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ATCC breast cancer cell lines mda mb 231
μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and <t>GFP</t> <t>+</t> <t>MDA-MB-231</t> cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.
Breast Cancer Cell Lines 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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Silimed Inc silicone gel-filled breast implants textured surface
μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and <t>GFP</t> <t>+</t> <t>MDA-MB-231</t> cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.
Silicone Gel Filled Breast Implants Textured Surface, supplied by Silimed 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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Silimed Inc silicone gel-filled breast implants polyurethane foam covered surface
μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and <t>GFP</t> <t>+</t> <t>MDA-MB-231</t> cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.
Silicone Gel Filled Breast Implants Polyurethane Foam Covered Surface, supplied by Silimed Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/silicone gel-filled breast implants polyurethane foam covered surface/product/Silimed Inc
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Silimed Inc breast implant smooth surface
μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and <t>GFP</t> <t>+</t> <t>MDA-MB-231</t> cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.
Breast Implant Smooth Surface, supplied by Silimed Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/breast implant smooth surface/product/Silimed Inc
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Thermo Fisher oncomine breast cfdna assay
μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and <t>GFP</t> <t>+</t> <t>MDA-MB-231</t> cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.
Oncomine Breast Cfdna Assay, supplied by Thermo Fisher, 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 human breast cancer cell lines skbr3
EBA impairs cancer stem cell-like properties. (A) BT474 and <t>SKBR3</t> cells were treated with EBA for 48 h, and ALDH1 activity was assessed by flow cytometry using the Aldefluor assay. DEAB was used to define the baseline of Aldefluor-positive fluorescence. (B) BT474 cells (5x10 4 cells/ml) were plated in ultra-low attachment dishes and cultured in the presence or absence of EBA for 5 days. The number and volume of mammospheres were measured by microscopy. (C) Overall survival of patients with breast cancer stratified by the co-expression of ALDH1A1 and CD44. (D) Spearman correlation analysis of ALDH1A1 and CD44 mRNA levels in patients with HER2-positive breast cancer from The Cancer Genome Atlas cohort (n=76). Kaplan-Meier survival analyses of patients with HER2-overexpressing breast cancer stratified by (E) ALDH1A1 and (F) CD44 expression. Patients were divided into high- and low-expression groups based on the median gene expression. Statistical significance was determined using the log-rank test. (G) JIMT-1 cells were treated with EBA (3 μ M) for 48 h and the CD44 high /CD24 low cell populations were identified by flow cytometry. (H) JIMT-1 cells (1.5x10 4 cells/ml) were cultured under serum-free suspension conditions in the presence of EBA (3 μ M) for 8 days. Mammosphere number and volumes were quantified. ** P<0.01 and **** P<0.0001 vs. vehicle-treated control (0 μ M EBA). EBA, ebastine; ALDH, aldehyde dehydrogenase; DEAB, diethylaminobenzaldehyde; CTL, control; ISO, isotype.
Human Breast Cancer Cell Lines Skbr3, supplied by ATCC, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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human breast cancer cell lines skbr3 - by Bioz Stars, 2026-03
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ATCC human breast cancer cells
EBA impairs cancer stem cell-like properties. (A) BT474 and <t>SKBR3</t> cells were treated with EBA for 48 h, and ALDH1 activity was assessed by flow cytometry using the Aldefluor assay. DEAB was used to define the baseline of Aldefluor-positive fluorescence. (B) BT474 cells (5x10 4 cells/ml) were plated in ultra-low attachment dishes and cultured in the presence or absence of EBA for 5 days. The number and volume of mammospheres were measured by microscopy. (C) Overall survival of patients with breast cancer stratified by the co-expression of ALDH1A1 and CD44. (D) Spearman correlation analysis of ALDH1A1 and CD44 mRNA levels in patients with HER2-positive breast cancer from The Cancer Genome Atlas cohort (n=76). Kaplan-Meier survival analyses of patients with HER2-overexpressing breast cancer stratified by (E) ALDH1A1 and (F) CD44 expression. Patients were divided into high- and low-expression groups based on the median gene expression. Statistical significance was determined using the log-rank test. (G) JIMT-1 cells were treated with EBA (3 μ M) for 48 h and the CD44 high /CD24 low cell populations were identified by flow cytometry. (H) JIMT-1 cells (1.5x10 4 cells/ml) were cultured under serum-free suspension conditions in the presence of EBA (3 μ M) for 8 days. Mammosphere number and volumes were quantified. ** P<0.01 and **** P<0.0001 vs. vehicle-treated control (0 μ M EBA). EBA, ebastine; ALDH, aldehyde dehydrogenase; DEAB, diethylaminobenzaldehyde; CTL, control; ISO, isotype.
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
https://www.bioz.com/result/human breast cancer cells/product/ATCC
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human breast cancer cells - by Bioz Stars, 2026-03
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ATCC 4t1 breast tumour cells
Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or <t>4T1</t> tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.
4t1 Breast Tumour 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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4t1 breast tumour cells - by Bioz Stars, 2026-03
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Image Search Results


μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and GFP + MDA-MB-231 cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.

