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hcc1937  (ATCC)


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    Structured Review

    ATCC hcc1937
    Hcc1937, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1229 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 1229 article reviews
    hcc1937 - by Bioz Stars, 2026-06
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    ATCC hcc1937 breast cancer cell lines
    A) Scheme of treatment used in the experiment. B, C, D) Treatment of MDA-MB-231, <t>HCC1937,</t> and MCF7 cells with Olaparib and PF4708671 (PF47) alone or with PF47 pretreatment followed by olaparib treatment (PF + Ola). The PF47 dose used for all cells was 20 µM for 24 hours. The olaparib dose used for MDA-MB-231 and HCC1937 was 80 µM, and for MCF7 it was 160 µM for 6 days. Two-way ANOVA with Dunnett’s post-hoc test was used for statistical analysis and results are presented as mean ± SD of 3 biological replicates. **=p<0.01; ***=p<00.1; ****=p<000.1.
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    ATCC atcc human tnbc cells
    Antiproliferative effects of CPC on <t>TNBC</t> cells in vitro and in vivo. (A) Cell viability of CPC and cisplatin in 24 h ATP assay. Two types of TNBC <t>cells</t> <t>(MDA‐MB‐231</t> and <t>HCC1937)</t> and normal breast cells (M10) were included. Cells (left) were treated with 0 (vehicle control containing 0.1% DMSO), 0.5, 1.5, and 2 μg/mL of CPC for 24 h. Moreover, cells (right) were treated with 0, 0.5, 1.5, 2, 4, 6, 8, and 10 μg/mL of cisplatin for 24 h. (B) Recovery of CPC‐induced antiproliferation by NAC. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters in the same cell line differ significantly ( p < 0.05) (Tukey HSD post hoc test). Taking panel (B) as an example (MDA‐MB‐231 cells), the “a” (with overlapping letters) labeling the control, NAC, and NAC/CPC (0.5, 1.5, and 2) treatments indicates that their differences were non‐significant. In contrast, the “a, b, and c” (without overlapping letters) labeling the control, CPC 0.5, and CPC 1.5 μg/mL indicates significant differences in multi‐comparisons. Cell experimental data are displayed as means ± SD ( n = 3). (C) TNBC xenograft tumor suppression of CPC. MDA‐MB‐231‐xenografted mice were treated with CPC (0, 50, and 200 μg: CPC0, CPC50, and CPC200) for 5 weeks. Body weight and tumor volume were monitored twice weekly, and tumor weights were measured at 5 weeks. Animal experiment data are expressed as means ± SD ( n = 6).
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    ATCC human hcc1937
    Antiproliferative effects of CPC on <t>TNBC</t> cells in vitro and in vivo. (A) Cell viability of CPC and cisplatin in 24 h ATP assay. Two types of TNBC <t>cells</t> <t>(MDA‐MB‐231</t> and <t>HCC1937)</t> and normal breast cells (M10) were included. Cells (left) were treated with 0 (vehicle control containing 0.1% DMSO), 0.5, 1.5, and 2 μg/mL of CPC for 24 h. Moreover, cells (right) were treated with 0, 0.5, 1.5, 2, 4, 6, 8, and 10 μg/mL of cisplatin for 24 h. (B) Recovery of CPC‐induced antiproliferation by NAC. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters in the same cell line differ significantly ( p < 0.05) (Tukey HSD post hoc test). Taking panel (B) as an example (MDA‐MB‐231 cells), the “a” (with overlapping letters) labeling the control, NAC, and NAC/CPC (0.5, 1.5, and 2) treatments indicates that their differences were non‐significant. In contrast, the “a, b, and c” (without overlapping letters) labeling the control, CPC 0.5, and CPC 1.5 μg/mL indicates significant differences in multi‐comparisons. Cell experimental data are displayed as means ± SD ( n = 3). (C) TNBC xenograft tumor suppression of CPC. MDA‐MB‐231‐xenografted mice were treated with CPC (0, 50, and 200 μg: CPC0, CPC50, and CPC200) for 5 weeks. Body weight and tumor volume were monitored twice weekly, and tumor weights were measured at 5 weeks. Animal experiment data are expressed as means ± SD ( n = 6).
    Human Hcc1937, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    crl  (ATCC)
    97
    ATCC crl
    Antiproliferative effects of CPC on <t>TNBC</t> cells in vitro and in vivo. (A) Cell viability of CPC and cisplatin in 24 h ATP assay. Two types of TNBC <t>cells</t> <t>(MDA‐MB‐231</t> and <t>HCC1937)</t> and normal breast cells (M10) were included. Cells (left) were treated with 0 (vehicle control containing 0.1% DMSO), 0.5, 1.5, and 2 μg/mL of CPC for 24 h. Moreover, cells (right) were treated with 0, 0.5, 1.5, 2, 4, 6, 8, and 10 μg/mL of cisplatin for 24 h. (B) Recovery of CPC‐induced antiproliferation by NAC. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters in the same cell line differ significantly ( p < 0.05) (Tukey HSD post hoc test). Taking panel (B) as an example (MDA‐MB‐231 cells), the “a” (with overlapping letters) labeling the control, NAC, and NAC/CPC (0.5, 1.5, and 2) treatments indicates that their differences were non‐significant. In contrast, the “a, b, and c” (without overlapping letters) labeling the control, CPC 0.5, and CPC 1.5 μg/mL indicates significant differences in multi‐comparisons. Cell experimental data are displayed as means ± SD ( n = 3). (C) TNBC xenograft tumor suppression of CPC. MDA‐MB‐231‐xenografted mice were treated with CPC (0, 50, and 200 μg: CPC0, CPC50, and CPC200) for 5 weeks. Body weight and tumor volume were monitored twice weekly, and tumor weights were measured at 5 weeks. Animal experiment data are expressed as means ± SD ( n = 6).
    Crl, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    A) Scheme of treatment used in the experiment. B, C, D) Treatment of MDA-MB-231, HCC1937, and MCF7 cells with Olaparib and PF4708671 (PF47) alone or with PF47 pretreatment followed by olaparib treatment (PF + Ola). The PF47 dose used for all cells was 20 µM for 24 hours. The olaparib dose used for MDA-MB-231 and HCC1937 was 80 µM, and for MCF7 it was 160 µM for 6 days. Two-way ANOVA with Dunnett’s post-hoc test was used for statistical analysis and results are presented as mean ± SD of 3 biological replicates. **=p<0.01; ***=p<00.1; ****=p<000.1.

