bt20  (ATCC)


Bioz Verified Symbol ATCC is a verified supplier
Bioz Manufacturer Symbol ATCC manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 95

    Structured Review

    ATCC bt20
    PD-L1 is an unpredictable biomarker of response to PD-1/PD-L1 Inhibition. (A) PD-L1 mRNA and protein expression levels and (B and C) surface PD-L1 expression in MCF7, <t>BT20,</t> and MDA-MB-231 cells; (D) western blot analysis for PD-1 expression and ELISA assay for IL-2 and IFNγ levels in activated Jurkat T cells after PMA (50 ng/mL) and Ionomycin (1 µg/mL) treatment; (E) Caspase 3/7 activity of PD-L1(-) MCF7 cells, co-cultured with activated Jurkat T cells; Caspase 3/7 activity of PD-L1(+) (F) BT20 and (G) MDA-MB-231 cells, co-cultured with activated Jurkat T cells, after treatment of PD-1/PD-L1 inhibitor for 24 h.
    Bt20, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bt20/product/ATCC
    Average 95 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    bt20 - by Bioz Stars, 2022-09
    95/100 stars

    Images

    1) Product Images from "Blockade of CCL2 expression overcomes intrinsic PD-1/PD-L1 inhibitor-resistance in transglutaminase 2-induced PD-L1 positive triple negative breast cancer"

    Article Title: Blockade of CCL2 expression overcomes intrinsic PD-1/PD-L1 inhibitor-resistance in transglutaminase 2-induced PD-L1 positive triple negative breast cancer

    Journal: American Journal of Cancer Research

    doi:

    PD-L1 is an unpredictable biomarker of response to PD-1/PD-L1 Inhibition. (A) PD-L1 mRNA and protein expression levels and (B and C) surface PD-L1 expression in MCF7, BT20, and MDA-MB-231 cells; (D) western blot analysis for PD-1 expression and ELISA assay for IL-2 and IFNγ levels in activated Jurkat T cells after PMA (50 ng/mL) and Ionomycin (1 µg/mL) treatment; (E) Caspase 3/7 activity of PD-L1(-) MCF7 cells, co-cultured with activated Jurkat T cells; Caspase 3/7 activity of PD-L1(+) (F) BT20 and (G) MDA-MB-231 cells, co-cultured with activated Jurkat T cells, after treatment of PD-1/PD-L1 inhibitor for 24 h.
    Figure Legend Snippet: PD-L1 is an unpredictable biomarker of response to PD-1/PD-L1 Inhibition. (A) PD-L1 mRNA and protein expression levels and (B and C) surface PD-L1 expression in MCF7, BT20, and MDA-MB-231 cells; (D) western blot analysis for PD-1 expression and ELISA assay for IL-2 and IFNγ levels in activated Jurkat T cells after PMA (50 ng/mL) and Ionomycin (1 µg/mL) treatment; (E) Caspase 3/7 activity of PD-L1(-) MCF7 cells, co-cultured with activated Jurkat T cells; Caspase 3/7 activity of PD-L1(+) (F) BT20 and (G) MDA-MB-231 cells, co-cultured with activated Jurkat T cells, after treatment of PD-1/PD-L1 inhibitor for 24 h.

    Techniques Used: Biomarker Assay, Inhibition, Expressing, Multiple Displacement Amplification, Western Blot, Enzyme-linked Immunosorbent Assay, Activity Assay, Cell Culture

    TG2 induces PD-L1 expression by blocking PTEN and activating NF-κB in TNBC cells. (A) Fold change in TG2 in MDA-MB-231 and BT20 cells, and western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7 and MDA-MB-231 cells, with β-Actin as a loading control. (B) Western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7/Mock, MCF7/TG2, MDA-MB-231, and MDA-MB-231/TG2 siRNA cells, with β-Actin as a loading control. (C) Cell Immunohistochemistry and (D) FACS analysis for surface PD-L1 expression level in MCF7/Mock, MCF7/TG2, MDA-MB-231 and MDA-MB-231/TG2 siRNA. (E) Incidence of TG2 and PD-L1 expression in Formalin-Fixed Paraffin-Embedded (FFPE) tissue samples of 648 TNBC patients.
    Figure Legend Snippet: TG2 induces PD-L1 expression by blocking PTEN and activating NF-κB in TNBC cells. (A) Fold change in TG2 in MDA-MB-231 and BT20 cells, and western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7 and MDA-MB-231 cells, with β-Actin as a loading control. (B) Western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7/Mock, MCF7/TG2, MDA-MB-231, and MDA-MB-231/TG2 siRNA cells, with β-Actin as a loading control. (C) Cell Immunohistochemistry and (D) FACS analysis for surface PD-L1 expression level in MCF7/Mock, MCF7/TG2, MDA-MB-231 and MDA-MB-231/TG2 siRNA. (E) Incidence of TG2 and PD-L1 expression in Formalin-Fixed Paraffin-Embedded (FFPE) tissue samples of 648 TNBC patients.

    Techniques Used: Expressing, Blocking Assay, Multiple Displacement Amplification, Western Blot, Immunohistochemistry, FACS, Formalin-fixed Paraffin-Embedded

