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bt549 triple negative breast cancer cells  (ATCC)


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    ATCC bt549 triple negative breast cancer cells
    Bt549 Triple Negative Breast Cancer Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2891 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 99 stars, based on 2891 article reviews
    bt549 triple negative breast cancer cells - by Bioz Stars, 2026-06
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    ATCC triple negative breast cancer tnbc cell lines bt549
    YH395A inhibited breast cancer cell proliferation. (A) Breast cancer cell lines (MDA-MB-231, MDA-MB-468, <t>BT549,</t> SUM159, and BT-20), normal mammary epithelial cells (MCF-10 A), human gastric mucosal epithelial cells (GES-1), and human embryonic lung fibroblast cells (MRC-5) were treated with the indicated concentrations of YH395A or YR-290. After 96 h, SRB assay was performed. The bars indicate the mean ± SD. (B) Colony formation assays of breast cancer cells
    Triple Negative Breast Cancer Tnbc Cell Lines Bt549, 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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    Mendeley Ltd bt549 triple negative breast cancer cells
    (A) Venn plots of gene co-expression in NU7441-added and control cells, the overlapping area shows the number of co-expressed genes in the two samples. Control represents <t>BT549</t> cells without drug treatment and inhibition represents BT549 cells after NU7441 treatment (B). Histograms of genes differentially expressed in the NU7441-treated group compared to the control group. The differential genes selected according to |log2(FoldChange)| >= 1 & padj<= 0.05.(C)Volcano plot of differential genes in the NU7441-treated group compared to the control group. 680 genes were up-regulated and 1365 genes were down-regulated in BT549 cells treated with NU7441 according to |log2(FoldChange)| >= 1 & padj<= 0.05.
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    ATCC triple negative breast cancer cell lines bt549
    (A) Venn plots of gene co-expression in NU7441-added and control cells, the overlapping area shows the number of co-expressed genes in the two samples. Control represents <t>BT549</t> cells without drug treatment and inhibition represents BT549 cells after NU7441 treatment (B). Histograms of genes differentially expressed in the NU7441-treated group compared to the control group. The differential genes selected according to |log2(FoldChange)| >= 1 & padj<= 0.05.(C)Volcano plot of differential genes in the NU7441-treated group compared to the control group. 680 genes were up-regulated and 1365 genes were down-regulated in BT549 cells treated with NU7441 according to |log2(FoldChange)| >= 1 & padj<= 0.05.
    Triple Negative Breast Cancer Cell Lines Bt549, 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 triple negative breast cancer tnbc bt549 cells
    Ectopic miR-126-3p downregulates AKT2. ( a ) Predicted miR-126-3p target site on AKT2 3′UTR, as recognized by TargetScan Human 8.0 software. The sequence of wild type (wt) and mutant (mut) AKT2 3′UTR is shown; bold letters indicate the miR-126-3p seed sequence. Region cloned into the pGL3-Control Luciferase Reporter Vector is also indicated (dashed line). ( b ) Dual luciferase assay of wild type (wt) and mutated (mut) AKT2 3′UTR after transfection with scramble oligo (scramble), miR-126-3p-mimic (miR-126), or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells, arbitrarily set to 100%. Results are shown as mean ± S.E.M. of four different measures from three independent experiments. * p < 0.01 versus scramble, # p < 0.01 versus wt AKT2 3′UTR. ( c ) Western blot of AKT2 and PIK3R2 in <t>BT549</t> cells left untreated (NT) or transfected with either scramble oligo (scramble) or miR-126-3p mimic (miR-126) or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. Blots are representative of five independent experiments and results are shown as mean ± S.E.M. * p < 0.01 versus scramble, # p < 0.01 versus miR-126.
