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breast cancer cell lines mda mb 231  (ATCC)


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    Structured Review

    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 27245 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Ribbon-shaped microgels as bioinks for 3D bioprinting of anisotropic tissue structures"

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

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2025.12.040

    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.
    Figure Legend 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.

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



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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
    https://www.bioz.com/result/breast cancer cell lines mda mb 231/product/ATCC
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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: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC sw620 human colorectal cancer cell line
    Oxidative stress markers in nude mice colon treated with <t>SW620,</t> AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 in MDA and a non-significant change at p > 0.05 in SOD and catalase activity. Values presented as mean ± S.E., a, b different superscripts within columns are significantly different ( P < 0.05).
    Sw620 Human Colorectal Cancer Cell Line, 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/sw620 human colorectal cancer cell line/product/ATCC
    Average 99 stars, based on 1 article reviews
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    ATCC human breast cancer mda mb 231 cell lines
    Oxidative stress markers in nude mice colon treated with <t>SW620,</t> AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 in MDA and a non-significant change at p > 0.05 in SOD and catalase activity. Values presented as mean ± S.E., a, b different superscripts within columns are significantly different ( P < 0.05).
    Human Breast Cancer Mda Mb 231 Cell Lines, 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 mda mb 231 cell lines/product/ATCC
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    ATCC ovarian cancer cell lines skov3
    The pre-targeting complex of NIR-PIT induces the release of ICD markers (A) Flow cytometric histograms show cell surface expression of calreticulin, HSP70, and HSP90 compared to untreated controls in <t>SKOV3</t> cells with scFv-tisotumab-Zip2-Zip1-SNAP-IR700. (B) OVCAR3 cells treated with scFv-Sacituzumab-Zip2-Zip1-SNAP-IR700. (C) IGROV1 cells treated with scFv-Farletuzumab-Zip2-Zip1-SNAP-IR700. Only viable cells were included in the analysis. Bar graphs show the mean fluorescence intensity (MFI) of cell surface calreticulin, HSP70, and HSP90. Data are represented as mean ± SD from three biological replicates. Cells exposed to NIR light irradiation without incubation with NIR-PIT agents were used as control. Statistical significance was determined by a one-way ANOVA and Dunnett's test. ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001.
    Ovarian Cancer Cell Lines Skov3, 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 lung cancer cell lines a549
    IFNs mediate immunotherapy-associated gene expression in tumors and activate immune cells in healthy PBMCs. A qPCR was used to detect the PD-L1 expression in <t>A549</t> (5 × 10 5 in a 6-well plate) treated with IFNα and IFNγ (20 ng/mL for each, incubated for 2 h). B The expression of the top 8 up-regulated genes from RNAseq analysis (Table S2), including ICAM1, BATF, IRF1, SOCS1, HAPLN3, TAP1, PSMB9, and MAFF, were validated by qPCR analysis in A549 treated with IFNα and IFNγ (20 ng/mL for each, incubated for 2 h). C The healthy PBMCs (1 × 10 6 in a 6-well plate) treated with IFNs (20 ng/mL for each, incubated for 24 h), co-cultured with A549, IFNα- and IFNγ (3 h)-pretreated A549 at a 20:1 ratio, and IFNα, IFNγ, and A549 concurrently treated for 24 h were analyzed by flow cytometry to (D and E) detect the activation marker CD107a levels in CD4 + T, CD8 + T cells, and CD45 + CD3 − (nonT) PBMCs (n = 3). CD4 + T and CD8 + T were gated by staining with anti-CD45-Pacific blue, anti-CD3-APC/Cy7, anti-CD8-Alexa488, and anti-CD4-PE. CD107a was detected using anti-CD107a-BV605. (F) In addition, the activation markers IFNG, and cytotoxic marker granzyme B (GZMB) were detected by qPCR in the collected PBMCs after individual treatments. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001
    Human Lung Cancer Cell Lines A549, 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 colorectal cancer cell line sw620
    Ongoing copy number alterations in model systems. A, Schematic of the method used to obtain and sequence single cells from cultured colorectal cancer cell line <t>SW620</t> and patient-derived organoid (PDO) 3994-1117. Cell line SW620 underwent single-cell dispensing using the cellenONE system, followed by direct library prep (DLP) while the 10× Genomics Chromium was used to prepare single-cell libraries from the patient-derived organoid 3994-1117. B, Heatmap showing CNAs in single cells from colorectal cancer cell line SW620 and ( C ) from patient-derived organoid 3994-1117. Red = gain, blue = loss. D, Phylogenetic tree constructed using CNAs in the colorectal cancer cell line SW620. E, Frequency of copy number gains and losses at the tips of the SW620 phylogenetic tree. F, Phylogenetic tree constructed using CNAs in the colorectal cancer organoid 3994-117. G, Frequency of copy number gains and losses at the tips of the 3994-117 phylogenetic tree (as in E ).
    Colorectal Cancer Cell Line Sw620, 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 cell culture human grade 4 bladder cancer cell line htb 5
    Ongoing copy number alterations in model systems. A, Schematic of the method used to obtain and sequence single cells from cultured colorectal cancer cell line <t>SW620</t> and patient-derived organoid (PDO) 3994-1117. Cell line SW620 underwent single-cell dispensing using the cellenONE system, followed by direct library prep (DLP) while the 10× Genomics Chromium was used to prepare single-cell libraries from the patient-derived organoid 3994-1117. B, Heatmap showing CNAs in single cells from colorectal cancer cell line SW620 and ( C ) from patient-derived organoid 3994-1117. Red = gain, blue = loss. D, Phylogenetic tree constructed using CNAs in the colorectal cancer cell line SW620. E, Frequency of copy number gains and losses at the tips of the SW620 phylogenetic tree. F, Phylogenetic tree constructed using CNAs in the colorectal cancer organoid 3994-117. G, Frequency of copy number gains and losses at the tips of the 3994-117 phylogenetic tree (as in E ).
    Cell Culture Human Grade 4 Bladder Cancer Cell Line Htb 5, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    ATCC bladder cancer cell lines
    Ongoing copy number alterations in model systems. A, Schematic of the method used to obtain and sequence single cells from cultured colorectal cancer cell line <t>SW620</t> and patient-derived organoid (PDO) 3994-1117. Cell line SW620 underwent single-cell dispensing using the cellenONE system, followed by direct library prep (DLP) while the 10× Genomics Chromium was used to prepare single-cell libraries from the patient-derived organoid 3994-1117. B, Heatmap showing CNAs in single cells from colorectal cancer cell line SW620 and ( C ) from patient-derived organoid 3994-1117. Red = gain, blue = loss. D, Phylogenetic tree constructed using CNAs in the colorectal cancer cell line SW620. E, Frequency of copy number gains and losses at the tips of the SW620 phylogenetic tree. F, Phylogenetic tree constructed using CNAs in the colorectal cancer organoid 3994-117. G, Frequency of copy number gains and losses at the tips of the 3994-117 phylogenetic tree (as in E ).
    Bladder Cancer Cell Lines, 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