    CCL2 induction by TG2 contributes to PD-L1 inhibitor-resistance via regulation of negatively cytotoxic T cells in TNBC cells. The level of (A) PD-L1 and (B) CCL2 mRNA expression in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells measured by qRT-PCR analysis; (C) western blot analysis to check expression levels of TG2, P-AKT, IκBα, PD-L1, CCL2, and β-Actin in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells; (D) the expression of TG2, PD-L1, and CCL2 in MCF7/TG2 and MDA-MB-231 cells tested by western blotting analysis after TG2 siRNA transfection; (E) expression of PD-1 and CCR2 in Jurkat T cells with or without treatment of PMA (50 ng/mL) and Ionomycin (1 µg/mL) for 24 h measured by western blotting; (F and G) the protein levels of cPARP, IκBα, PD-L1, and CCL2 in MCF7/TG and MDA-MB-231 cells with or without activated Jurkat T cell co-culture for 24 h measured by western blotting after CCL2 siRNA transfection, Avelumab (20 µg/mL) treatment, or dual combination treatment and Caspase 3/7 activity measured by Caspase 3/7 assay using proteins from MCF7/TG and MDA-MB-231 cells.
    Figure Legend Snippet: CCL2 induction by TG2 contributes to PD-L1 inhibitor-resistance via regulation of negatively cytotoxic T cells in TNBC cells. The level of (A) PD-L1 and (B) CCL2 mRNA expression in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells measured by qRT-PCR analysis; (C) western blot analysis to check expression levels of TG2, P-AKT, IκBα, PD-L1, CCL2, and β-Actin in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells; (D) the expression of TG2, PD-L1, and CCL2 in MCF7/TG2 and MDA-MB-231 cells tested by western blotting analysis after TG2 siRNA transfection; (E) expression of PD-1 and CCR2 in Jurkat T cells with or without treatment of PMA (50 ng/mL) and Ionomycin (1 µg/mL) for 24 h measured by western blotting; (F and G) the protein levels of cPARP, IκBα, PD-L1, and CCL2 in MCF7/TG and MDA-MB-231 cells with or without activated Jurkat T cell co-culture for 24 h measured by western blotting after CCL2 siRNA transfection, Avelumab (20 µg/mL) treatment, or dual combination treatment and Caspase 3/7 activity measured by Caspase 3/7 assay using proteins from MCF7/TG and MDA-MB-231 cells.

    Techniques Used: Expressing, Multiple Displacement Amplification, Quantitative RT-PCR, Western Blot, Transfection, Co-Culture Assay, Activity Assay

    2) Product Images from "SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells"

    Article Title: SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells

    Journal: Cell Communication and Signaling : CCS

    doi: 10.1186/s12964-018-0286-2

    Dasatinib treatment inhibits the in vitro functional activity induced by P-cadherin expression. a Western blotting for pSRC(Tyr416), total Src, P-cadherin, E-cadherin and p120ctn in P-cadherin overexpressing cells after dasatinib treatment (100 nM) for 48 h. Protein levels of β-actin were analyzed and used as the loading control. b Representative experiment from a wound healing migration assay, in both P-cadherin overexpressing BCC (MCF-7/AZ.Pcad and BT20), treated with 100 nM of dasatinib or DMSO for 24 h. c Fold change in the number of invasive cells, evaluated by the matrigel invasion assay for both MCF-7/AZ.Pcad and BT20 treated with DMSO or 100 nM of dasatinib. d Zymography for MMP2 activity and Western blotting for sP-cad, using the conditioned medium from cells treated with DMSO or 100 nM of dasatinib for 48 h, in both MCF-7/AZ.Pcad and BT20 BCC models. e Mammosphere forming assay was performed for both cell models. The P -values indicate the statistically significant difference between DMSO and dasatinib treated cells, in both P-cadherin BCC models. f Average values of Work (J), representing the cell-cell adhesion strength, of both BCC cancer cell models treated with DMSO and dasatinib, using AFM Force Spectroscopy analysis. g Box-plot quantification of the length (μm) and h number of invasive protrusions of MCF-7/AZ.Pcad spheroids, treated with DMSO or 100 nM dasatinib, for 24 h. P -values
    Figure Legend Snippet: Dasatinib treatment inhibits the in vitro functional activity induced by P-cadherin expression. a Western blotting for pSRC(Tyr416), total Src, P-cadherin, E-cadherin and p120ctn in P-cadherin overexpressing cells after dasatinib treatment (100 nM) for 48 h. Protein levels of β-actin were analyzed and used as the loading control. b Representative experiment from a wound healing migration assay, in both P-cadherin overexpressing BCC (MCF-7/AZ.Pcad and BT20), treated with 100 nM of dasatinib or DMSO for 24 h. c Fold change in the number of invasive cells, evaluated by the matrigel invasion assay for both MCF-7/AZ.Pcad and BT20 treated with DMSO or 100 nM of dasatinib. d Zymography for MMP2 activity and Western blotting for sP-cad, using the conditioned medium from cells treated with DMSO or 100 nM of dasatinib for 48 h, in both MCF-7/AZ.Pcad and BT20 BCC models. e Mammosphere forming assay was performed for both cell models. The P -values indicate the statistically significant difference between DMSO and dasatinib treated cells, in both P-cadherin BCC models. f Average values of Work (J), representing the cell-cell adhesion strength, of both BCC cancer cell models treated with DMSO and dasatinib, using AFM Force Spectroscopy analysis. g Box-plot quantification of the length (μm) and h number of invasive protrusions of MCF-7/AZ.Pcad spheroids, treated with DMSO or 100 nM dasatinib, for 24 h. P -values

    Techniques Used: In Vitro, Functional Assay, Activity Assay, Expressing, Western Blot, Migration, Invasion Assay, Zymography, Spectroscopy