    Human Triple Negative Breast Cancer Tnbc Bt549 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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    Asterand Inc bt549 human triple-negative breast cancer cell line
    Ectopic miR-126-3p downregulates AKT2. ( a ) Predicted miR-126-3p target site on AKT2 3′UTR, as recognized by TargetScan Human 8.0 software. The sequence of wild type (wt) and mutant (mut) AKT2 3′UTR is shown; bold letters indicate the miR-126-3p seed sequence. Region cloned into the pGL3-Control Luciferase Reporter Vector is also indicated (dashed line). ( b ) Dual luciferase assay of wild type (wt) and mutated (mut) AKT2 3′UTR after transfection with scramble oligo (scramble), miR-126-3p-mimic (miR-126), or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells, arbitrarily set to 100%. Results are shown as mean ± S.E.M. of four different measures from three independent experiments. * p < 0.01 versus scramble, # p < 0.01 versus wt AKT2 3′UTR. ( c ) Western blot of AKT2 and PIK3R2 in <t>BT549</t> cells left untreated (NT) or transfected with either scramble oligo (scramble) or miR-126-3p mimic (miR-126) or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. Blots are representative of five independent experiments and results are shown as mean ± S.E.M. * p < 0.01 versus scramble, # p < 0.01 versus miR-126.
    Bt549 Human Triple Negative Breast Cancer Cell Line, supplied by Asterand Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC triple negative breast cancer cell line bt549
    Ectopic miR-126-3p downregulates AKT2. ( a ) Predicted miR-126-3p target site on AKT2 3′UTR, as recognized by TargetScan Human 8.0 software. The sequence of wild type (wt) and mutant (mut) AKT2 3′UTR is shown; bold letters indicate the miR-126-3p seed sequence. Region cloned into the pGL3-Control Luciferase Reporter Vector is also indicated (dashed line). ( b ) Dual luciferase assay of wild type (wt) and mutated (mut) AKT2 3′UTR after transfection with scramble oligo (scramble), miR-126-3p-mimic (miR-126), or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells, arbitrarily set to 100%. Results are shown as mean ± S.E.M. of four different measures from three independent experiments. * p < 0.01 versus scramble, # p < 0.01 versus wt AKT2 3′UTR. ( c ) Western blot of AKT2 and PIK3R2 in <t>BT549</t> cells left untreated (NT) or transfected with either scramble oligo (scramble) or miR-126-3p mimic (miR-126) or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. Blots are representative of five independent experiments and results are shown as mean ± S.E.M. * p < 0.01 versus scramble, # p < 0.01 versus miR-126.
    Triple Negative Breast Cancer Cell Line Bt549, 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 triple negative breast cancer cells lines bt549
    Ectopic miR-126-3p downregulates AKT2. ( a ) Predicted miR-126-3p target site on AKT2 3′UTR, as recognized by TargetScan Human 8.0 software. The sequence of wild type (wt) and mutant (mut) AKT2 3′UTR is shown; bold letters indicate the miR-126-3p seed sequence. Region cloned into the pGL3-Control Luciferase Reporter Vector is also indicated (dashed line). ( b ) Dual luciferase assay of wild type (wt) and mutated (mut) AKT2 3′UTR after transfection with scramble oligo (scramble), miR-126-3p-mimic (miR-126), or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells, arbitrarily set to 100%. Results are shown as mean ± S.E.M. of four different measures from three independent experiments. * p < 0.01 versus scramble, # p < 0.01 versus wt AKT2 3′UTR. ( c ) Western blot of AKT2 and PIK3R2 in <t>BT549</t> cells left untreated (NT) or transfected with either scramble oligo (scramble) or miR-126-3p mimic (miR-126) or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. Blots are representative of five independent experiments and results are shown as mean ± S.E.M. * p < 0.01 versus scramble, # p < 0.01 versus miR-126.
    Triple Negative Breast Cancer Cells Lines Bt549, 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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    Image Search Results


