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human her2 breast cancer cell lines skbr3  (ATCC)


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    ATCC human her2 breast cancer cell lines skbr3
    Human Her2 Breast Cancer Cell Lines Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7115 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 7115 article reviews
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    ATCC human her2 breast cancer cell lines skbr3
    Human Her2 Breast Cancer Cell Lines Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human breast cancer cell skbr3 her2
    Srsf3 knockout promotes Htatip2 expression in liver cancer but reduces Htatip2 expression in breast cancer visualized by IGV (A). Srsf3 KD in Hepa 1-6 cells, a murine hepatoma cell line, led to increased expression of Htatip2. Hepa1-6 cells were transfected with 40 nM of Srsf3-specific siRNA (si-Srsf3) or non-targeting siRNA (si-NC) and harvested at 48h upon transfection for analysis. Srsf3 KD efficiency was confirmed by Western blot, with Gapdh serving as a sample loading control (B). (C) Srsf3 KD in Hepa 1-6 cells led to increased expression of Htatip2 examined by TaqMan RT-qPCR in three independent experiments. *, p< 0.05 by Student’s t-test.. (D-E) Knockdown (KD) of Srsf3/SRSF3 promotes exon 11 inclusion in Eif4a2 RNA splicing leading to reduction of eIF4A2 protein in mouse and human breast cancer cells. Total cell RNA was extracted from the cultured individual cell lines transfected with 40 nM of the indicated siRNAs and harvested at 48 h after transfection and used for RT-PCR assays with a forward primer from exon 10 and backward primer from exon 12 (D). Total cell extracts from corresponding cell lines prepared at the 48 h after siRNA transfection were immunoblotted for the protein expression of eIF4A2, SRSF3, and GAPDH with the corresponding antibodies (E).
    Human Breast Cancer Cell Skbr3 Her2, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human her2 positive breast cancer cell line skbr3
    Srsf3 knockout promotes Htatip2 expression in liver cancer but reduces Htatip2 expression in breast cancer visualized by IGV (A). Srsf3 KD in Hepa 1-6 cells, a murine hepatoma cell line, led to increased expression of Htatip2. Hepa1-6 cells were transfected with 40 nM of Srsf3-specific siRNA (si-Srsf3) or non-targeting siRNA (si-NC) and harvested at 48h upon transfection for analysis. Srsf3 KD efficiency was confirmed by Western blot, with Gapdh serving as a sample loading control (B). (C) Srsf3 KD in Hepa 1-6 cells led to increased expression of Htatip2 examined by TaqMan RT-qPCR in three independent experiments. *, p< 0.05 by Student’s t-test.. (D-E) Knockdown (KD) of Srsf3/SRSF3 promotes exon 11 inclusion in Eif4a2 RNA splicing leading to reduction of eIF4A2 protein in mouse and human breast cancer cells. Total cell RNA was extracted from the cultured individual cell lines transfected with 40 nM of the indicated siRNAs and harvested at 48 h after transfection and used for RT-PCR assays with a forward primer from exon 10 and backward primer from exon 12 (D). Total cell extracts from corresponding cell lines prepared at the 48 h after siRNA transfection were immunoblotted for the protein expression of eIF4A2, SRSF3, and GAPDH with the corresponding antibodies (E).
    Human Her2 Positive Breast Cancer Cell Line Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC human her2 expressing breast cancer cell lines skbr3
    Srsf3 knockout promotes Htatip2 expression in liver cancer but reduces Htatip2 expression in breast cancer visualized by IGV (A). Srsf3 KD in Hepa 1-6 cells, a murine hepatoma cell line, led to increased expression of Htatip2. Hepa1-6 cells were transfected with 40 nM of Srsf3-specific siRNA (si-Srsf3) or non-targeting siRNA (si-NC) and harvested at 48h upon transfection for analysis. Srsf3 KD efficiency was confirmed by Western blot, with Gapdh serving as a sample loading control (B). (C) Srsf3 KD in Hepa 1-6 cells led to increased expression of Htatip2 examined by TaqMan RT-qPCR in three independent experiments. *, p< 0.05 by Student’s t-test.. (D-E) Knockdown (KD) of Srsf3/SRSF3 promotes exon 11 inclusion in Eif4a2 RNA splicing leading to reduction of eIF4A2 protein in mouse and human breast cancer cells. Total cell RNA was extracted from the cultured individual cell lines transfected with 40 nM of the indicated siRNAs and harvested at 48 h after transfection and used for RT-PCR assays with a forward primer from exon 10 and backward primer from exon 12 (D). Total cell extracts from corresponding cell lines prepared at the 48 h after siRNA transfection were immunoblotted for the protein expression of eIF4A2, SRSF3, and GAPDH with the corresponding antibodies (E).