    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

    Oxidative stress markers in nude mice colon treated with SW620, AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 in MDA and a non-significant change at p > 0.05 in SOD and catalase activity. Values presented as mean ± S.E., a, b different superscripts within columns are significantly different ( P < 0.05).

    Journal: Journal of Genetic Engineering & Biotechnology

    Article Title: Potential role of Adansonia digitata nanoparticles on colorectal cancer induced by colorectal cancer cells (SW620) in nude mice

    doi: 10.1016/j.jgeb.2026.100659

    Figure Lengend Snippet: Oxidative stress markers in nude mice colon treated with SW620, AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 in MDA and a non-significant change at p > 0.05 in SOD and catalase activity. Values presented as mean ± S.E., a, b different superscripts within columns are significantly different ( P < 0.05).

    Article Snippet: The SW620 human colorectal cancer cell line was obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

    Techniques: Activity Assay

    Anti-apoptotic/pro-apoptotic protein level markers in nude mice colon treated with SW620, AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 compared to the SW620 group in cytochrome c and a non-significant change at p > 0.05 in caspase3, BAX, and BCL-2. Values presented as mean ± S.E., a, b different superscripts within columns are significantly different ( P < 0.05).

    Journal: Journal of Genetic Engineering & Biotechnology

    Article Title: Potential role of Adansonia digitata nanoparticles on colorectal cancer induced by colorectal cancer cells (SW620) in nude mice

    doi: 10.1016/j.jgeb.2026.100659

    Figure Lengend Snippet: Anti-apoptotic/pro-apoptotic protein level markers in nude mice colon treated with SW620, AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 compared to the SW620 group in cytochrome c and a non-significant change at p > 0.05 in caspase3, BAX, and BCL-2. Values presented as mean ± S.E., a, b different superscripts within columns are significantly different ( P < 0.05).