    Dasatinib treatment affects the in vivo tumorigenic and metastatic capacity of P-cadherin overexpressing tumors. a Kaplan-Meyer survival curve for the overall survival of mice treated with DMSO and dasatinib 10 mg/kg, for a maximum period of 210 days. P-value was calculated using a log-rank test to assess significant differences for mice overall survival. b Percentage of tumours with vascular invasion, observed by HE staining. Presence or absence of clusters of tumour cells inside blood vessels surrounding the primary tumour was quantified in control versus dasatinib treated mice (10 mg/kg). c Tumour volume measured at week 5, post inoculation of cancer cells, from control and dasatinib treated groups, in all BCC models (SUM149, BT20 and MDA-MB-468). d Immunofluorescence for p120ctn (red) and DAPI (blue in the primary tumours from control and dasatinib treated animals. Scale bar = 50 μm. e Immunohistochemistry for p120ctn and pSRC(Tyr416) in the primary tumours from control and dasatinib treated animals. The images shown are representative ones. f Quantification of the p120ctn cytoplasmic intensity expression in primary tumours from control and dasatinib treated animals. g Quantification of the p120ctn membrane intensity. Each dot represents the mean of p120ctn membrane intensity of 100 pairs of cells from a single biological replicate. Student’s t-tests were used to determine statistically significant differences, and P-values are indicated in the figure. Scale bar = 50 μm. h Proximity ligation assay for E-cadherin and p120ctn, from tumours recovered from different mice from control and dasatinib treated groups. i Box-plot for the average number of blobs/cells, quantified using the images of the proximity ligation assay for E-cadherin and p120ctn, between tumours from control and dasatinib treated mice. Student’s t-tests were used to determine statistically significant differences, and the P-value are indicated in the figure. Scale bar = 50 μm
    Figure Legend Snippet: Dasatinib treatment affects the in vivo tumorigenic and metastatic capacity of P-cadherin overexpressing tumors. a Kaplan-Meyer survival curve for the overall survival of mice treated with DMSO and dasatinib 10 mg/kg, for a maximum period of 210 days. P-value was calculated using a log-rank test to assess significant differences for mice overall survival. b Percentage of tumours with vascular invasion, observed by HE staining. Presence or absence of clusters of tumour cells inside blood vessels surrounding the primary tumour was quantified in control versus dasatinib treated mice (10 mg/kg). c Tumour volume measured at week 5, post inoculation of cancer cells, from control and dasatinib treated groups, in all BCC models (SUM149, BT20 and MDA-MB-468). d Immunofluorescence for p120ctn (red) and DAPI (blue in the primary tumours from control and dasatinib treated animals. Scale bar = 50 μm. e Immunohistochemistry for p120ctn and pSRC(Tyr416) in the primary tumours from control and dasatinib treated animals. The images shown are representative ones. f Quantification of the p120ctn cytoplasmic intensity expression in primary tumours from control and dasatinib treated animals. g Quantification of the p120ctn membrane intensity. Each dot represents the mean of p120ctn membrane intensity of 100 pairs of cells from a single biological replicate. Student’s t-tests were used to determine statistically significant differences, and P-values are indicated in the figure. Scale bar = 50 μm. h Proximity ligation assay for E-cadherin and p120ctn, from tumours recovered from different mice from control and dasatinib treated groups. i Box-plot for the average number of blobs/cells, quantified using the images of the proximity ligation assay for E-cadherin and p120ctn, between tumours from control and dasatinib treated mice. Student’s t-tests were used to determine statistically significant differences, and the P-value are indicated in the figure. Scale bar = 50 μm

    Techniques Used: In Vivo, Mouse Assay, Staining, Multiple Displacement Amplification, Immunofluorescence, Immunohistochemistry, Expressing, Proximity Ligation Assay

    3) Product Images from "Astaxanthin Reduces Stemness Markers in BT20 and T47D Breast Cancer Stem Cells by Inhibiting Expression of Pontin and Mutant p53"

    Article Title: Astaxanthin Reduces Stemness Markers in BT20 and T47D Breast Cancer Stem Cells by Inhibiting Expression of Pontin and Mutant p53

    Journal: Marine Drugs

    doi: 10.3390/md18110577

    Effects of pontin-targeting siRNAs on expression levels of Oct4, Nanog, and mutp53 in T47D and BT20 breast cancer cell lines. Cells were transfected with pontin-targeting or control siRNA. ( A ) Cell lysates were prepared from T47D and BT20 cells, and the expression levels of Oct4, Nanog, and mutp53 were detected by Western blotting. ( B ) Total RNA was extracted, and the expression levels of Oct4, Nanog, and mutp53 were evaluated via qRT-PCR. All experiments were normalized by comparison with glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Data represent the mean ± SD of three independent experiments (* p
    Figure Legend Snippet: Effects of pontin-targeting siRNAs on expression levels of Oct4, Nanog, and mutp53 in T47D and BT20 breast cancer cell lines. Cells were transfected with pontin-targeting or control siRNA. ( A ) Cell lysates were prepared from T47D and BT20 cells, and the expression levels of Oct4, Nanog, and mutp53 were detected by Western blotting. ( B ) Total RNA was extracted, and the expression levels of Oct4, Nanog, and mutp53 were evaluated via qRT-PCR. All experiments were normalized by comparison with glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Data represent the mean ± SD of three independent experiments (* p

    Techniques Used: Expressing, Transfection, Western Blot, Quantitative RT-PCR

    Pontin knockdown attenuated the proliferation of T47D and BT20 cells. ( A ) Cell cycle analyses of T47D and BT20 cells after targeted pontin knockdown. Cells were harvested 3 days after transfection of pontin siRNAs or control siRNA. Similar results were obtained from three independent experiments. ( B ) Ki67 incorporation was used to determine the proportions of cells in each cell cycle phase. Cells were harvested 3 days after transfection of control siRNA or pontin siRNAs. Proportions of Ki67-positive cells are shown. Results are expressed as the mean ± SD of three independent experiments. * p
    Figure Legend Snippet: Pontin knockdown attenuated the proliferation of T47D and BT20 cells. ( A ) Cell cycle analyses of T47D and BT20 cells after targeted pontin knockdown. Cells were harvested 3 days after transfection of pontin siRNAs or control siRNA. Similar results were obtained from three independent experiments. ( B ) Ki67 incorporation was used to determine the proportions of cells in each cell cycle phase. Cells were harvested 3 days after transfection of control siRNA or pontin siRNAs. Proportions of Ki67-positive cells are shown. Results are expressed as the mean ± SD of three independent experiments. * p

    Techniques Used: Transfection

    Rottlerin reduced expression levels of Oct4, Nanog, and mutp53 in T47D and BT20 breast cancer cell lines. Cell lysates were prepared from T47D and BT20 cells that had been subjected to rottlerin treatment. Expression levels of Oct4, Nanog, and mutp53 were detected via Western blotting analyses and qRT-PCR. ( A ) Cell lysates were prepared from T47D and BT20 cells, and the expression levels of Oct4, Nanog, and mutp53 were detected by Western blotting. ( B ) Total RNA was extracted, and the expression levels of Oct4, Nanog, and mutp53 were evaluated by qRT-PCR. All expression levels were normalized to GAPDH. Data represent the mean ± SD of three independent experiments (* p
    Figure Legend Snippet: Rottlerin reduced expression levels of Oct4, Nanog, and mutp53 in T47D and BT20 breast cancer cell lines. Cell lysates were prepared from T47D and BT20 cells that had been subjected to rottlerin treatment. Expression levels of Oct4, Nanog, and mutp53 were detected via Western blotting analyses and qRT-PCR. ( A ) Cell lysates were prepared from T47D and BT20 cells, and the expression levels of Oct4, Nanog, and mutp53 were detected by Western blotting. ( B ) Total RNA was extracted, and the expression levels of Oct4, Nanog, and mutp53 were evaluated by qRT-PCR. All expression levels were normalized to GAPDH. Data represent the mean ± SD of three independent experiments (* p