    Journal: bioRxiv

    Article Title: S6K1 and S6K2 regulate homologous recombination DNA repair through control of BRCA1 protein stability

    doi: 10.64898/2026.04.28.721439

    Figure Lengend Snippet: A) Scheme of treatment used in the experiment. B, C, D) Treatment of MDA-MB-231, HCC1937, and MCF7 cells with Olaparib and PF4708671 (PF47) alone or with PF47 pretreatment followed by olaparib treatment (PF + Ola). The PF47 dose used for all cells was 20 µM for 24 hours. The olaparib dose used for MDA-MB-231 and HCC1937 was 80 µM, and for MCF7 it was 160 µM for 6 days. Two-way ANOVA with Dunnett’s post-hoc test was used for statistical analysis and results are presented as mean ± SD of 3 biological replicates. **=p<0.01; ***=p<00.1; ****=p<000.1.

    Article Snippet: MCF7, MDA-MB-231 and HCC1937 breast cancer cell lines were originally obtained from the ATCC and were a gift from Prof. Sandra Martha Gomes Dias.

    Techniques:

    Antiproliferative effects of CPC on TNBC cells in vitro and in vivo. (A) Cell viability of CPC and cisplatin in 24 h ATP assay. Two types of TNBC cells (MDA‐MB‐231 and HCC1937) and normal breast cells (M10) were included. Cells (left) were treated with 0 (vehicle control containing 0.1% DMSO), 0.5, 1.5, and 2 μg/mL of CPC for 24 h. Moreover, cells (right) were treated with 0, 0.5, 1.5, 2, 4, 6, 8, and 10 μg/mL of cisplatin for 24 h. (B) Recovery of CPC‐induced antiproliferation by NAC. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters in the same cell line differ significantly ( p < 0.05) (Tukey HSD post hoc test). Taking panel (B) as an example (MDA‐MB‐231 cells), the “a” (with overlapping letters) labeling the control, NAC, and NAC/CPC (0.5, 1.5, and 2) treatments indicates that their differences were non‐significant. In contrast, the “a, b, and c” (without overlapping letters) labeling the control, CPC 0.5, and CPC 1.5 μg/mL indicates significant differences in multi‐comparisons. Cell experimental data are displayed as means ± SD ( n = 3). (C) TNBC xenograft tumor suppression of CPC. MDA‐MB‐231‐xenografted mice were treated with CPC (0, 50, and 200 μg: CPC0, CPC50, and CPC200) for 5 weeks. Body weight and tumor volume were monitored twice weekly, and tumor weights were measured at 5 weeks. Animal experiment data are expressed as means ± SD ( n = 6).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: Antiproliferative effects of CPC on TNBC cells in vitro and in vivo. (A) Cell viability of CPC and cisplatin in 24 h ATP assay. Two types of TNBC cells (MDA‐MB‐231 and HCC1937) and normal breast cells (M10) were included. Cells (left) were treated with 0 (vehicle control containing 0.1% DMSO), 0.5, 1.5, and 2 μg/mL of CPC for 24 h. Moreover, cells (right) were treated with 0, 0.5, 1.5, 2, 4, 6, 8, and 10 μg/mL of cisplatin for 24 h. (B) Recovery of CPC‐induced antiproliferation by NAC. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters in the same cell line differ significantly ( p < 0.05) (Tukey HSD post hoc test). Taking panel (B) as an example (MDA‐MB‐231 cells), the “a” (with overlapping letters) labeling the control, NAC, and NAC/CPC (0.5, 1.5, and 2) treatments indicates that their differences were non‐significant. In contrast, the “a, b, and c” (without overlapping letters) labeling the control, CPC 0.5, and CPC 1.5 μg/mL indicates significant differences in multi‐comparisons. Cell experimental data are displayed as means ± SD ( n = 3). (C) TNBC xenograft tumor suppression of CPC. MDA‐MB‐231‐xenografted mice were treated with CPC (0, 50, and 200 μg: CPC0, CPC50, and CPC200) for 5 weeks. Body weight and tumor volume were monitored twice weekly, and tumor weights were measured at 5 weeks. Animal experiment data are expressed as means ± SD ( n = 6).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: In Vitro, In Vivo, ATP Assay, Control, Incubation, Labeling

    CPC treatment disturbed the cell cycle of TNBC cells. M10 is a normal cell, and others are TNBC cells. (A) Cell cycle detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. (B) Cell cycle detection and statistical analysis showed NAC's recovery of different incubation times of CPC treatment. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 12 and 24 h, i.e., CPC and NAC/CPC. For CPC post‐incubation, cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Cell cycle phases such as subG1, G1, S, and G2/M were defined as indicated in the flow cytometry panel. Columns labeled without overlapping letters differ significantly in the same phase of the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC treatment disturbed the cell cycle of TNBC cells. M10 is a normal cell, and others are TNBC cells. (A) Cell cycle detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. (B) Cell cycle detection and statistical analysis showed NAC's recovery of different incubation times of CPC treatment. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 12 and 24 h, i.e., CPC and NAC/CPC. For CPC post‐incubation, cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Cell cycle phases such as subG1, G1, S, and G2/M were defined as indicated in the flow cytometry panel. Columns labeled without overlapping letters differ significantly in the same phase of the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Control, Incubation, Flow Cytometry, Labeling