    YH395A inhibited breast cancer cell proliferation. (A) Breast cancer cell lines (MDA-MB-231, MDA-MB-468, BT549, SUM159, and BT-20), normal mammary epithelial cells (MCF-10 A), human gastric mucosal epithelial cells (GES-1), and human embryonic lung fibroblast cells (MRC-5) were treated with the indicated concentrations of YH395A or YR-290. After 96 h, SRB assay was performed. The bars indicate the mean ± SD. (B) Colony formation assays of breast cancer cells

    Journal: Cell Communication and Signaling : CCS

    Article Title: Artificial intelligence-driven discovery of YH395A: A novel TGFβR1 inhibitor with potent anti-tumor activity against triple-negative breast cancer

    doi: 10.1186/s12964-025-02337-2

    Figure Lengend Snippet: YH395A inhibited breast cancer cell proliferation. (A) Breast cancer cell lines (MDA-MB-231, MDA-MB-468, BT549, SUM159, and BT-20), normal mammary epithelial cells (MCF-10 A), human gastric mucosal epithelial cells (GES-1), and human embryonic lung fibroblast cells (MRC-5) were treated with the indicated concentrations of YH395A or YR-290. After 96 h, SRB assay was performed. The bars indicate the mean ± SD. (B) Colony formation assays of breast cancer cells

    Article Snippet: The MCF-10 A, GES-1, MRC-5, and triple-negative breast cancer (TNBC) cell lines BT549 (RRID: CVCL_0062), MDA-MB-468 (RRID: CVCL_0419), BT-20 (RRID: CVCL_0169), and MDA-MB-231(RRID: CVCL_0063) were sourced from the American Type Culture Collection (ATCC, USA), while SUM159 cells were generously donated by Dr. Yuzhu Zhang (Guangdong Academy of Chinese Medicine, China).

    Techniques: Sulforhodamine B Assay

    (A) Venn plots of gene co-expression in NU7441-added and control cells, the overlapping area shows the number of co-expressed genes in the two samples. Control represents BT549 cells without drug treatment and inhibition represents BT549 cells after NU7441 treatment (B). Histograms of genes differentially expressed in the NU7441-treated group compared to the control group. The differential genes selected according to |log2(FoldChange)| >= 1 & padj<= 0.05.(C)Volcano plot of differential genes in the NU7441-treated group compared to the control group. 680 genes were up-regulated and 1365 genes were down-regulated in BT549 cells treated with NU7441 according to |log2(FoldChange)| >= 1 & padj<= 0.05.

    Journal: Data in Brief

    Article Title: Transcriptomic data of BT549 triple negative breast cancer cells treated with 20 µM NU7441, a DNA-dependent kinase inhibitor

    doi: 10.1016/j.dib.2024.110183

    Figure Lengend Snippet: (A) Venn plots of gene co-expression in NU7441-added and control cells, the overlapping area shows the number of co-expressed genes in the two samples. Control represents BT549 cells without drug treatment and inhibition represents BT549 cells after NU7441 treatment (B). Histograms of genes differentially expressed in the NU7441-treated group compared to the control group. The differential genes selected according to |log2(FoldChange)| >= 1 & padj<= 0.05.(C)Volcano plot of differential genes in the NU7441-treated group compared to the control group. 680 genes were up-regulated and 1365 genes were down-regulated in BT549 cells treated with NU7441 according to |log2(FoldChange)| >= 1 & padj<= 0.05.

    Article Snippet: Transcriptomic data of BT549 triple negative breast cancer cells treated with 20μM NU7441,a DNA-dependent kinase inhibitor (Original data) (Mendeley Data).

    Techniques: Expressing, Control, Inhibition

    Journal: Data in Brief

    Article Title: Transcriptomic data of BT549 triple negative breast cancer cells treated with 20 µM NU7441, a DNA-dependent kinase inhibitor

    doi: 10.1016/j.dib.2024.110183

    Figure Lengend Snippet:

    Article Snippet: Transcriptomic data of BT549 triple negative breast cancer cells treated with 20μM NU7441,a DNA-dependent kinase inhibitor (Original data) (Mendeley Data).

