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u87 mg luc2 cells  (ATCC)


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    ATCC u87 mg luc2 cells
    U87 Mg Luc2 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 42 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u87 mg luc2 cells/product/ATCC
    Average 94 stars, based on 42 article reviews
    u87 mg luc2 cells - by Bioz Stars, 2026-05
    94/100 stars

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    ATCC human glioblastoma gbm cell line u87 mg luc2
    Pretreatment with Dox and TMZ enhances the in vivo antitumor activity of anti-HLA-G CAR-NK cells. (A) Treatment protocol used for the TNBC animal model. MDA-MB-231 cells (1×10 6 /mouse) were implanted orthotopically on day 0. On day 6 and for the following 3 weeks, mice received a weekly injection of normal saline or 0.5 mg/kg Dox via the tail vein. On day 7, mice were injected with normal saline or with 1.5×10 7 mock or anti-HLA-G CAR-NK cells, followed by infusion of 5×10 6 mock or anti-HLA-G CAR-NK cells each subsequent week for 3 weeks. (B) Representative IVIS images of MDA-MB231 tumors treated according to the protocols described in (A). Images were taken weekly. (C) Tumor progression, as measured by bioluminescence photometry. The luminoscore was calculated as the sum of flux values from the front and back views. (D) Survival was plotted using the Kaplan-Meier method. Mice were considered dead when the tumor volume exceeded 2000 mm 3 or the greatest dimension was >1.5 cm in any direction, as measured using an electronic manual caliper. (E) Treatment protocol for the GBM animal model. <t>U87</t> cells (1×10 6 /mouse) were implanted intracranially on day 0. On day 6 and for the following 3 weeks, mice were treated weekly (or not) with 3 mg/kg TMZ by oral gavage. Mice were injected with normal saline, or 1.5×10 7 mock or anti-HLA-G CAR-NK cells, on day 7, followed by infusion of 5×10 6 mock or anti-HLA-G CAR-NK cells each subsequent week for 3 weeks. (F) Representative weekly IVIS images of U87 tumors treated according to the protocols described in (E). (G) Tumor progression, as measured by bioluminescence photometry. (H) Survival plotted using the Kaplan-Meier method (*p<0.05, **p<0.01, ***p<0.001). CAR, chimeric antigen receptor; Dox, doxorubicin; GBM, glioblastoma; HLA-G, human leukocyte antigen G; IL, interleukin; NK, natural killer; TMZ, temozolomide; TNBC, triple-negative breast cancer.
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    ATCC brain glioma cell u87 mg luc2
    Relative expression of miR-124 in <t>U87</t> brain glioma stem cells after transfection. The RT-qPCR results showed that the relative expression of miR-124 in cells of miR-124 mimic group was significantly higher than that of miR-124 inhibitor and miR-control groups, while miR-124 inhibitor group was lower than miR-control group. *P<0.05.
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    Pretreatment with Dox and TMZ enhances the in vivo antitumor activity of anti-HLA-G CAR-NK cells. (A) Treatment protocol used for the TNBC animal model. MDA-MB-231 cells (1×10 6 /mouse) were implanted orthotopically on day 0. On day 6 and for the following 3 weeks, mice received a weekly injection of normal saline or 0.5 mg/kg Dox via the tail vein. On day 7, mice were injected with normal saline or with 1.5×10 7 mock or anti-HLA-G CAR-NK cells, followed by infusion of 5×10 6 mock or anti-HLA-G CAR-NK cells each subsequent week for 3 weeks. (B) Representative IVIS images of MDA-MB231 tumors treated according to the protocols described in (A). Images were taken weekly. (C) Tumor progression, as measured by bioluminescence photometry. The luminoscore was calculated as the sum of flux values from the front and back views. (D) Survival was plotted using the Kaplan-Meier method. Mice were considered dead when the tumor volume exceeded 2000 mm 3 or the greatest dimension was >1.5 cm in any direction, as measured using an electronic manual caliper. (E) Treatment protocol for the GBM animal model. U87 cells (1×10 6 /mouse) were implanted intracranially on day 0. On day 6 and for the following 3 weeks, mice were treated weekly (or not) with 3 mg/kg TMZ by oral gavage. Mice were injected with normal saline, or 1.5×10 7 mock or anti-HLA-G CAR-NK cells, on day 7, followed by infusion of 5×10 6 mock or anti-HLA-G CAR-NK cells each subsequent week for 3 weeks. (F) Representative weekly IVIS images of U87 tumors treated according to the protocols described in (E). (G) Tumor progression, as measured by bioluminescence photometry. (H) Survival plotted using the Kaplan-Meier method (*p<0.05, **p<0.01, ***p<0.001). CAR, chimeric antigen receptor; Dox, doxorubicin; GBM, glioblastoma; HLA-G, human leukocyte antigen G; IL, interleukin; NK, natural killer; TMZ, temozolomide; TNBC, triple-negative breast cancer.