    Human Her2 Expressing Breast Cancer Cell Lines Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC skbr3 her2 human breast cancer cells
    Phase-contrast photomicrography of scratch wounds in MDA-MB-231 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) DMEM medium supplemented with 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.
    Skbr3 Her2 Human Breast Cancer Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC mda-mb-231
    Phase-contrast photomicrography of scratch wounds in MDA-MB-231 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) DMEM medium supplemented with 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.
    Mda Mb 231, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC her2 skbr3 human breast adenocarcinoma cancer cells
    MitoQ selectively represses mitochondrial superoxide production by human breast cancer cells. Cells were treated ± MitoQ 100 nM for 48 h. ( a ) The oxygen consumption rate (OCR) of MDA-MB-231 cells was measured using Seahorse oximetry. The graph represents OCR measurements over time with the sequential addition of oligomycin, FCCP, and rotenone (Rot) together with antimycin A (AA). From Seahorse traces, basal, maximal and ATP-linked mitochondrial oxygen consumption rates (mtOCRs) were calculated ( n = 8–18). ( b ) The mitochondrial potential (Δψ) of MDA-MB-231 cells was measured using JC-10 ( n = 16). ( c ) Mitochondrial superoxide (mtO 2 − ) levels were measured using electron paramagnetic resonance (EPR) with MitoTEMPO-H as a selective mtO 2 − sensor ± PEG-SOD2 ( n = 6). ( d ) Seahorse oximetry as in a, but using human <t>SkBr3</t> breast cancer cells ( n = 29–41). ( e ) Δψ measurement as in b, but using SkBr3 cells ( n = 16). ( f ) Determination of mtO 2 − levels as in c, but using SkBr3 cells ( n = 4). ( g ) Seahorse oximetry as in a, but using human MDA-MB-436 breast cancer cells ( n = 16). Note that SEMs are smaller than symbols in the left graph showing oximetry traces. ( h ) Δψ measurement as in b, but using MDA-MB-436 cells ( n = 8). ( i ) Determination of mtO 2 − levels as in c, but using MDA-MB-436 cells. ( n = 4). ( j ) Seahorse oximetry as in a, but using nonmalignant MCF10A human breast epithelial cells ( n = 18–24). ( k ) Δψ measurement as in b, but using MCF10A cells ( n = 8). ( l ) Determination of mtO 2 − levels as in c, but using MCF10A cells ( n = 3). All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t -test ( a – l ).
    Her2 Skbr3 Human Breast Adenocarcinoma Cancer Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Srsf3 knockout promotes Htatip2 expression in liver cancer but reduces Htatip2 expression in breast cancer visualized by IGV (A). Srsf3 KD in Hepa 1-6 cells, a murine hepatoma cell line, led to increased expression of Htatip2. Hepa1-6 cells were transfected with 40 nM of Srsf3-specific siRNA (si-Srsf3) or non-targeting siRNA (si-NC) and harvested at 48h upon transfection for analysis. Srsf3 KD efficiency was confirmed by Western blot, with Gapdh serving as a sample loading control (B). (C) Srsf3 KD in Hepa 1-6 cells led to increased expression of Htatip2 examined by TaqMan RT-qPCR in three independent experiments. *, p< 0.05 by Student’s t-test.. (D-E) Knockdown (KD) of Srsf3/SRSF3 promotes exon 11 inclusion in Eif4a2 RNA splicing leading to reduction of eIF4A2 protein in mouse and human breast cancer cells. Total cell RNA was extracted from the cultured individual cell lines transfected with 40 nM of the indicated siRNAs and harvested at 48 h after transfection and used for RT-PCR assays with a forward primer from exon 10 and backward primer from exon 12 (D). Total cell extracts from corresponding cell lines prepared at the 48 h after siRNA transfection were immunoblotted for the protein expression of eIF4A2, SRSF3, and GAPDH with the corresponding antibodies (E).