    CPC induces apoptosis (annexin V) in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A) Apoptosis (annexin V) detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Annexin V‐positive population indicated apoptosis (+). (B) Apoptosis (annexin V) detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced apoptosis. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. (C) Apoptosis (annexin V) detection and statistical analysis of different concentrations of cisplatin treatment. Cells were treated with 0, 1.5, and 2 μg/mL of cisplatin for 24 h. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC induces apoptosis (annexin V) in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A) Apoptosis (annexin V) detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Annexin V‐positive population indicated apoptosis (+). (B) Apoptosis (annexin V) detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced apoptosis. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. (C) Apoptosis (annexin V) detection and statistical analysis of different concentrations of cisplatin treatment. Cells were treated with 0, 1.5, and 2 μg/mL of cisplatin for 24 h. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Control, Incubation, Labeling

    CPC induces extrinsic apoptosis (PARP, caspase 3, and caspase 8 activation) but not intrinsic apoptosis (caspase 9) in TNBC cells. With pretreatments of vehicle, NAC (10 mM for 1 h), or Z‐VAD (50 μM for 2 h), cells were treated with 2 μg/mL of CPC for 0, 12, and 24 h. M10 is a normal cell, and others are TNBC cells. (A) Expression of cleaved forms of PARP, caspase 3, and caspase 8 were detected using Western blotting. (B) Statistical analysis. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3). c‐PARP, c‐Cas 3, c‐Cas 8, and c‐Cas 9 indicate the cleaved forms of PARP, caspases 3, 8, and 9.

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC induces extrinsic apoptosis (PARP, caspase 3, and caspase 8 activation) but not intrinsic apoptosis (caspase 9) in TNBC cells. With pretreatments of vehicle, NAC (10 mM for 1 h), or Z‐VAD (50 μM for 2 h), cells were treated with 2 μg/mL of CPC for 0, 12, and 24 h. M10 is a normal cell, and others are TNBC cells. (A) Expression of cleaved forms of PARP, caspase 3, and caspase 8 were detected using Western blotting. (B) Statistical analysis. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3). c‐PARP, c‐Cas 3, c‐Cas 8, and c‐Cas 9 indicate the cleaved forms of PARP, caspases 3, 8, and 9.

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Activation Assay, Expressing, Western Blot, Labeling

    CPC induces apoptosis (caspase 3 and 8 activation) in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A, C) Caspase 3/8 detection and statistical analysis for different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Symbol (+) represents caspase 3/8 (+) in flow cytometry. (B, D) Caspase 3/8 detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced apoptosis in flow cytometry. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated without or with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. (E, F) Caspase 3/7 and 8 detection and statistical analysis for different concentrations of cisplatin treatment in luminescence assays. Cells were treated with 0, 1.5, and 2 μg/mL of cisplatin for 24 h. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC induces apoptosis (caspase 3 and 8 activation) in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A, C) Caspase 3/8 detection and statistical analysis for different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Symbol (+) represents caspase 3/8 (+) in flow cytometry. (B, D) Caspase 3/8 detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced apoptosis in flow cytometry. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated without or with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. (E, F) Caspase 3/7 and 8 detection and statistical analysis for different concentrations of cisplatin treatment in luminescence assays. Cells were treated with 0, 1.5, and 2 μg/mL of cisplatin for 24 h. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Activation Assay, Control, Flow Cytometry, Incubation, Labeling

    CPC overexpresses ROS and MitoSOX in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A, C) ROS detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Symbol (+) represents high levels of ROS. (B, D) ROS and MitoSOX detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced ROS and MitoSOX. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as mean ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC overexpresses ROS and MitoSOX in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A, C) ROS detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. Symbol (+) represents high levels of ROS. (B, D) ROS and MitoSOX detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced ROS and MitoSOX. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as mean ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Control, Incubation, Labeling

    CPC triggers MMP depletion in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A) MMP detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. JC‐1 red and green represent the polymers and monomers of JC‐1. High JC‐1 ratio (green/red) indicates MMP depletion. (B) MMP detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced MMP depletion. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC triggers MMP depletion in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A) MMP detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. JC‐1 red and green represent the polymers and monomers of JC‐1. High JC‐1 ratio (green/red) indicates MMP depletion. (B) MMP detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced MMP depletion. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Control, Incubation, Labeling