    Journal: Journal for Immunotherapy of Cancer

    Article Title: Targeting human leukocyte antigen G with chimeric antigen receptors of natural killer cells convert immunosuppression to ablate solid tumors

    doi: 10.1136/jitc-2021-003050

    Figure Lengend Snippet: Pretreatment with Dox and TMZ enhances the in vivo antitumor activity of anti-HLA-G CAR-NK cells. (A) Treatment protocol used for the TNBC animal model. MDA-MB-231 cells (1×10 6 /mouse) were implanted orthotopically on day 0. On day 6 and for the following 3 weeks, mice received a weekly injection of normal saline or 0.5 mg/kg Dox via the tail vein. On day 7, mice were injected with normal saline or with 1.5×10 7 mock or anti-HLA-G CAR-NK cells, followed by infusion of 5×10 6 mock or anti-HLA-G CAR-NK cells each subsequent week for 3 weeks. (B) Representative IVIS images of MDA-MB231 tumors treated according to the protocols described in (A). Images were taken weekly. (C) Tumor progression, as measured by bioluminescence photometry. The luminoscore was calculated as the sum of flux values from the front and back views. (D) Survival was plotted using the Kaplan-Meier method. Mice were considered dead when the tumor volume exceeded 2000 mm 3 or the greatest dimension was >1.5 cm in any direction, as measured using an electronic manual caliper. (E) Treatment protocol for the GBM animal model. U87 cells (1×10 6 /mouse) were implanted intracranially on day 0. On day 6 and for the following 3 weeks, mice were treated weekly (or not) with 3 mg/kg TMZ by oral gavage. Mice were injected with normal saline, or 1.5×10 7 mock or anti-HLA-G CAR-NK cells, on day 7, followed by infusion of 5×10 6 mock or anti-HLA-G CAR-NK cells each subsequent week for 3 weeks. (F) Representative weekly IVIS images of U87 tumors treated according to the protocols described in (E). (G) Tumor progression, as measured by bioluminescence photometry. (H) Survival plotted using the Kaplan-Meier method (*p<0.05, **p<0.01, ***p<0.001). CAR, chimeric antigen receptor; Dox, doxorubicin; GBM, glioblastoma; HLA-G, human leukocyte antigen G; IL, interleukin; NK, natural killer; TMZ, temozolomide; TNBC, triple-negative breast cancer.

    Article Snippet: The Luc-expressing human glioblastoma (GBM) cell line U87 MG-Luc2 (ATCC) and SVGp12 (ATCC) were cultured in Eagle’s minimal essential medium (Thermo Fisher Scientific).

    Techniques: In Vivo, Activity Assay, Animal Model, Injection, Saline

    Relative expression of miR-124 in U87 brain glioma stem cells after transfection. The RT-qPCR results showed that the relative expression of miR-124 in cells of miR-124 mimic group was significantly higher than that of miR-124 inhibitor and miR-control groups, while miR-124 inhibitor group was lower than miR-control group. *P<0.05.

    Journal: Experimental and Therapeutic Medicine

    Article Title: miR-124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

    doi: 10.3892/etm.2019.7914

    Figure Lengend Snippet: Relative expression of miR-124 in U87 brain glioma stem cells after transfection. The RT-qPCR results showed that the relative expression of miR-124 in cells of miR-124 mimic group was significantly higher than that of miR-124 inhibitor and miR-control groups, while miR-124 inhibitor group was lower than miR-control group. *P<0.05.

    Article Snippet: Brain glioma cell U87 MG-Luc2 was purchased from ATCC (ATCCHTB-14-LUC2), hereinafter referred to as U87 cells and has been authenticated by STR profiling (Beijing Microread Genetics Co., Ltd.).

