triple negative breast cancer

    doi: 10.1038/sdata.2019.33

    Figure Lengend Snippet: ( a ) Row-linked heatmaps show RPKM normalized number of reads across a 4 kb genomic interval in 40 bp bins relative to the TSS. Heatmaps were generated from merged biological replicate pairs for each data set. Regions are sorted in descending order based on average row tag density for Pol II. Each row represents a gene, with 18,793 genes displayed. Red and blue reflect high and low read densities, respectively. ( b ) Composite plots below each heatmap quantify the normalized tag density. The central trace denotes the average tag density for each 40 bp bin and the orange fill reflects the standard deviation. ( c ) Genome browser view of PRO-seq and ChIP-exo signal for the indicated targets in HCC1806 cells shown at the MYC gene. Tag distributions were smoothed and RPKM normalized using deepTOOLS. Traces were generated from merged biological replicate pairs.

    Article Snippet: The human HCC1806 triple negative breast cancer cell line, basal-like 2 subtype (ATCC) was maintained at 37 ° C in 5% CO 2 between 20–80% confluency in RPMI 1640 (Roswell Park Memorial Institute, Gibco 11875-093) containing 10% bovine calf serum (Gibco 16170-078), 1% L-glutamine (Gibco 25030-081), and 1% Penicillin/Streptomycin (Gibco-15146-122).

    Techniques: Generated, Standard Deviation