    Techniques Used: Expressing, Western Blot, Quantitative RT-PCR

    Pontin knockdown reduced migration and invasion in breast cancer cells. Pontin knockdown by siRNA attenuated migration of ( A ) T47D and ( B ) BT20 cells, as determined by transwell migration assays. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field (×200 magnification). Pontin knockdown by siRNA attenuated invasion of ( C ) T47D and ( D ) BT20 cells, determined using Matrigel-coated transwell invasion assays. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field (×200 magnification). Data represent the mean ± SD of three independent experiments (* p
    Figure Legend Snippet: Pontin knockdown reduced migration and invasion in breast cancer cells. Pontin knockdown by siRNA attenuated migration of ( A ) T47D and ( B ) BT20 cells, as determined by transwell migration assays. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field (×200 magnification). Pontin knockdown by siRNA attenuated invasion of ( C ) T47D and ( D ) BT20 cells, determined using Matrigel-coated transwell invasion assays. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field (×200 magnification). Data represent the mean ± SD of three independent experiments (* p

    Techniques Used: Migration

    Pontin knockdown reduced colony and spheroid formation abilities in T47D and BT20 cells. Pontin knockdown with siRNA attenuated colony formation by ( A ) T47D and ( B ) BT20 cells. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field. Pontin knockdown with siRNA attenuated spheroid formation by ( C ) T47D and ( D ) BT20 cells. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field. Data represent the mean ± SD of three independent experiments (* p
    Figure Legend Snippet: Pontin knockdown reduced colony and spheroid formation abilities in T47D and BT20 cells. Pontin knockdown with siRNA attenuated colony formation by ( A ) T47D and ( B ) BT20 cells. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field. Pontin knockdown with siRNA attenuated spheroid formation by ( C ) T47D and ( D ) BT20 cells. Left panel, representative images from a portion of field; right panel, quantification of average number of migrated cells/field. Data represent the mean ± SD of three independent experiments (* p

    Techniques Used:

    AST reduced the expression levels of pontin, mutp53, Oct4, and Nanog in T47D and BT20 breast cancer cell lines, thereby inhibiting cell proliferation. ( A ) Spheroid formation abilities of SKBR3, T47D, and BT20 breast cancer cell lines. ( B ) Expression levels of mutp53, pontin, Oct4, and Nanog were determined via Western blotting of T47D and BT20 cells after AST treatment. Actin was used as a loading control. ( C ) Cells were incubated for 48 h at 37 °C at the indicated concentrations of AST in a 96-well plate. Then, CCK-8 was added and the cells were incubated for 3 h at 37 °C. Absorbance was measured with a spectrophotometer at 450 nm. Data are expressed as the mean ± standard deviation (SD) of three independent experiments. * p
    Figure Legend Snippet: AST reduced the expression levels of pontin, mutp53, Oct4, and Nanog in T47D and BT20 breast cancer cell lines, thereby inhibiting cell proliferation. ( A ) Spheroid formation abilities of SKBR3, T47D, and BT20 breast cancer cell lines. ( B ) Expression levels of mutp53, pontin, Oct4, and Nanog were determined via Western blotting of T47D and BT20 cells after AST treatment. Actin was used as a loading control. ( C ) Cells were incubated for 48 h at 37 °C at the indicated concentrations of AST in a 96-well plate. Then, CCK-8 was added and the cells were incubated for 3 h at 37 °C. Absorbance was measured with a spectrophotometer at 450 nm. Data are expressed as the mean ± standard deviation (SD) of three independent experiments. * p

    Techniques Used: AST Assay, Expressing, Western Blot, Incubation, CCK-8 Assay, Spectrophotometry, Standard Deviation

    4) Product Images from "Identification of CETP as a molecular target for estrogen positive breast cancer cell death by cholesterol depleting agents"

    Article Title: Identification of CETP as a molecular target for estrogen positive breast cancer cell death by cholesterol depleting agents

    Journal: Genes & Cancer

    doi: 10.18632/genesandcancer.122

    AP disrupts lipid rafts and modulates cholesterol levels in vitro and in vivo (A) Lipid raft and filipin staining in MCF-7 cells after treatment with 10 μM PL or AP for 30 min and 1 h. Images are representative of three independent experiments (n = 3). (B) Comparison of cholesterol depletion in BJ, BT20, and MCF-7 cells after treatment with 10 μM PL and AP for 2 h; 5 mg/ml MBCD was used as a positive control. (C) Cholesterol pre-incubation blocked apoptosis induction in 10 μM PL and AP, and 5 mg/ml MBCD treated cells for 2 h. 5 mMH 2 O 2 was used as a positive apoptotic control. Data shown (B and C) are representative of the mean ± SD of quadruplicate wells/ condition in at least three independent experiments (n=3) (P ≤ 0.05, t -test). (D) Levels of total cholesterol, cholesterol esters, and unbound free cholesterol. Data shown as mean ± SD of vehicle group (n = 4), PL treated (n = 4) and AP treated (n = 5) groups.
    Figure Legend Snippet: AP disrupts lipid rafts and modulates cholesterol levels in vitro and in vivo (A) Lipid raft and filipin staining in MCF-7 cells after treatment with 10 μM PL or AP for 30 min and 1 h. Images are representative of three independent experiments (n = 3). (B) Comparison of cholesterol depletion in BJ, BT20, and MCF-7 cells after treatment with 10 μM PL and AP for 2 h; 5 mg/ml MBCD was used as a positive control. (C) Cholesterol pre-incubation blocked apoptosis induction in 10 μM PL and AP, and 5 mg/ml MBCD treated cells for 2 h. 5 mMH 2 O 2 was used as a positive apoptotic control. Data shown (B and C) are representative of the mean ± SD of quadruplicate wells/ condition in at least three independent experiments (n=3) (P ≤ 0.05, t -test). (D) Levels of total cholesterol, cholesterol esters, and unbound free cholesterol. Data shown as mean ± SD of vehicle group (n = 4), PL treated (n = 4) and AP treated (n = 5) groups.