    Article Snippet: The SW620 human colorectal cancer cell line was obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

    Techniques:

    TGF-β, TNF-α, INOS, and IL-1β mRNA expression in nude mice colon treated with SW620, AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 compared to the SW620 group in TGF-β, and a non-significant change at p > 0.05 in TNF-α, IL-1β, and INOS. Values presented as mean ± S.E., a, b, c different superscripts within columns are significantly different ( P < 0.05).

    Journal: Journal of Genetic Engineering & Biotechnology

    Article Title: Potential role of Adansonia digitata nanoparticles on colorectal cancer induced by colorectal cancer cells (SW620) in nude mice

    doi: 10.1016/j.jgeb.2026.100659

    Figure Lengend Snippet: TGF-β, TNF-α, INOS, and IL-1β mRNA expression in nude mice colon treated with SW620, AD, ADNPs1, and ADNPs2. A significant change at p < 0.05 compared to the SW620 group in TGF-β, and a non-significant change at p > 0.05 in TNF-α, IL-1β, and INOS. Values presented as mean ± S.E., a, b, c different superscripts within columns are significantly different ( P < 0.05).

    Article Snippet: The SW620 human colorectal cancer cell line was obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

    Techniques: Expressing

    The pre-targeting complex of NIR-PIT induces the release of ICD markers (A) Flow cytometric histograms show cell surface expression of calreticulin, HSP70, and HSP90 compared to untreated controls in SKOV3 cells with scFv-tisotumab-Zip2-Zip1-SNAP-IR700. (B) OVCAR3 cells treated with scFv-Sacituzumab-Zip2-Zip1-SNAP-IR700. (C) IGROV1 cells treated with scFv-Farletuzumab-Zip2-Zip1-SNAP-IR700. Only viable cells were included in the analysis. Bar graphs show the mean fluorescence intensity (MFI) of cell surface calreticulin, HSP70, and HSP90. Data are represented as mean ± SD from three biological replicates. Cells exposed to NIR light irradiation without incubation with NIR-PIT agents were used as control. Statistical significance was determined by a one-way ANOVA and Dunnett's test. ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001.

    Journal: iScience

    Article Title: Synthetic zipper mediated pre-targeting system for near-infrared photoimmunotherapy

    doi: 10.1016/j.isci.2025.114558

    Figure Lengend Snippet: The pre-targeting complex of NIR-PIT induces the release of ICD markers (A) Flow cytometric histograms show cell surface expression of calreticulin, HSP70, and HSP90 compared to untreated controls in SKOV3 cells with scFv-tisotumab-Zip2-Zip1-SNAP-IR700. (B) OVCAR3 cells treated with scFv-Sacituzumab-Zip2-Zip1-SNAP-IR700. (C) IGROV1 cells treated with scFv-Farletuzumab-Zip2-Zip1-SNAP-IR700. Only viable cells were included in the analysis. Bar graphs show the mean fluorescence intensity (MFI) of cell surface calreticulin, HSP70, and HSP90. Data are represented as mean ± SD from three biological replicates. Cells exposed to NIR light irradiation without incubation with NIR-PIT agents were used as control. Statistical significance was determined by a one-way ANOVA and Dunnett's test. ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001.

    Article Snippet: Ovarian cancer cell lines SKOV3 (HTB-77), OVCAR3 (HTB-161), IGROV1 (SCC-203), A2780 (ECACC-93112519), and HEK293T (CRL-11268) were obtained from the American Type Culture Collection, the European Collection of Authenticated Cell Cultures, and Sigma-Aldrich.