    Techniques: Gene Expression, Control, Sequencing, Sample Prep

    Ectopic miR-126-3p downregulates AKT2. ( a ) Predicted miR-126-3p target site on AKT2 3′UTR, as recognized by TargetScan Human 8.0 software. The sequence of wild type (wt) and mutant (mut) AKT2 3′UTR is shown; bold letters indicate the miR-126-3p seed sequence. Region cloned into the pGL3-Control Luciferase Reporter Vector is also indicated (dashed line). ( b ) Dual luciferase assay of wild type (wt) and mutated (mut) AKT2 3′UTR after transfection with scramble oligo (scramble), miR-126-3p-mimic (miR-126), or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells, arbitrarily set to 100%. Results are shown as mean ± S.E.M. of four different measures from three independent experiments. * p < 0.01 versus scramble, # p < 0.01 versus wt AKT2 3′UTR. ( c ) Western blot of AKT2 and PIK3R2 in BT549 cells left untreated (NT) or transfected with either scramble oligo (scramble) or miR-126-3p mimic (miR-126) or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. Blots are representative of five independent experiments and results are shown as mean ± S.E.M. * p < 0.01 versus scramble, # p < 0.01 versus miR-126.

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: Ectopic miR-126-3p downregulates AKT2. ( a ) Predicted miR-126-3p target site on AKT2 3′UTR, as recognized by TargetScan Human 8.0 software. The sequence of wild type (wt) and mutant (mut) AKT2 3′UTR is shown; bold letters indicate the miR-126-3p seed sequence. Region cloned into the pGL3-Control Luciferase Reporter Vector is also indicated (dashed line). ( b ) Dual luciferase assay of wild type (wt) and mutated (mut) AKT2 3′UTR after transfection with scramble oligo (scramble), miR-126-3p-mimic (miR-126), or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells, arbitrarily set to 100%. Results are shown as mean ± S.E.M. of four different measures from three independent experiments. * p < 0.01 versus scramble, # p < 0.01 versus wt AKT2 3′UTR. ( c ) Western blot of AKT2 and PIK3R2 in BT549 cells left untreated (NT) or transfected with either scramble oligo (scramble) or miR-126-3p mimic (miR-126) or inhibitor (anti-miR-126). Values are reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. Blots are representative of five independent experiments and results are shown as mean ± S.E.M. * p < 0.01 versus scramble, # p < 0.01 versus miR-126.

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Software, Sequencing, Mutagenesis, Clone Assay, Control, Luciferase, Plasmid Preparation, Transfection, Western Blot

    miR-126-3p/AKT2 axis reduces migration of BT549 cells. ( a ) Scratch wound assay performed on BT549 cells left untreated (NT) or transiently transfected with either scramble oligo (scramble) or miR-126-3p-mimic (miR-126) or AKT2 siRNA. Migration was monitored for up to 18 h. The leading edge of the wound is highlighted red. ( b ) Graphical view showing the wound width (µm), in relation to incubation times. Results are representative of three independent experiments, each performed in quintuplicate and reported as mean ± S.E.M. * p < 0.01 and ** p < 0.05 versus scramble. Scale bars: 400 µM.

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: miR-126-3p/AKT2 axis reduces migration of BT549 cells. ( a ) Scratch wound assay performed on BT549 cells left untreated (NT) or transiently transfected with either scramble oligo (scramble) or miR-126-3p-mimic (miR-126) or AKT2 siRNA. Migration was monitored for up to 18 h. The leading edge of the wound is highlighted red. ( b ) Graphical view showing the wound width (µm), in relation to incubation times. Results are representative of three independent experiments, each performed in quintuplicate and reported as mean ± S.E.M. * p < 0.01 and ** p < 0.05 versus scramble. Scale bars: 400 µM.

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Migration, Scratch Wound Assay Assay, Transfection, Incubation

    miR-126-3p/AKT2 axis reduces invasion of BC cells. Transwell migration assay performed with BT549 ( a ), and MCF-7 ( b ) cells left untreated (NT) or transiently transfected with either scramble oligo (scramble), miR-126-3p-mimic (miR-126), miR-126-3p-inhibitor (anti-miR-126), or AKT2 siRNA. Photographs are representative of four independent experiments. ( c ) Histograms show the number of invading cells, reported as percentage of relative scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100% (absolute cell number = 608.12 ± 21.72 and 161.62 ± 14.67 for BT549 and MCF-7 cells, respectively). Data are shown as mean ± SEM. *: p < 0.01 versus relative scramble. Scale bars: 250 µm.