    Journal: bioRxiv

    Article Title: SRSF3 is oncogenic in breast but tumor-suppressive in liver by differential regulation of gene expression

    doi: 10.1101/2025.03.14.643315

    Figure Lengend Snippet: Srsf3 knockout promotes Htatip2 expression in liver cancer but reduces Htatip2 expression in breast cancer visualized by IGV (A). Srsf3 KD in Hepa 1-6 cells, a murine hepatoma cell line, led to increased expression of Htatip2. Hepa1-6 cells were transfected with 40 nM of Srsf3-specific siRNA (si-Srsf3) or non-targeting siRNA (si-NC) and harvested at 48h upon transfection for analysis. Srsf3 KD efficiency was confirmed by Western blot, with Gapdh serving as a sample loading control (B). (C) Srsf3 KD in Hepa 1-6 cells led to increased expression of Htatip2 examined by TaqMan RT-qPCR in three independent experiments. *, p< 0.05 by Student’s t-test.. (D-E) Knockdown (KD) of Srsf3/SRSF3 promotes exon 11 inclusion in Eif4a2 RNA splicing leading to reduction of eIF4A2 protein in mouse and human breast cancer cells. Total cell RNA was extracted from the cultured individual cell lines transfected with 40 nM of the indicated siRNAs and harvested at 48 h after transfection and used for RT-PCR assays with a forward primer from exon 10 and backward primer from exon 12 (D). Total cell extracts from corresponding cell lines prepared at the 48 h after siRNA transfection were immunoblotted for the protein expression of eIF4A2, SRSF3, and GAPDH with the corresponding antibodies (E).

    Article Snippet: Mouse breast cancer cell NF639 expressing c-neu oncogene, human breast cancer cell SKBR3 (HER2+) and MCF7 (ER+) was purchased from ATCC.

    Techniques: Knock-Out, Expressing, Transfection, Western Blot, Control, Quantitative RT-PCR, Knockdown, Cell Culture, Reverse Transcription Polymerase Chain Reaction

    Phase-contrast photomicrography of scratch wounds in MDA-MB-231 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) DMEM medium supplemented with 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.

    Journal: Pharmaceutics

    Article Title: Hybrid Nanosystem Formed by DOX-Loaded Liposomes and Extracellular Vesicles from MDA-MB-231 Is Effective against Breast Cancer Cells with Different Molecular Profiles

    doi: 10.3390/pharmaceutics16060739

    Figure Lengend Snippet: Phase-contrast photomicrography of scratch wounds in MDA-MB-231 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) DMEM medium supplemented with 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.

    Article Snippet: The MDA-MB-231 (triple negative), MCF7 (ER+/PR+/HER2+), and SKBR3 (HER2+) human breast cancer cells were purchased from the American Type Culture Collection (ATCC) (Manassas, VA, USA).

    Techniques: Control

    Phase-contrast photomicrography of scratch wounds in MCF-7 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) MEM medium supplemented with insulin (10 mg/L) and 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.

    Journal: Pharmaceutics

    Article Title: Hybrid Nanosystem Formed by DOX-Loaded Liposomes and Extracellular Vesicles from MDA-MB-231 Is Effective against Breast Cancer Cells with Different Molecular Profiles

    doi: 10.3390/pharmaceutics16060739

    Figure Lengend Snippet: Phase-contrast photomicrography of scratch wounds in MCF-7 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) MEM medium supplemented with insulin (10 mg/L) and 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.

    Article Snippet: The MDA-MB-231 (triple negative), MCF7 (ER+/PR+/HER2+), and SKBR3 (HER2+) human breast cancer cells were purchased from the American Type Culture Collection (ATCC) (Manassas, VA, USA).

    Techniques: Control

    Phase-contrast photomicrography of scratch wounds in SKBR-3 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) McCoy medium supplemented with 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.

    Journal: Pharmaceutics

    Article Title: Hybrid Nanosystem Formed by DOX-Loaded Liposomes and Extracellular Vesicles from MDA-MB-231 Is Effective against Breast Cancer Cells with Different Molecular Profiles

    doi: 10.3390/pharmaceutics16060739

    Figure Lengend Snippet: Phase-contrast photomicrography of scratch wounds in SKBR-3 breast cancer cell line at ( A ) time zero and after 24 h of exposure to ( B ) McCoy medium supplemented with 1% FBS (control), ( C ) free DOX, ( D ) pHSL-DOX, ( E ) DOXOPEG ® , ( F ) HF-pHSL/EV-DOX, ( G ) blank HF-pHSL/EV. The images are representative of three independent experiments. Magnification at 5×.