    Techniques: Expressing, Fluorescence, Irradiation, Incubation, Control

    IFNs mediate immunotherapy-associated gene expression in tumors and activate immune cells in healthy PBMCs. A qPCR was used to detect the PD-L1 expression in A549 (5 × 10 5 in a 6-well plate) treated with IFNα and IFNγ (20 ng/mL for each, incubated for 2 h). B The expression of the top 8 up-regulated genes from RNAseq analysis (Table S2), including ICAM1, BATF, IRF1, SOCS1, HAPLN3, TAP1, PSMB9, and MAFF, were validated by qPCR analysis in A549 treated with IFNα and IFNγ (20 ng/mL for each, incubated for 2 h). C The healthy PBMCs (1 × 10 6 in a 6-well plate) treated with IFNs (20 ng/mL for each, incubated for 24 h), co-cultured with A549, IFNα- and IFNγ (3 h)-pretreated A549 at a 20:1 ratio, and IFNα, IFNγ, and A549 concurrently treated for 24 h were analyzed by flow cytometry to (D and E) detect the activation marker CD107a levels in CD4 + T, CD8 + T cells, and CD45 + CD3 − (nonT) PBMCs (n = 3). CD4 + T and CD8 + T were gated by staining with anti-CD45-Pacific blue, anti-CD3-APC/Cy7, anti-CD8-Alexa488, and anti-CD4-PE. CD107a was detected using anti-CD107a-BV605. (F) In addition, the activation markers IFNG, and cytotoxic marker granzyme B (GZMB) were detected by qPCR in the collected PBMCs after individual treatments. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Radiotherapy enhances M1 macrophage immunogenic activity through IFNs induction and stimulation in TP53-wild type tumors

    doi: 10.1007/s00262-026-04300-7

    Figure Lengend Snippet: IFNs mediate immunotherapy-associated gene expression in tumors and activate immune cells in healthy PBMCs. A qPCR was used to detect the PD-L1 expression in A549 (5 × 10 5 in a 6-well plate) treated with IFNα and IFNγ (20 ng/mL for each, incubated for 2 h). B The expression of the top 8 up-regulated genes from RNAseq analysis (Table S2), including ICAM1, BATF, IRF1, SOCS1, HAPLN3, TAP1, PSMB9, and MAFF, were validated by qPCR analysis in A549 treated with IFNα and IFNγ (20 ng/mL for each, incubated for 2 h). C The healthy PBMCs (1 × 10 6 in a 6-well plate) treated with IFNs (20 ng/mL for each, incubated for 24 h), co-cultured with A549, IFNα- and IFNγ (3 h)-pretreated A549 at a 20:1 ratio, and IFNα, IFNγ, and A549 concurrently treated for 24 h were analyzed by flow cytometry to (D and E) detect the activation marker CD107a levels in CD4 + T, CD8 + T cells, and CD45 + CD3 − (nonT) PBMCs (n = 3). CD4 + T and CD8 + T were gated by staining with anti-CD45-Pacific blue, anti-CD3-APC/Cy7, anti-CD8-Alexa488, and anti-CD4-PE. CD107a was detected using anti-CD107a-BV605. (F) In addition, the activation markers IFNG, and cytotoxic marker granzyme B (GZMB) were detected by qPCR in the collected PBMCs after individual treatments. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The human lung cancer cell lines A549, HepG2, and PLC5 used in this study were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Gene Expression, Expressing, Incubation, RNA sequencing, Cell Culture, Flow Cytometry, Activation Assay, Marker, Staining, Two Tailed Test

    Radiotherapy increases IFNs and promotes immunogenic activity but distinct gene expression in the IFNγ- and 8 Gy-treated A549 cells. A A549 cells (5 × 10 5 in a 6-well plate) treated with irradiation (0, 1, 2, 4, 8 Gy) and further incubated for 24 h were collected to detect the p53-downstream gene CDKN1A, MDM2, and tumor marker MKI67 by qPCR. Statistical analysis was achieved by one-way ANOVA. B In addition, IFNA and IFNG and their downstream PD-L1 expression in the irradiated A549 cells and C MDM2 inhibitor Nutlin-3a-treated A549 cells were measured by qPCR. D The healthy PBMCs (1 × 10 6 in a 6-well plate) treated with IFNα and IFNγ (20 ng/mL for each) for 2 h and 24 h were collected and analyzed for the immune activation marker IFNG and cytotoxic marker granzyme B (GZMB) expression using qPCR. E M1 markers TNFA and CXCL10, and M2 markers ARG1 and IL-10 were also investigated in the collected PBMCs with the individual treatments by qPCR. F The healthy PBMCs (1 × 10 6 in a 6-well plate) incubated with irradiation-treated A549 (0, 4, 8 Gy) at a ratio of 20:1 for 24 h were collected and investigated for the immune activation marker IFNG and cytotoxic marker GZMB expression using qPCR. G Meanwhile, M1 markers TNFA, CXCL10, and M2 markers ARG1, IL-10 were also investigated in the collected PBMCs with the individual treatments by qPCR. (H) RNAseq was used to search for the differential genes in the A549 cells (5 × 10 5 in a 6-well plate) treated with IFNγ (20 ng /mL, incubated for 2 h) and x-ray irradiation (8 Gy was selected based on the highest CDKN1A and MDM2 induction, 24 h post-irradiation). There were 75 up-regulated and 12 down-regulated genes selected in IFNγ-treated A549 and 88 up-regulated and 202 down-regulated genes selected in 8 Gy-treated A549 according to log2 fold change > 1 or < -1 with p value < 0.05 (Table S2-4). There was no overlapped gene between IFNγ and 8 Gy treatment. I The 75 and 88 up-regulated genes in IFNγ- and irradiated A549 cells were analyzed by NetworkAnalyst ( https://www.networkanalyst.ca/ ) based on the KEGG dataset, revealing that the differential genes were involved in STATs and p53 signaling pathways, respectively. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, non-significant