    Techniques Used: In Vitro, In Vivo, Staining, Positive Control, Incubation

    5) Product Images from "Safety and efficacy of intratumoral injections of chimeric antigen receptor (CAR) T cells in metastatic breast cancer"

    Article Title: Safety and efficacy of intratumoral injections of chimeric antigen receptor (CAR) T cells in metastatic breast cancer

    Journal: Cancer immunology research

    doi: 10.1158/2326-6066.CIR-17-0189

    Cytotoxicity of c-Met-CAR T cells Chromium release cytolytic activity assays of mRNA CAR T cells in two breast cancer cell lines, BT20 and TB129. Each assay was performed in duplicates and repeated in at least three independent experiments. A) Upper panel, BT20 tumor cell lysis induced by CAR T directed against c-Met (cMet.BBz, solid triangles), mesothelin (SS1.BBz, solid squares) or CD19 (CD19.BBz, solid circles) at various effector T cell:tumor cell (E:T) ratios. mRNA c-Met-CAR T cells were more effective than mRNA meso-CAR T cells in inducing CAR T cell directed tumor cell lysis. Lower panel, histograms of flow cytometry analyses of c-Met and mesothelin expression on BT20 cells as stained by antibodies against c-Met and mesothelin. B) Upper panel, TB129 tumor cell lysis induced by CAR T directed against c-Met (cMet.BBz, solid triangles), mesothelin (SS1.BBz, solid squares) or CD19 (CD19.BBz, solid circles) at various E:T ratios. mRNA c-Met-CAR T cells cytolytic activity was similar to that of mRNA meso-CAR T cells in inducing CAR T directed tumor cell lysis. Lower panel, histograms of flow cytometry analyses of TB129 cells as stained by antibodies against c-Met and mesothelin.
    Figure Legend Snippet: Cytotoxicity of c-Met-CAR T cells Chromium release cytolytic activity assays of mRNA CAR T cells in two breast cancer cell lines, BT20 and TB129. Each assay was performed in duplicates and repeated in at least three independent experiments. A) Upper panel, BT20 tumor cell lysis induced by CAR T directed against c-Met (cMet.BBz, solid triangles), mesothelin (SS1.BBz, solid squares) or CD19 (CD19.BBz, solid circles) at various effector T cell:tumor cell (E:T) ratios. mRNA c-Met-CAR T cells were more effective than mRNA meso-CAR T cells in inducing CAR T cell directed tumor cell lysis. Lower panel, histograms of flow cytometry analyses of c-Met and mesothelin expression on BT20 cells as stained by antibodies against c-Met and mesothelin. B) Upper panel, TB129 tumor cell lysis induced by CAR T directed against c-Met (cMet.BBz, solid triangles), mesothelin (SS1.BBz, solid squares) or CD19 (CD19.BBz, solid circles) at various E:T ratios. mRNA c-Met-CAR T cells cytolytic activity was similar to that of mRNA meso-CAR T cells in inducing CAR T directed tumor cell lysis. Lower panel, histograms of flow cytometry analyses of TB129 cells as stained by antibodies against c-Met and mesothelin.

    Techniques Used: Activity Assay, Lysis, Flow Cytometry, Cytometry, Expressing, Staining

    Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • bt20  (ATCC)
    97
    ATCC bt20
    PD-L1 is an unpredictable biomarker of response to PD-1/PD-L1 Inhibition. (A) PD-L1 mRNA and protein expression levels and (B and C) surface PD-L1 expression in MCF7, <t>BT20,</t> and MDA-MB-231 cells; (D) western blot analysis for PD-1 expression and ELISA assay for IL-2 and IFNγ levels in activated Jurkat T cells after PMA (50 ng/mL) and Ionomycin (1 µg/mL) treatment; (E) Caspase 3/7 activity of PD-L1(-) MCF7 cells, co-cultured with activated Jurkat T cells; Caspase 3/7 activity of PD-L1(+) (F) BT20 and (G) MDA-MB-231 cells, co-cultured with activated Jurkat T cells, after treatment of PD-1/PD-L1 inhibitor for 24 h.
    Bt20, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bt20/product/ATCC
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bt20 - by Bioz Stars, 2022-09
    97/100 stars
      Buy from Supplier

    bt474  (ATCC)
    97
    ATCC bt474
    The effect of lidocaine on the viability of breast cancer cell lines. ( A ). Bar charts: [lidocaine] ≥ 0.3 mM inhibited AU565 viability, [lidocaine] ≥ 1 mM suppressed the viability of all cell lines except that [lidocaine] = 3 mM was needed for inhibition of <t>BT474</t> and MCF-7 viability. “*” indicates the significant differences ( p
    Bt474, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bt474/product/ATCC
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    bt474 - by Bioz Stars, 2022-09
    97/100 stars
      Buy from Supplier

    Image Search Results


    PD-L1 is an unpredictable biomarker of response to PD-1/PD-L1 Inhibition. (A) PD-L1 mRNA and protein expression levels and (B and C) surface PD-L1 expression in MCF7, BT20, and MDA-MB-231 cells; (D) western blot analysis for PD-1 expression and ELISA assay for IL-2 and IFNγ levels in activated Jurkat T cells after PMA (50 ng/mL) and Ionomycin (1 µg/mL) treatment; (E) Caspase 3/7 activity of PD-L1(-) MCF7 cells, co-cultured with activated Jurkat T cells; Caspase 3/7 activity of PD-L1(+) (F) BT20 and (G) MDA-MB-231 cells, co-cultured with activated Jurkat T cells, after treatment of PD-1/PD-L1 inhibitor for 24 h.