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: miR-126-3p/AKT2 axis reduces invasion of BC cells. Transwell migration assay performed with BT549 ( a ), and MCF-7 ( b ) cells left untreated (NT) or transiently transfected with either scramble oligo (scramble), miR-126-3p-mimic (miR-126), miR-126-3p-inhibitor (anti-miR-126), or AKT2 siRNA. Photographs are representative of four independent experiments. ( c ) Histograms show the number of invading cells, reported as percentage of relative scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100% (absolute cell number = 608.12 ± 21.72 and 161.62 ± 14.67 for BT549 and MCF-7 cells, respectively). Data are shown as mean ± SEM. *: p < 0.01 versus relative scramble. Scale bars: 250 µm.

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Transwell Migration Assay, Transfection

    miR-126-3p/AKT2 axis decreases cofilin activity. BT549 and MCF-7 cells were left untreated (NT) or transiently transfected with scramble oligo (scramble), miR-126-3p mimic (miR-126), or AKT2 siRNA before investigating the expression of total and phosphorylated (Ser3) cofilin by Western blot. Histogram shows densitometric analysis; values are reported as p-cofilin (Ser3)/total cofilin ratio compared to scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. GAPDH was used as loading control. Blots are representative of five independent experiments and results are reported as mean ± SEM. *: p < 0.01 versus scramble.

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: miR-126-3p/AKT2 axis decreases cofilin activity. BT549 and MCF-7 cells were left untreated (NT) or transiently transfected with scramble oligo (scramble), miR-126-3p mimic (miR-126), or AKT2 siRNA before investigating the expression of total and phosphorylated (Ser3) cofilin by Western blot. Histogram shows densitometric analysis; values are reported as p-cofilin (Ser3)/total cofilin ratio compared to scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100%. GAPDH was used as loading control. Blots are representative of five independent experiments and results are reported as mean ± SEM. *: p < 0.01 versus scramble.

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Activity Assay, Transfection, Expressing, Western Blot, Control

    miR-126-3p/AKT2 axis reduces the clonogenic potential of BC cells. Colony forming unit (CFU) assay performed with BT549 ( a ) and MCF-7 ( b ) cells left untreated (NT) or transiently transfected with either scramble oligo (scramble), miR-126-3p-mimic (miR-126), miR-126-3p-inhibitor (anti-miR-126), or AKT2 siRNA. Photographs are representative of three independent experiments. ( c ) Histograms show the colony number reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100% (absolute colony number = 94.67 ± 2.21 and 33.12 ± 0.18 for BT549 and MCF-7 cells, respectively). Data are shown as mean ± SEM. *: p < 0.01 versus relative scramble.

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: miR-126-3p/AKT2 axis reduces the clonogenic potential of BC cells. Colony forming unit (CFU) assay performed with BT549 ( a ) and MCF-7 ( b ) cells left untreated (NT) or transiently transfected with either scramble oligo (scramble), miR-126-3p-mimic (miR-126), miR-126-3p-inhibitor (anti-miR-126), or AKT2 siRNA. Photographs are representative of three independent experiments. ( c ) Histograms show the colony number reported as percentage of scramble-transfected cells (not statistically differing from NT cells), arbitrarily set to 100% (absolute colony number = 94.67 ± 2.21 and 33.12 ± 0.18 for BT549 and MCF-7 cells, respectively). Data are shown as mean ± SEM. *: p < 0.01 versus relative scramble.