    Techniques: Expressing, Transfection, Quantitative RT-PCR, Control

    Expression of Nogo-A and NgR protein in  U87  brain glioma stem cells.

    Journal: Experimental and Therapeutic Medicine

    Article Title: miR-124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

    doi: 10.3892/etm.2019.7914

    Figure Lengend Snippet: Expression of Nogo-A and NgR protein in U87 brain glioma stem cells.

    Article Snippet: Brain glioma cell U87 MG-Luc2 was purchased from ATCC (ATCCHTB-14-LUC2), hereinafter referred to as U87 cells and has been authenticated by STR profiling (Beijing Microread Genetics Co., Ltd.).

    Techniques: Expressing

    (A) Expressions level of Nogo-A protein in U87 brain glioma stem cells after transfection. The relative expression of Nogo-A protein in cells of miR-124 mimic group was significantly lower than that of miR-124 inhibitor and miR-control groups, while the miR-124 inhibitor group was higher than miR-control group. (B) Expression level of NgR protein in U87 brain glioma stem cells after transfection. The relative expression of NgR protein in cells of miR-124 mimic group was significantly lower than that of miR-124 inhibitor and miR-control groups, while the miR-124 inhibitor group was higher than miR-control group. *P<0.05.

    Journal: Experimental and Therapeutic Medicine

    Article Title: miR-124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

    doi: 10.3892/etm.2019.7914

    Figure Lengend Snippet: (A) Expressions level of Nogo-A protein in U87 brain glioma stem cells after transfection. The relative expression of Nogo-A protein in cells of miR-124 mimic group was significantly lower than that of miR-124 inhibitor and miR-control groups, while the miR-124 inhibitor group was higher than miR-control group. (B) Expression level of NgR protein in U87 brain glioma stem cells after transfection. The relative expression of NgR protein in cells of miR-124 mimic group was significantly lower than that of miR-124 inhibitor and miR-control groups, while the miR-124 inhibitor group was higher than miR-control group. *P<0.05.

    Article Snippet: Brain glioma cell U87 MG-Luc2 was purchased from ATCC (ATCCHTB-14-LUC2), hereinafter referred to as U87 cells and has been authenticated by STR profiling (Beijing Microread Genetics Co., Ltd.).

    Techniques: Transfection, Expressing, Control

    Detection results of U87 brain glioma stem cells by MTT proliferation in vitro . The absorbance values of the cells in the miR-124 mimic and miR-control groups were significantly lower than those in the miR-124 inhibitor group at each time point, while the miR-124 mimic group was significantly lower than miR-control group. *P<0.05, compared with miR-control group; # P<0.05, compared with miR-124 inhibitor group.

    Journal: Experimental and Therapeutic Medicine

    Article Title: miR-124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

    doi: 10.3892/etm.2019.7914

    Figure Lengend Snippet: Detection results of U87 brain glioma stem cells by MTT proliferation in vitro . The absorbance values of the cells in the miR-124 mimic and miR-control groups were significantly lower than those in the miR-124 inhibitor group at each time point, while the miR-124 mimic group was significantly lower than miR-control group. *P<0.05, compared with miR-control group; # P<0.05, compared with miR-124 inhibitor group.

    Article Snippet: Brain glioma cell U87 MG-Luc2 was purchased from ATCC (ATCCHTB-14-LUC2), hereinafter referred to as U87 cells and has been authenticated by STR profiling (Beijing Microread Genetics Co., Ltd.).

    Techniques: In Vitro, Control

    Detection results of CD133 + U87 brain glioma stem cells. The level of CD133 + cells in miR-124 mimic group was significantly lower than that in miR-124 inhibitor and miR-control groups, while the miR-124 inhibitor group was higher than miR-control group. *P<0.05.

    Journal: Experimental and Therapeutic Medicine

    Article Title: miR-124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

    doi: 10.3892/etm.2019.7914

    Figure Lengend Snippet: Detection results of CD133 + U87 brain glioma stem cells. The level of CD133 + cells in miR-124 mimic group was significantly lower than that in miR-124 inhibitor and miR-control groups, while the miR-124 inhibitor group was higher than miR-control group. *P<0.05.

    Article Snippet: Brain glioma cell U87 MG-Luc2 was purchased from ATCC (ATCCHTB-14-LUC2), hereinafter referred to as U87 cells and has been authenticated by STR profiling (Beijing Microread Genetics Co., Ltd.).

    Techniques: Control