    Journal: American Journal of Cancer Research

    Article Title: Blockade of CCL2 expression overcomes intrinsic PD-1/PD-L1 inhibitor-resistance in transglutaminase 2-induced PD-L1 positive triple negative breast cancer

    doi:

    Figure Lengend Snippet: PD-L1 is an unpredictable biomarker of response to PD-1/PD-L1 Inhibition. (A) PD-L1 mRNA and protein expression levels and (B and C) surface PD-L1 expression in MCF7, BT20, and MDA-MB-231 cells; (D) western blot analysis for PD-1 expression and ELISA assay for IL-2 and IFNγ levels in activated Jurkat T cells after PMA (50 ng/mL) and Ionomycin (1 µg/mL) treatment; (E) Caspase 3/7 activity of PD-L1(-) MCF7 cells, co-cultured with activated Jurkat T cells; Caspase 3/7 activity of PD-L1(+) (F) BT20 and (G) MDA-MB-231 cells, co-cultured with activated Jurkat T cells, after treatment of PD-1/PD-L1 inhibitor for 24 h.

    Article Snippet: The human breast cancer cell lines, BT20, MCF7 and MDA-MB-231, were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Biomarker Assay, Inhibition, Expressing, Multiple Displacement Amplification, Western Blot, Enzyme-linked Immunosorbent Assay, Activity Assay, Cell Culture

    TG2 induces PD-L1 expression by blocking PTEN and activating NF-κB in TNBC cells. (A) Fold change in TG2 in MDA-MB-231 and BT20 cells, and western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7 and MDA-MB-231 cells, with β-Actin as a loading control. (B) Western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7/Mock, MCF7/TG2, MDA-MB-231, and MDA-MB-231/TG2 siRNA cells, with β-Actin as a loading control. (C) Cell Immunohistochemistry and (D) FACS analysis for surface PD-L1 expression level in MCF7/Mock, MCF7/TG2, MDA-MB-231 and MDA-MB-231/TG2 siRNA. (E) Incidence of TG2 and PD-L1 expression in Formalin-Fixed Paraffin-Embedded (FFPE) tissue samples of 648 TNBC patients.

    Journal: American Journal of Cancer Research

    Article Title: Blockade of CCL2 expression overcomes intrinsic PD-1/PD-L1 inhibitor-resistance in transglutaminase 2-induced PD-L1 positive triple negative breast cancer

    doi:

    Figure Lengend Snippet: TG2 induces PD-L1 expression by blocking PTEN and activating NF-κB in TNBC cells. (A) Fold change in TG2 in MDA-MB-231 and BT20 cells, and western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7 and MDA-MB-231 cells, with β-Actin as a loading control. (B) Western blot analysis of TG2, PD-L1, PTEN, pAKT, and IκBα in MCF7/Mock, MCF7/TG2, MDA-MB-231, and MDA-MB-231/TG2 siRNA cells, with β-Actin as a loading control. (C) Cell Immunohistochemistry and (D) FACS analysis for surface PD-L1 expression level in MCF7/Mock, MCF7/TG2, MDA-MB-231 and MDA-MB-231/TG2 siRNA. (E) Incidence of TG2 and PD-L1 expression in Formalin-Fixed Paraffin-Embedded (FFPE) tissue samples of 648 TNBC patients.

    Article Snippet: The human breast cancer cell lines, BT20, MCF7 and MDA-MB-231, were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Blocking Assay, Multiple Displacement Amplification, Western Blot, Immunohistochemistry, FACS, Formalin-fixed Paraffin-Embedded

    CCL2 induction by TG2 contributes to PD-L1 inhibitor-resistance via regulation of negatively cytotoxic T cells in TNBC cells. The level of (A) PD-L1 and (B) CCL2 mRNA expression in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells measured by qRT-PCR analysis; (C) western blot analysis to check expression levels of TG2, P-AKT, IκBα, PD-L1, CCL2, and β-Actin in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells; (D) the expression of TG2, PD-L1, and CCL2 in MCF7/TG2 and MDA-MB-231 cells tested by western blotting analysis after TG2 siRNA transfection; (E) expression of PD-1 and CCR2 in Jurkat T cells with or without treatment of PMA (50 ng/mL) and Ionomycin (1 µg/mL) for 24 h measured by western blotting; (F and G) the protein levels of cPARP, IκBα, PD-L1, and CCL2 in MCF7/TG and MDA-MB-231 cells with or without activated Jurkat T cell co-culture for 24 h measured by western blotting after CCL2 siRNA transfection, Avelumab (20 µg/mL) treatment, or dual combination treatment and Caspase 3/7 activity measured by Caspase 3/7 assay using proteins from MCF7/TG and MDA-MB-231 cells.

    Journal: American Journal of Cancer Research

    Article Title: Blockade of CCL2 expression overcomes intrinsic PD-1/PD-L1 inhibitor-resistance in transglutaminase 2-induced PD-L1 positive triple negative breast cancer

    doi:

    Figure Lengend Snippet: CCL2 induction by TG2 contributes to PD-L1 inhibitor-resistance via regulation of negatively cytotoxic T cells in TNBC cells. The level of (A) PD-L1 and (B) CCL2 mRNA expression in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells measured by qRT-PCR analysis; (C) western blot analysis to check expression levels of TG2, P-AKT, IκBα, PD-L1, CCL2, and β-Actin in MCF7, BT20, MCF7/TG2, and MDA-MB-231 cells; (D) the expression of TG2, PD-L1, and CCL2 in MCF7/TG2 and MDA-MB-231 cells tested by western blotting analysis after TG2 siRNA transfection; (E) expression of PD-1 and CCR2 in Jurkat T cells with or without treatment of PMA (50 ng/mL) and Ionomycin (1 µg/mL) for 24 h measured by western blotting; (F and G) the protein levels of cPARP, IκBα, PD-L1, and CCL2 in MCF7/TG and MDA-MB-231 cells with or without activated Jurkat T cell co-culture for 24 h measured by western blotting after CCL2 siRNA transfection, Avelumab (20 µg/mL) treatment, or dual combination treatment and Caspase 3/7 activity measured by Caspase 3/7 assay using proteins from MCF7/TG and MDA-MB-231 cells.

    Article Snippet: The human breast cancer cell lines, BT20, MCF7 and MDA-MB-231, were obtained from the American Type Culture Collection (Manassas, VA, USA).