    Article Snippet: The MDA-MB-231 (triple negative), MCF7 (ER+/PR+/HER2+), and SKBR3 (HER2+) human breast cancer cells were purchased from the American Type Culture Collection (ATCC) (Manassas, VA, USA).

    Techniques: Control

    MitoQ selectively represses mitochondrial superoxide production by human breast cancer cells. Cells were treated ± MitoQ 100 nM for 48 h. ( a ) The oxygen consumption rate (OCR) of MDA-MB-231 cells was measured using Seahorse oximetry. The graph represents OCR measurements over time with the sequential addition of oligomycin, FCCP, and rotenone (Rot) together with antimycin A (AA). From Seahorse traces, basal, maximal and ATP-linked mitochondrial oxygen consumption rates (mtOCRs) were calculated ( n = 8–18). ( b ) The mitochondrial potential (Δψ) of MDA-MB-231 cells was measured using JC-10 ( n = 16). ( c ) Mitochondrial superoxide (mtO 2 − ) levels were measured using electron paramagnetic resonance (EPR) with MitoTEMPO-H as a selective mtO 2 − sensor ± PEG-SOD2 ( n = 6). ( d ) Seahorse oximetry as in a, but using human SkBr3 breast cancer cells ( n = 29–41). ( e ) Δψ measurement as in b, but using SkBr3 cells ( n = 16). ( f ) Determination of mtO 2 − levels as in c, but using SkBr3 cells ( n = 4). ( g ) Seahorse oximetry as in a, but using human MDA-MB-436 breast cancer cells ( n = 16). Note that SEMs are smaller than symbols in the left graph showing oximetry traces. ( h ) Δψ measurement as in b, but using MDA-MB-436 cells ( n = 8). ( i ) Determination of mtO 2 − levels as in c, but using MDA-MB-436 cells. ( n = 4). ( j ) Seahorse oximetry as in a, but using nonmalignant MCF10A human breast epithelial cells ( n = 18–24). ( k ) Δψ measurement as in b, but using MCF10A cells ( n = 8). ( l ) Determination of mtO 2 − levels as in c, but using MCF10A cells ( n = 3). All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t -test ( a – l ).

    Journal: Cancers

    Article Title: MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

    doi: 10.3390/cancers14061516

    Figure Lengend Snippet: MitoQ selectively represses mitochondrial superoxide production by human breast cancer cells. Cells were treated ± MitoQ 100 nM for 48 h. ( a ) The oxygen consumption rate (OCR) of MDA-MB-231 cells was measured using Seahorse oximetry. The graph represents OCR measurements over time with the sequential addition of oligomycin, FCCP, and rotenone (Rot) together with antimycin A (AA). From Seahorse traces, basal, maximal and ATP-linked mitochondrial oxygen consumption rates (mtOCRs) were calculated ( n = 8–18). ( b ) The mitochondrial potential (Δψ) of MDA-MB-231 cells was measured using JC-10 ( n = 16). ( c ) Mitochondrial superoxide (mtO 2 − ) levels were measured using electron paramagnetic resonance (EPR) with MitoTEMPO-H as a selective mtO 2 − sensor ± PEG-SOD2 ( n = 6). ( d ) Seahorse oximetry as in a, but using human SkBr3 breast cancer cells ( n = 29–41). ( e ) Δψ measurement as in b, but using SkBr3 cells ( n = 16). ( f ) Determination of mtO 2 − levels as in c, but using SkBr3 cells ( n = 4). ( g ) Seahorse oximetry as in a, but using human MDA-MB-436 breast cancer cells ( n = 16). Note that SEMs are smaller than symbols in the left graph showing oximetry traces. ( h ) Δψ measurement as in b, but using MDA-MB-436 cells ( n = 8). ( i ) Determination of mtO 2 − levels as in c, but using MDA-MB-436 cells. ( n = 4). ( j ) Seahorse oximetry as in a, but using nonmalignant MCF10A human breast epithelial cells ( n = 18–24). ( k ) Δψ measurement as in b, but using MCF10A cells ( n = 8). ( l ) Determination of mtO 2 − levels as in c, but using MCF10A cells ( n = 3). All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t -test ( a – l ).