    CPC causes γH2AX and 8‐OHdG DNA damage in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A, C) γH2AX and 8‐OHdG DNA damage detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. The symbol (+) represents high levels of γH2AX and 8‐OHdG. (B, D) γH2AX and 8‐OHdG detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced γH2AX and 8‐OHdG DNA damage. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC causes γH2AX and 8‐OHdG DNA damage in TNBC cells. M10 is a normal cell, and others are TNBC cells. (A, C) γH2AX and 8‐OHdG DNA damage detection and statistical analysis of different concentrations of CPC treatment. Cells were treated with 0 (control containing 0.1% DMSO), 1.5, and 2 μg/mL of CPC for 24 h. The symbol (+) represents high levels of γH2AX and 8‐OHdG. (B, D) γH2AX and 8‐OHdG detection and statistical analysis showed NAC's recovery of different incubation times of CPC‐induced γH2AX and 8‐OHdG DNA damage. Cells were pre‐incubated without or with NAC (10 mM for 1 h) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL), i.e., CPC and NAC/CPC. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Control, Incubation, Labeling

    CPC causes MAPK activation in TNBC cells. Cells were pre‐incubated without or with NAC (10 mM for 1 h) or MAPK inhibitors (JNK, p38 or ERK) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL). (A) Cell viability of MAPK inhibitors in CPC‐treated TNBC cells. (B) Phosphorylation of MAPKs by CPC on TNBC cells. (C) Apoptosis of JNKi/CPC, p38i/CPC, and ERKi/CPC in TNBC cells. (D) Caspase 3/7 and 8 activations of JNKi/CPC, p38i/CPC, and ERKi/CPC in TNBC cells. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: CPC causes MAPK activation in TNBC cells. Cells were pre‐incubated without or with NAC (10 mM for 1 h) or MAPK inhibitors (JNK, p38 or ERK) and post‐incubated with CPC for 0, 12, and 24 h (2 μg/mL). (A) Cell viability of MAPK inhibitors in CPC‐treated TNBC cells. (B) Phosphorylation of MAPKs by CPC on TNBC cells. (C) Apoptosis of JNKi/CPC, p38i/CPC, and ERKi/CPC in TNBC cells. (D) Caspase 3/7 and 8 activations of JNKi/CPC, p38i/CPC, and ERKi/CPC in TNBC cells. Columns labeled without overlapping letters differ significantly in the same cell line ( p < 0.05) (Tukey HSD post hoc test). Data are expressed as means ± SD ( n = 3).

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Activation Assay, Incubation, Phospho-proteomics, Labeling

    Overview of CPC's anti‐TNBC cell proliferation effect and mechanism. CPC caused selective oxidative stress, MAPK activation, apoptosis, and DNA damage in TNBC cells, leading to the selective inhibition of TNBC cell proliferation compared with normal cells. These selective anti‐TNBC effects of CPC were dependent on oxidative stress, confirmed by the pretreatments of NAC or MAPK inhibitors.

    Journal: Drug Development Research

    Article Title: Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model

    doi: 10.1002/ddr.70286

    Figure Lengend Snippet: Overview of CPC's anti‐TNBC cell proliferation effect and mechanism. CPC caused selective oxidative stress, MAPK activation, apoptosis, and DNA damage in TNBC cells, leading to the selective inhibition of TNBC cell proliferation compared with normal cells. These selective anti‐TNBC effects of CPC were dependent on oxidative stress, confirmed by the pretreatments of NAC or MAPK inhibitors.

    Article Snippet: ATCC human TNBC cells (MDA‐MB‐231 and HCC1937) were included and maintained in mixed Dulbecco's Modified Eagle's Medium (DMEM)/F12 medium (3:2) and RPMI Medium 1640 (Gibco).

    Techniques: Activation Assay, Inhibition