    Techniques: Expressing, Multiple Displacement Amplification, Quantitative RT-PCR, Western Blot, Transfection, Co-Culture Assay, Activity Assay

    Dasatinib treatment inhibits the in vitro functional activity induced by P-cadherin expression. a Western blotting for pSRC(Tyr416), total Src, P-cadherin, E-cadherin and p120ctn in P-cadherin overexpressing cells after dasatinib treatment (100 nM) for 48 h. Protein levels of β-actin were analyzed and used as the loading control. b Representative experiment from a wound healing migration assay, in both P-cadherin overexpressing BCC (MCF-7/AZ.Pcad and BT20), treated with 100 nM of dasatinib or DMSO for 24 h. c Fold change in the number of invasive cells, evaluated by the matrigel invasion assay for both MCF-7/AZ.Pcad and BT20 treated with DMSO or 100 nM of dasatinib. d Zymography for MMP2 activity and Western blotting for sP-cad, using the conditioned medium from cells treated with DMSO or 100 nM of dasatinib for 48 h, in both MCF-7/AZ.Pcad and BT20 BCC models. e Mammosphere forming assay was performed for both cell models. The P -values indicate the statistically significant difference between DMSO and dasatinib treated cells, in both P-cadherin BCC models. f Average values of Work (J), representing the cell-cell adhesion strength, of both BCC cancer cell models treated with DMSO and dasatinib, using AFM Force Spectroscopy analysis. g Box-plot quantification of the length (μm) and h number of invasive protrusions of MCF-7/AZ.Pcad spheroids, treated with DMSO or 100 nM dasatinib, for 24 h. P -values

    Journal: Cell Communication and Signaling : CCS

    Article Title: SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells

    doi: 10.1186/s12964-018-0286-2

    Figure Lengend Snippet: Dasatinib treatment inhibits the in vitro functional activity induced by P-cadherin expression. a Western blotting for pSRC(Tyr416), total Src, P-cadherin, E-cadherin and p120ctn in P-cadherin overexpressing cells after dasatinib treatment (100 nM) for 48 h. Protein levels of β-actin were analyzed and used as the loading control. b Representative experiment from a wound healing migration assay, in both P-cadherin overexpressing BCC (MCF-7/AZ.Pcad and BT20), treated with 100 nM of dasatinib or DMSO for 24 h. c Fold change in the number of invasive cells, evaluated by the matrigel invasion assay for both MCF-7/AZ.Pcad and BT20 treated with DMSO or 100 nM of dasatinib. d Zymography for MMP2 activity and Western blotting for sP-cad, using the conditioned medium from cells treated with DMSO or 100 nM of dasatinib for 48 h, in both MCF-7/AZ.Pcad and BT20 BCC models. e Mammosphere forming assay was performed for both cell models. The P -values indicate the statistically significant difference between DMSO and dasatinib treated cells, in both P-cadherin BCC models. f Average values of Work (J), representing the cell-cell adhesion strength, of both BCC cancer cell models treated with DMSO and dasatinib, using AFM Force Spectroscopy analysis. g Box-plot quantification of the length (μm) and h number of invasive protrusions of MCF-7/AZ.Pcad spheroids, treated with DMSO or 100 nM dasatinib, for 24 h. P -values

    Article Snippet: Human breast cancer cell (BCC) lines were obtained as follows: MCF-7/AZ was provided by Prof. Marc Mareel (Ghent University, Belgium); SUM-149 was kindly provided by Dr. Stephen Ethier (University of Michigan, USA); BT20 and MDA-MB-468 were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: In Vitro, Functional Assay, Activity Assay, Expressing, Western Blot, Migration, Invasion Assay, Zymography, Spectroscopy

    Dasatinib treatment affects the in vivo tumorigenic and metastatic capacity of P-cadherin overexpressing tumors. a Kaplan-Meyer survival curve for the overall survival of mice treated with DMSO and dasatinib 10 mg/kg, for a maximum period of 210 days. P-value was calculated using a log-rank test to assess significant differences for mice overall survival. b Percentage of tumours with vascular invasion, observed by HE staining. Presence or absence of clusters of tumour cells inside blood vessels surrounding the primary tumour was quantified in control versus dasatinib treated mice (10 mg/kg). c Tumour volume measured at week 5, post inoculation of cancer cells, from control and dasatinib treated groups, in all BCC models (SUM149, BT20 and MDA-MB-468). d Immunofluorescence for p120ctn (red) and DAPI (blue in the primary tumours from control and dasatinib treated animals. Scale bar = 50 μm. e Immunohistochemistry for p120ctn and pSRC(Tyr416) in the primary tumours from control and dasatinib treated animals. The images shown are representative ones. f Quantification of the p120ctn cytoplasmic intensity expression in primary tumours from control and dasatinib treated animals. g Quantification of the p120ctn membrane intensity. Each dot represents the mean of p120ctn membrane intensity of 100 pairs of cells from a single biological replicate. Student’s t-tests were used to determine statistically significant differences, and P-values are indicated in the figure. Scale bar = 50 μm. h Proximity ligation assay for E-cadherin and p120ctn, from tumours recovered from different mice from control and dasatinib treated groups. i Box-plot for the average number of blobs/cells, quantified using the images of the proximity ligation assay for E-cadherin and p120ctn, between tumours from control and dasatinib treated mice. Student’s t-tests were used to determine statistically significant differences, and the P-value are indicated in the figure. Scale bar = 50 μm