    Article Snippet: HER2+ SkBr3 human breast adenocarcinoma cancer cells (catalogue #HTB-30), triple-negative MDA-MB-436 human breast adenocarcinoma cancer cells (catalogue #HTB-130) and MCF10A human nonmalignant breast epithelial cells (catalogue #CRL-10317) were from ATCC (Manassas, VA, USA).

    Techniques: Electron Paramagnetic Resonance, Control

    MitoQ increases glucose consumption and lactate release by human breast cancer cells, and is cytostatic at doses ≥ 250 nM. ( a ) MDA-MB-231 cells were treated ± MitoQ 100 nM for 48 h. Glucose consumption (left), lactate production (middle) and the lactate/glucose ratio (right) were then determined using enzymatic assays on a CMA600 analyzer ( n = 3 all). ( b ) Viable MDA-MB-231 cells were counted on a SpectraMax i3 spectrophotometer at the indicated time points after treatment with increasing doses of MitoQ ( n = 4). ( c ) Enzymatic measurements of glucose and lactate consumption as in a, but using SkBr3 cells ( n = 10). ( d ) SkBr3 cell viability was determined as in b ( n = 8). ( e ) Enzymatic measurements of glucose and lactate consumption as in a, but using MDA-MB-436 cells ( n = 10). ( f ) MDA-MB-436 cell viability was determined as in b ( n = 8). ( g ) Enzymatic measurements of glucose and lactate consumption as in a, but using MCF10A normal epithelial breast cells ( n = 4). ( h ) MCF10A cell viability was determined as in b ( n = 8). All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t -test ( a , c , e , g ) or 2-way ANOVA with Tukey’s post hoc test ( b , d , f , h ).

    Journal: Cancers

    Article Title: MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

    doi: 10.3390/cancers14061516

    Figure Lengend Snippet: MitoQ increases glucose consumption and lactate release by human breast cancer cells, and is cytostatic at doses ≥ 250 nM. ( a ) MDA-MB-231 cells were treated ± MitoQ 100 nM for 48 h. Glucose consumption (left), lactate production (middle) and the lactate/glucose ratio (right) were then determined using enzymatic assays on a CMA600 analyzer ( n = 3 all). ( b ) Viable MDA-MB-231 cells were counted on a SpectraMax i3 spectrophotometer at the indicated time points after treatment with increasing doses of MitoQ ( n = 4). ( c ) Enzymatic measurements of glucose and lactate consumption as in a, but using SkBr3 cells ( n = 10). ( d ) SkBr3 cell viability was determined as in b ( n = 8). ( e ) Enzymatic measurements of glucose and lactate consumption as in a, but using MDA-MB-436 cells ( n = 10). ( f ) MDA-MB-436 cell viability was determined as in b ( n = 8). ( g ) Enzymatic measurements of glucose and lactate consumption as in a, but using MCF10A normal epithelial breast cells ( n = 4). ( h ) MCF10A cell viability was determined as in b ( n = 8). All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t -test ( a , c , e , g ) or 2-way ANOVA with Tukey’s post hoc test ( b , d , f , h ).

    Article Snippet: HER2+ SkBr3 human breast adenocarcinoma cancer cells (catalogue #HTB-30), triple-negative MDA-MB-436 human breast adenocarcinoma cancer cells (catalogue #HTB-130) and MCF10A human nonmalignant breast epithelial cells (catalogue #CRL-10317) were from ATCC (Manassas, VA, USA).

