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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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1) Product Images from "Cryptocaryone Exhibits ROS/MAPK‐Dependent Antiproliferative and Apoptosis‐Inducing Effects on Triple‐Negative Breast Cancer Cells and Proof‐of‐Concept Breast Cancer Mouse Model"

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

Journal: Drug Development Research

doi: 10.1002/ddr.70286

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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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.

Figure Legend 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.

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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.

Figure Legend 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.

Techniques Used: Activation Assay, Inhibition

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Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Journal: Drug Development Research

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

Dose-dependent cytotoxic effects of GNT and Apigenin on HCC1937 cells evaluated by the MTT assay. ( A ) Dose–response curves showing percentage cell viability plotted against the logarithm of compound concentration (µM). ( B ) Bar graph representation of cell viability at increasing concentrations (10–400 µM) compared to control. Data are presented as mean ± SD ( n = 6)

Journal: BMC Pharmacology & Toxicology

Article Title: Integrated in silico and in vitro evaluation of Genistein and Apigenin as dual inhibitors of PARP1 and ESR1 in breast cancer

doi: 10.1186/s40360-025-01082-z

Figure Lengend Snippet: Dose-dependent cytotoxic effects of GNT and Apigenin on HCC1937 cells evaluated by the MTT assay. ( A ) Dose–response curves showing percentage cell viability plotted against the logarithm of compound concentration (µM). ( B ) Bar graph representation of cell viability at increasing concentrations (10–400 µM) compared to control. Data are presented as mean ± SD ( n = 6)

Article Snippet: HCC1937 human triple-negative breast cancer (TNBC) cells were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA; Cat. No. CRL-2336).

Techniques: MTT Assay, Concentration Assay, Control

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