Journal: Bioactive Materials

Article Title: Ribbon-shaped microgels as bioinks for 3D bioprinting of anisotropic tissue structures

doi: 10.1016/j.bioactmat.2025.12.040

Figure Lengend Snippet: μRB bioinks support multicellular patterning to model breast cancer-bone invasion at tissue interface. (A) Schematic of experimental design: bioprinting of MSCs and osteogenic differentiation to derive bone grid, followed by injection of breast cancer bioink, and monitoring invasion over time using confocal microscopy. (B) Confocal images of MSCs (red) after printing (Scale bar = 1 mm). (C) Confocal images of scaffold sections containing CellTracker-labeled MSCs (red) after 28 days of osteogenic differentiation and GFP + MDA-MB-231 cells extruded into the open pores of the grids (green) (Scale bar = 200 μm). (D) Confocal images of patterned MSC-derived bone (red) with MDA-MB-231 and MCF-7 breast cancer cells (green) after 14 days of co-culture (Scale bar = 1 mm). (E) Quantification of breast cancer cell invasion: percentage that remain in open pores vs. invading into the MSC-bone compartment (n = 5 per group). Values are reported as mean ± S.D. and p-values were determined by two-way analysis of variance (ANOVA) with Tukey's multiple comparisons test; ∗∗p ≤ 0.01, ∗∗∗p ≤ 0.005, ∗∗∗∗p ≤ 0.001.

Article Snippet: Breast cancer cell lines MDA-MB-231 (ATCC) and MCF-7 (ATCC) were lentivirus transduced to express GFP and cultured in DMEM media (4.5 g L −1 glucose) supplemented with 10 % (v/v) fetal bovine serum and 1 % (v/v) penicillin-streptomycin.

Techniques: Injection, Confocal Microscopy, Labeling, Derivative Assay, Co-Culture Assay

EBA impairs cancer stem cell-like properties. (A) BT474 and SKBR3 cells were treated with EBA for 48 h, and ALDH1 activity was assessed by flow cytometry using the Aldefluor assay. DEAB was used to define the baseline of Aldefluor-positive fluorescence. (B) BT474 cells (5x10 4 cells/ml) were plated in ultra-low attachment dishes and cultured in the presence or absence of EBA for 5 days. The number and volume of mammospheres were measured by microscopy. (C) Overall survival of patients with breast cancer stratified by the co-expression of ALDH1A1 and CD44. (D) Spearman correlation analysis of ALDH1A1 and CD44 mRNA levels in patients with HER2-positive breast cancer from The Cancer Genome Atlas cohort (n=76). Kaplan-Meier survival analyses of patients with HER2-overexpressing breast cancer stratified by (E) ALDH1A1 and (F) CD44 expression. Patients were divided into high- and low-expression groups based on the median gene expression. Statistical significance was determined using the log-rank test. (G) JIMT-1 cells were treated with EBA (3 μ M) for 48 h and the CD44 high /CD24 low cell populations were identified by flow cytometry. (H) JIMT-1 cells (1.5x10 4 cells/ml) were cultured under serum-free suspension conditions in the presence of EBA (3 μ M) for 8 days. Mammosphere number and volumes were quantified. ** P<0.01 and **** P<0.0001 vs. vehicle-treated control (0 μ M EBA). EBA, ebastine; ALDH, aldehyde dehydrogenase; DEAB, diethylaminobenzaldehyde; CTL, control; ISO, isotype.

Journal: International Journal of Molecular Medicine

Article Title: Ebastine targets HER2/HER3 signaling and cancer stem cell traits to overcome trastuzumab resistance in HER2-positive breast cancer

doi: 10.3892/ijmm.2026.5751

Figure Lengend Snippet: EBA impairs cancer stem cell-like properties. (A) BT474 and SKBR3 cells were treated with EBA for 48 h, and ALDH1 activity was assessed by flow cytometry using the Aldefluor assay. DEAB was used to define the baseline of Aldefluor-positive fluorescence. (B) BT474 cells (5x10 4 cells/ml) were plated in ultra-low attachment dishes and cultured in the presence or absence of EBA for 5 days. The number and volume of mammospheres were measured by microscopy. (C) Overall survival of patients with breast cancer stratified by the co-expression of ALDH1A1 and CD44. (D) Spearman correlation analysis of ALDH1A1 and CD44 mRNA levels in patients with HER2-positive breast cancer from The Cancer Genome Atlas cohort (n=76). Kaplan-Meier survival analyses of patients with HER2-overexpressing breast cancer stratified by (E) ALDH1A1 and (F) CD44 expression. Patients were divided into high- and low-expression groups based on the median gene expression. Statistical significance was determined using the log-rank test. (G) JIMT-1 cells were treated with EBA (3 μ M) for 48 h and the CD44 high /CD24 low cell populations were identified by flow cytometry. (H) JIMT-1 cells (1.5x10 4 cells/ml) were cultured under serum-free suspension conditions in the presence of EBA (3 μ M) for 8 days. Mammosphere number and volumes were quantified. ** P<0.01 and **** P<0.0001 vs. vehicle-treated control (0 μ M EBA). EBA, ebastine; ALDH, aldehyde dehydrogenase; DEAB, diethylaminobenzaldehyde; CTL, control; ISO, isotype.

Article Snippet: The human breast cancer cell lines SKBR3, BT474, MDA-MB-453 (American Type Culture Collection) and JIMT-1 (Leibnitz Institute DSMZ-German Collection of Microorganisms and Cell Cultures GmbH) were cultured in DMEM, MEM or RPMI-1640 (all Sigma-Aldrich; Merck KGaA) supplemented with 10% FBS (Gibco; Thermo Fisher Scientific, Inc.) and 100 U/ml penicillin-streptomycin at 37°C in a humidified atmosphere of 5% CO 2 .

Techniques: Activity Assay, Flow Cytometry, Fluorescence, Cell Culture, Microscopy, Expressing, Gene Expression, Suspension, Control

Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Journal: Journal of Bone Oncology

Article Title: Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype

doi: 10.1016/j.jbo.2026.100754

Figure Lengend Snippet: Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Article Snippet: PC3 prostate tumour cells (ATCC CRL-1435), 4T1 breast tumour cells (CRL-2539) and K562 leukemia tumour cells (CCL-243) were obtained from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Co-Culture Assay, Control, Isolation, Cell Characterization