    Techniques: Spectrophotometry, Control

    MitoQ has mitigated effects on the epithelial to mesenchymal transition (EMT) of human breast cancer cells. Cells were treated ± MitoQ for 48 h. ( a ) Representative immunocytological pictures where MDA-MB-231, SkBr3 and MDA-MB-436 cells are stained with hematoxylin and eosin. Bars = 1 mm. ( b ) Cells were stained with primary antibodies anti-vimentin and anti-E-cadherin (green fluorescence), and nuclei were stained with DAPI (blue). Representative pictures are shown on top, and the graphs on the bottom show the fluorescence intensity for MDA-MB-231 ( n = 9–12), SkBr3 ( n = 9–12) and MDA-MB-436 ( n = 11-12) cells. Bars = 20 µm. ( c ) mRNA expression of EMT markers vimentin ( VIM ), SNAIL ( SNAI1 ), SLUG ( SNAI2 ), ZEB1 and TWIST1 in MDA-MB-231 cancer cells treated ± 500 nM MitoQ for 48 h ( n = 6–9). ( d ) Western blots (WBs) of the corresponding proteins with β-actin as a loading control. ( e ) mRNA expression in c, but in SkBr3 cells ( n = 3–9). ( f ) WBs as in d, but using SkBr3 cells. ( g ) mRNA expression in c, but in MDA-MB-436 cells ( n = 6–9). ( h ) WBs as in d, but using MDA-MB-436 cells. All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t test ( b , c , e , g ).

    Journal: Cancers

    Article Title: MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

    doi: 10.3390/cancers14061516

    Figure Lengend Snippet: MitoQ has mitigated effects on the epithelial to mesenchymal transition (EMT) of human breast cancer cells. Cells were treated ± MitoQ for 48 h. ( a ) Representative immunocytological pictures where MDA-MB-231, SkBr3 and MDA-MB-436 cells are stained with hematoxylin and eosin. Bars = 1 mm. ( b ) Cells were stained with primary antibodies anti-vimentin and anti-E-cadherin (green fluorescence), and nuclei were stained with DAPI (blue). Representative pictures are shown on top, and the graphs on the bottom show the fluorescence intensity for MDA-MB-231 ( n = 9–12), SkBr3 ( n = 9–12) and MDA-MB-436 ( n = 11-12) cells. Bars = 20 µm. ( c ) mRNA expression of EMT markers vimentin ( VIM ), SNAIL ( SNAI1 ), SLUG ( SNAI2 ), ZEB1 and TWIST1 in MDA-MB-231 cancer cells treated ± 500 nM MitoQ for 48 h ( n = 6–9). ( d ) Western blots (WBs) of the corresponding proteins with β-actin as a loading control. ( e ) mRNA expression in c, but in SkBr3 cells ( n = 3–9). ( f ) WBs as in d, but using SkBr3 cells. ( g ) mRNA expression in c, but in MDA-MB-436 cells ( n = 6–9). ( h ) WBs as in d, but using MDA-MB-436 cells. All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t test ( b , c , e , g ).

    Article Snippet: HER2+ SkBr3 human breast adenocarcinoma cancer cells (catalogue #HTB-30), triple-negative MDA-MB-436 human breast adenocarcinoma cancer cells (catalogue #HTB-130) and MCF10A human nonmalignant breast epithelial cells (catalogue #CRL-10317) were from ATCC (Manassas, VA, USA).

    Techniques: Staining, Fluorescence, Expressing, Western Blot, Control

    MitoQ represses human breast cancer cell migration and invasion. Cells were treated for 48 h ± MitoQ (100 nM). ( a ) MDA-MB-231 (left, n = 6), SkBr3 (middle, n = 3–8) and MDA-MB-436 (right, n = 10–13) cancer cell migration over 24 h was determined using a scratch assay. Representative pictures are shown on top and quantification graphs on the bottom. Bars = 50 µm. ( b ) MDA-MB-231 (left, n = 3), SkBr3 (middle, n = 3) and MDA-MB-436 (right, n = 3) cancer cell invasion was quantified in a Boyden chamber assay. Representative images are shown together with overnight invasion data. All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; by Student t -test ( a , b ).

    Journal: Cancers

    Article Title: MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

    doi: 10.3390/cancers14061516

    Figure Lengend Snippet: MitoQ represses human breast cancer cell migration and invasion. Cells were treated for 48 h ± MitoQ (100 nM). ( a ) MDA-MB-231 (left, n = 6), SkBr3 (middle, n = 3–8) and MDA-MB-436 (right, n = 10–13) cancer cell migration over 24 h was determined using a scratch assay. Representative pictures are shown on top and quantification graphs on the bottom. Bars = 50 µm. ( b ) MDA-MB-231 (left, n = 3), SkBr3 (middle, n = 3) and MDA-MB-436 (right, n = 3) cancer cell invasion was quantified in a Boyden chamber assay. Representative images are shown together with overnight invasion data. All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; by Student t -test ( a , b ).