    Journal: Cell Communication and Signaling : CCS

    Article Title: SRC inhibition prevents P-cadherin mediated signaling and function in basal-like breast cancer cells

    doi: 10.1186/s12964-018-0286-2

    Figure Lengend Snippet: Dasatinib treatment affects the in vivo tumorigenic and metastatic capacity of P-cadherin overexpressing tumors. a Kaplan-Meyer survival curve for the overall survival of mice treated with DMSO and dasatinib 10 mg/kg, for a maximum period of 210 days. P-value was calculated using a log-rank test to assess significant differences for mice overall survival. b Percentage of tumours with vascular invasion, observed by HE staining. Presence or absence of clusters of tumour cells inside blood vessels surrounding the primary tumour was quantified in control versus dasatinib treated mice (10 mg/kg). c Tumour volume measured at week 5, post inoculation of cancer cells, from control and dasatinib treated groups, in all BCC models (SUM149, BT20 and MDA-MB-468). d Immunofluorescence for p120ctn (red) and DAPI (blue in the primary tumours from control and dasatinib treated animals. Scale bar = 50 μm. e Immunohistochemistry for p120ctn and pSRC(Tyr416) in the primary tumours from control and dasatinib treated animals. The images shown are representative ones. f Quantification of the p120ctn cytoplasmic intensity expression in primary tumours from control and dasatinib treated animals. g Quantification of the p120ctn membrane intensity. Each dot represents the mean of p120ctn membrane intensity of 100 pairs of cells from a single biological replicate. Student’s t-tests were used to determine statistically significant differences, and P-values are indicated in the figure. Scale bar = 50 μm. h Proximity ligation assay for E-cadherin and p120ctn, from tumours recovered from different mice from control and dasatinib treated groups. i Box-plot for the average number of blobs/cells, quantified using the images of the proximity ligation assay for E-cadherin and p120ctn, between tumours from control and dasatinib treated mice. Student’s t-tests were used to determine statistically significant differences, and the P-value are indicated in the figure. Scale bar = 50 μm

    Article Snippet: Human breast cancer cell (BCC) lines were obtained as follows: MCF-7/AZ was provided by Prof. Marc Mareel (Ghent University, Belgium); SUM-149 was kindly provided by Dr. Stephen Ethier (University of Michigan, USA); BT20 and MDA-MB-468 were obtained from American Type Culture Collection (Manassas, VA, USA).

    Techniques: In Vivo, Mouse Assay, Staining, Multiple Displacement Amplification, Immunofluorescence, Immunohistochemistry, Expressing, Proximity Ligation Assay

    The effect of lidocaine on the viability of breast cancer cell lines. ( A ). Bar charts: [lidocaine] ≥ 0.3 mM inhibited AU565 viability, [lidocaine] ≥ 1 mM suppressed the viability of all cell lines except that [lidocaine] = 3 mM was needed for inhibition of BT474 and MCF-7 viability. “*” indicates the significant differences ( p

    Journal: Cancers

    Article Title: Lidocaine Suppresses Viability and Migration of Human Breast Cancer Cells: TRPM7 as a Target for Some Breast Cancer Cell Lines

    doi: 10.3390/cancers13020234

    Figure Lengend Snippet: The effect of lidocaine on the viability of breast cancer cell lines. ( A ). Bar charts: [lidocaine] ≥ 0.3 mM inhibited AU565 viability, [lidocaine] ≥ 1 mM suppressed the viability of all cell lines except that [lidocaine] = 3 mM was needed for inhibition of BT474 and MCF-7 viability. “*” indicates the significant differences ( p

    Article Snippet: Cell Lines HEK293 human kidney embryo cell line (WT-HEK), breast cancer cell lines MDA-MB-231 (WT-231), AU565, T47D, MDA-MB-468, MCF-7, BT474, and BT-20 were purchased from ATCC® (Manassas, VA, USA).

    Techniques: Inhibition

    The effect of lidocaine on cell migration of breast cancer cell lines. ( A ). [lidocaine] ≥ 0.3 mM inhibited migration of MDA-MB-231, AU565, and BT474; [lidocaine] ≥ 1 mM suppressed the migration of all cell lines. “*” indicates the significant differences ( p

    Journal: Cancers

    Article Title: Lidocaine Suppresses Viability and Migration of Human Breast Cancer Cells: TRPM7 as a Target for Some Breast Cancer Cell Lines

    doi: 10.3390/cancers13020234

    Figure Lengend Snippet: The effect of lidocaine on cell migration of breast cancer cell lines. ( A ). [lidocaine] ≥ 0.3 mM inhibited migration of MDA-MB-231, AU565, and BT474; [lidocaine] ≥ 1 mM suppressed the migration of all cell lines. “*” indicates the significant differences ( p

    Article Snippet: Cell Lines HEK293 human kidney embryo cell line (WT-HEK), breast cancer cell lines MDA-MB-231 (WT-231), AU565, T47D, MDA-MB-468, MCF-7, BT474, and BT-20 were purchased from ATCC® (Manassas, VA, USA).

    Techniques: Migration, Multiple Displacement Amplification

    Basal level expression and DNA methylation for most of the genes in MT1 gene cluster show lower expression and higher methylation in breast cancer cell lines. (A) RT-qPCR gene expression and (B) averaged methylation profiles of MT1 genes in cell lines representing ERα + (MCF7 and BT474) and ERα − (BT20 and MDAMB231) subsets compared to normal (HMEC used for PCR and average of normal samples for DNA methylation) revealing lower levels of expression and higher levels of DNA methylation in cell lines compared to normal.

    Journal: Clinical Epigenetics

    Article Title: Genome-wide DNA methylation analysis reveals estrogen-mediated epigenetic repression of metallothionein-1 gene cluster in breast cancer

    doi: 10.1186/s13148-015-0045-9

    Figure Lengend Snippet: Basal level expression and DNA methylation for most of the genes in MT1 gene cluster show lower expression and higher methylation in breast cancer cell lines. (A) RT-qPCR gene expression and (B) averaged methylation profiles of MT1 genes in cell lines representing ERα + (MCF7 and BT474) and ERα − (BT20 and MDAMB231) subsets compared to normal (HMEC used for PCR and average of normal samples for DNA methylation) revealing lower levels of expression and higher levels of DNA methylation in cell lines compared to normal.

    Article Snippet: Cell culture Most of ICBP panel breast cell lines were obtained from NCI Cancer Biology Program at NCI in November 2008, except HMEC, MCF7, MDAMB134, BT474, BT20, and MDA-MB231 were obtained from American Type Culture Collection (ATCC) (ATCC Breast Cancer Cell Panel, Manassas, VA, USA).

    Techniques: Expressing, DNA Methylation Assay, Methylation, Quantitative RT-PCR, Polymerase Chain Reaction