cells  (ATCC)

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

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

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

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

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

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

Journal: Signal Transduction and Targeted Therapy

Article Title: Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth

doi: 10.1038/s41392-026-02650-3

Figure Lengend Snippet: Determination of anti-tumor activity of iMac with induced ACE expression, in vitro. a Proliferation of melanoma (SK-MEL-28), Triple Negative Breast Cancer (TNBC: HCC1806), and FP chemotherapy resistant HNSCC (FaDu/FP-R) cell lines cultured alone or indirectly co-cultured with iMac ( ± Dox) using 3.0 µm pore polyester membrane inserts for 5 days. Total and dead cell counts were determined via trypan blue exclusion on days 1, 3, and 5. b , c Quantification of iNOS and interleukin-12 (IL-12) production in Cnt-iMac and ACE-iMac treated with LPS (500 ng/ml, 12 h), ± Dox. d ROS production in ACE-iMac following LPS stimulation (1 µg/ml, 30 min) ±Dox, assessed by DCFDA (2’,7’-dichlorodihydrofluorescein diacetate) staining. Representative histograms (left) and mean fluorescence intensity (MFI) quantification (right) are shown. Nitric Oxide (NO) production in ACE-iMac stimulated with LPS (75 ng/ml) for 24 h ( e ), and/or conditioned with SK-MEL-28 supernatant for 24 h ( f ) ± Dox. g Perforin and IFN-γ levels in human peripheral blood NK and Tc cells, respectively, after co-culture with Cnt-iMac or ACE-iMac pretreated with LPS (24 h), followed by melanoma conditioning (24 h). To induce ACE expression, myeloid progenitors were differentiated in the presence of Dox and maintained at 1 µg/ml throughout all in vitro assays. Experiments were performed in triplicates across three independent replicates. Statistical analyses included one-way ANOVA ( a ), two-way ANOVA with Bonferroni correction ( b , c , g ), and two-sided unpaired Student’s t -test ( d – f ). Data are presented as means ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Article Snippet: The triple negative breast (TNB) cancer cell line HCC1806 and the melanoma cell line SK-MEL-28 were obtained from ATCC.

Techniques: Activity Assay, Expressing, In Vitro, Cell Culture, Membrane, Staining, Fluorescence, Co-Culture Assay

Journal: Signal Transduction and Targeted Therapy

Article Title: Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth

doi: 10.1038/s41392-026-02650-3

Figure Lengend Snippet: The effect of ACE-expressing iMac treatment on tumor growth in immunocompromised nude mice. To induce ACE expression, myeloid progenitors were differentiated in the presence of 1 µg/ml Dox (termed as ACE-iMac), while control iMac with basal ACE expression were differentiated in the absence of Dox. a Experimental scheme of iMac treatment. Mice were injected intratumorally with PBS, Cnt-iMac (±Dox) or ACE-iMac (±Dox) weekly (3–4 doses) as indicated by arrow. b Growth of melanoma xenografts derived from the SK-MEL-28 cell line. c Growth of breast cancer xenografts derived from the HCC1806 cell line. d Growth of HNSCC xenografts derived from the FaDu/FP-R cell line. For b – d Left panels show plots comparing tumor growth rates, the middle panels show representative images of tumors, and right panels show graphs comparing tumor weight. Following cell administration, Dox+ (ACE-iMac) mouse groups were provided with 150 µg/ml doxycycline in their drinking water throughout the duration of the study. Group comparisons were analyzed using one-way ANOVA with Bonferroni’s correction for multiple comparisons. Data are presented as means ± SEM ( n = 5–10). * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001

Article Snippet: The triple negative breast (TNB) cancer cell line HCC1806 and the melanoma cell line SK-MEL-28 were obtained from ATCC.

Techniques: Expressing, Control, Injection, Derivative Assay

Journal: Frontiers in Immunology

Article Title: Erythrocyte membrane–liposome coating sustains circulation stability and targeted tumor therapy of CAR-T cells

doi: 10.3389/fimmu.2026.1799107

Figure Lengend Snippet: Impact of Rlip modification on CD19 CAR-T cell binding efficiency, CAR expression, and functional phenotype. (A) . Schematic of the anti-CD19 CAR construct. (B) . Flow-cytometry histograms showing CD19 CAR expression in untransduced human T cells versus anti-CD19 CAR-T cells. (C). Flowcytometry histograms of RhB positivity in CAR-T and Rlip-CAR-T cells (reflecting Rlip binding efficiency). (D) . Flow-cytometry dot plots showing CD19 CAR expression levels in CAR-T and Rlip-CAR-T cells. (E) . Quantitative analysis of CD19 CAR expression ratios between CAR-T and Rlip-CART cells. (F) . Cytotoxic activity of CAR-T and Rlip-CAR-T cells against Nalm-6 and Raji cells at the indicated E:T ratios. (G) . Flow-cytometry dot plots showing memory-phenotype distribution of CAR-T and Rlip-CAR-T cells stained for CD62L and CD45RA. (H) . Quantitative analysis of T-cell memory subsets (TSCM, TCM, TEM, TTE) in CAR-T and Rlip-CAR-T cells. (I) . Quantitative analysis of activation-marker (CD69, CD25) expression in CAR-T and Rlip-CAR-T cells. (J) . Quantitative analysis of exhaustion-marker (PD-1, LAG-3) expression in CAR-T and Rlip-CAR-T cells. All data are obtained from at least three donors and presented as mean ± SD; ns, not significant. Cytotoxic activity (F) was analyzed by two-way ANOVA; all other quantitative comparisons (E, H–J) used two-tailed unpaired t-tests.

Article Snippet: Human breast cancer cell line HCC1806, ovarian cancer cell line OVCAR3, B-cell lymphoma cell line Raji, human monocytic leukemia cell line THP-1, and B-cell precursor leukemia cell line NALM-6 were purchased from the American Type Culture Collection (ATCC).

Techniques: Modification, Binding Assay, Expressing, Functional Assay, Construct, Flow Cytometry, Activity Assay, Staining, Activation Assay, Marker, Two Tailed Test