    Article Snippet: HER2+ SkBr3 human breast adenocarcinoma cancer cells (catalogue #HTB-30), triple-negative MDA-MB-436 human breast adenocarcinoma cancer cells (catalogue #HTB-130) and MCF10A human nonmalignant breast epithelial cells (catalogue #CRL-10317) were from ATCC (Manassas, VA, USA).

    Techniques: Migration, Wound Healing Assay, Boyden Chamber Assay, Control

    MitoQ represses human breast cancer cell clonogenicity, sphere formation and spheroid stability. ( a , b ) Cells were pretreated for 48 h with the indicated doses of MitoQ. ( a ) Clonogenic assay using adherent MDA-MB-231 (left, n = 6) and SkBr3 (right, n = 9) cells. Bars = 1 cm. ( b ) Clonogenic assay on soft agar using MDA-MB-231 ( n = 16), SkBr3 ( n = 16) and MDA-MB-436 ( n = 8) cells. ( c ) Shown are representative images of MDA-MB-231, SkBr3 and MDA-MB-436 spheroid formation over 4 days in the presence or not of 250 nM MitoQ. Bar = 250 µm. ( d ) Representative images of mature MDA-MB-231 spheroids before and after 4 days of treatment ± 250 nM MitoQ are shown on the left (Bar = 250 µm). On the right, the graph represents spheroid size determined using the bright field mode of phase contrast microscope ( n = 9–11). ( e ) As in d, but using MDA-MB-436 cells and a treatment of 7 days ( n = 6 all; bars = 50 µm for images on the top and 200 µm for images on the bottom). ( f ) mRNA expression of cancer stem cell markers MYC , POU5F1 (Oct4), NANOG and SOX2 in MDA-MB-231 (left, n = 3–7), SkBr3 (middle, n = 4–6) and MDA-MB-436 (right, n = 4–8) spheres treated for 48 h ± 250 nM MitoQ. All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t test ( a , d , f ) or one-way ANOVA followed by Dunnett’s post hoc test ( b , e ).

    Journal: Cancers

    Article Title: MitoQ Inhibits Human Breast Cancer Cell Migration, Invasion and Clonogenicity

    doi: 10.3390/cancers14061516

    Figure Lengend Snippet: MitoQ represses human breast cancer cell clonogenicity, sphere formation and spheroid stability. ( a , b ) Cells were pretreated for 48 h with the indicated doses of MitoQ. ( a ) Clonogenic assay using adherent MDA-MB-231 (left, n = 6) and SkBr3 (right, n = 9) cells. Bars = 1 cm. ( b ) Clonogenic assay on soft agar using MDA-MB-231 ( n = 16), SkBr3 ( n = 16) and MDA-MB-436 ( n = 8) cells. ( c ) Shown are representative images of MDA-MB-231, SkBr3 and MDA-MB-436 spheroid formation over 4 days in the presence or not of 250 nM MitoQ. Bar = 250 µm. ( d ) Representative images of mature MDA-MB-231 spheroids before and after 4 days of treatment ± 250 nM MitoQ are shown on the left (Bar = 250 µm). On the right, the graph represents spheroid size determined using the bright field mode of phase contrast microscope ( n = 9–11). ( e ) As in d, but using MDA-MB-436 cells and a treatment of 7 days ( n = 6 all; bars = 50 µm for images on the top and 200 µm for images on the bottom). ( f ) mRNA expression of cancer stem cell markers MYC , POU5F1 (Oct4), NANOG and SOX2 in MDA-MB-231 (left, n = 3–7), SkBr3 (middle, n = 4–6) and MDA-MB-436 (right, n = 4–8) spheres treated for 48 h ± 250 nM MitoQ. All data are shown as means ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to control; ns : p > 0.05 compared to control; by Student t test ( a , d , f ) or one-way ANOVA followed by Dunnett’s post hoc test ( b , e ).

    Article Snippet: HER2+ SkBr3 human breast adenocarcinoma cancer cells (catalogue #HTB-30), triple-negative MDA-MB-436 human breast adenocarcinoma cancer cells (catalogue #HTB-130) and MCF10A human nonmalignant breast epithelial cells (catalogue #CRL-10317) were from ATCC (Manassas, VA, USA).

    Techniques: Clonogenic Assay, Microscopy, Expressing, Control