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Colony-forming Unit Assay, Transfection

    miR-126-3p-enriched MVs derived from PUFA-treated platelets decrease tumorigenic properties of BT549 cells by directly targeting AKT2. ( a ) RT-PCR analysis of miR-126 content in MVs derived from resting (Ctrl) or AA plus DHA-treated (AA + DHA) platelets and ( b ) in BT549 cells after MV delivery. Histograms show miR-126 expression reported as percentage of relative Ctrl, arbitrarily set to 100%. ( c ) Western blot analysis of PIK3R2, AKT2, and phosphorylated cofilin levels in BT549 cells treated as in ( b ). Blots are representative of four independent experiments. Histograms represent the densitometric analysis, expressed as percentage of Ctrl, arbitrarily set to 100%. ( d ) Transwell invasion assay performed with BT549 cells treated as in ( b ). Images are representative of three independent experiments. Histogram shows the number of invading cells, reported as percentage of Ctrl, arbitrarily set to 100% (absolute cell number = 284 ± 17.24). ( e ) CFU assay performed with BT549 cells treated as in ( b ). Photographs are representative of three independent experiments. Histograms show colony number reported as percentage of Ctrl arbitrarily set to 100% (absolute colony number = 162.27 ± 4.3). Data in histograms are shown as mean ± SEM. * p < 0.01 and ** p < 0.05 versus relative Ctrl. Scale bars: 250 µm.

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: miR-126-3p-enriched MVs derived from PUFA-treated platelets decrease tumorigenic properties of BT549 cells by directly targeting AKT2. ( a ) RT-PCR analysis of miR-126 content in MVs derived from resting (Ctrl) or AA plus DHA-treated (AA + DHA) platelets and ( b ) in BT549 cells after MV delivery. Histograms show miR-126 expression reported as percentage of relative Ctrl, arbitrarily set to 100%. ( c ) Western blot analysis of PIK3R2, AKT2, and phosphorylated cofilin levels in BT549 cells treated as in ( b ). Blots are representative of four independent experiments. Histograms represent the densitometric analysis, expressed as percentage of Ctrl, arbitrarily set to 100%. ( d ) Transwell invasion assay performed with BT549 cells treated as in ( b ). Images are representative of three independent experiments. Histogram shows the number of invading cells, reported as percentage of Ctrl, arbitrarily set to 100% (absolute cell number = 284 ± 17.24). ( e ) CFU assay performed with BT549 cells treated as in ( b ). Photographs are representative of three independent experiments. Histograms show colony number reported as percentage of Ctrl arbitrarily set to 100% (absolute colony number = 162.27 ± 4.3). Data in histograms are shown as mean ± SEM. * p < 0.01 and ** p < 0.05 versus relative Ctrl. Scale bars: 250 µm.

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Derivative Assay, Reverse Transcription Polymerase Chain Reaction, Expressing, Western Blot, Transwell Invasion Assay, Colony-forming Unit Assay

    Kaplan–Meier survival analysis of BC patients based on miR-126 expression and AKT2 protein levels. Graphs were downloaded from the KM plotter website ( https://kmplot.com/analysis/ , accessed on 26 December 2021) . Comparison of 5-year overall survival between patients with high and low miR-126 expression levels in ( a ) all breast cancers, ( b ) luminal A, ( c ) luminal B, ( d ) HER2 positive, and ( e ) TNBC tumors. Data were from METABRIC database. ( f ) Comparison of 5-year overall survival between BC patients with high and low AKT2 protein levels. Data were from .

    Journal: International Journal of Molecular Sciences

    Article Title: Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay

    doi: 10.3390/ijms23105484

    Figure Lengend Snippet: Kaplan–Meier survival analysis of BC patients based on miR-126 expression and AKT2 protein levels. Graphs were downloaded from the KM plotter website ( https://kmplot.com/analysis/ , accessed on 26 December 2021) . Comparison of 5-year overall survival between patients with high and low miR-126 expression levels in ( a ) all breast cancers, ( b ) luminal A, ( c ) luminal B, ( d ) HER2 positive, and ( e ) TNBC tumors. Data were from METABRIC database. ( f ) Comparison of 5-year overall survival between BC patients with high and low AKT2 protein levels. Data were from .

    Article Snippet: Human triple negative breast cancer (TNBC) BT549 cells (ATCC HTB-122) were maintained in RPMI-1640 culture medium supplemented with 0.023 U/mL insulin; luminal A subtype MCF-7 cells (ATCC HTB-22) were grown in Dulbecco’s modified Eagle’s medium (DMEM).

    Techniques: Expressing, Comparison