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Radiotherapy enhances M1 macrophage immunogenic activity through IFNs induction and stimulation in TP53-wild type tumors

    doi: 10.1007/s00262-026-04300-7

    Figure Lengend Snippet: Radiotherapy increases IFNs and promotes immunogenic activity but distinct gene expression in the IFNγ- and 8 Gy-treated A549 cells. A A549 cells (5 × 10 5 in a 6-well plate) treated with irradiation (0, 1, 2, 4, 8 Gy) and further incubated for 24 h were collected to detect the p53-downstream gene CDKN1A, MDM2, and tumor marker MKI67 by qPCR. Statistical analysis was achieved by one-way ANOVA. B In addition, IFNA and IFNG and their downstream PD-L1 expression in the irradiated A549 cells and C MDM2 inhibitor Nutlin-3a-treated A549 cells were measured by qPCR. D The healthy PBMCs (1 × 10 6 in a 6-well plate) treated with IFNα and IFNγ (20 ng/mL for each) for 2 h and 24 h were collected and analyzed for the immune activation marker IFNG and cytotoxic marker granzyme B (GZMB) expression using qPCR. E M1 markers TNFA and CXCL10, and M2 markers ARG1 and IL-10 were also investigated in the collected PBMCs with the individual treatments by qPCR. F The healthy PBMCs (1 × 10 6 in a 6-well plate) incubated with irradiation-treated A549 (0, 4, 8 Gy) at a ratio of 20:1 for 24 h were collected and investigated for the immune activation marker IFNG and cytotoxic marker GZMB expression using qPCR. G Meanwhile, M1 markers TNFA, CXCL10, and M2 markers ARG1, IL-10 were also investigated in the collected PBMCs with the individual treatments by qPCR. (H) RNAseq was used to search for the differential genes in the A549 cells (5 × 10 5 in a 6-well plate) treated with IFNγ (20 ng /mL, incubated for 2 h) and x-ray irradiation (8 Gy was selected based on the highest CDKN1A and MDM2 induction, 24 h post-irradiation). There were 75 up-regulated and 12 down-regulated genes selected in IFNγ-treated A549 and 88 up-regulated and 202 down-regulated genes selected in 8 Gy-treated A549 according to log2 fold change > 1 or < -1 with p value < 0.05 (Table S2-4). There was no overlapped gene between IFNγ and 8 Gy treatment. I The 75 and 88 up-regulated genes in IFNγ- and irradiated A549 cells were analyzed by NetworkAnalyst ( https://www.networkanalyst.ca/ ) based on the KEGG dataset, revealing that the differential genes were involved in STATs and p53 signaling pathways, respectively. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001. ns, non-significant

    Article Snippet: The human lung cancer cell lines A549, HepG2, and PLC5 used in this study were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Activity Assay, Gene Expression, Irradiation, Incubation, Marker, Expressing, Activation Assay, RNA sequencing, Protein-Protein interactions, Two Tailed Test

    Radiotherapy specifically suppresses TP53-wild type tumors. A Flow cytometry based on fluorescent Annexin V staining was used to detect apoptosis in the irradiation (0, 4, and 8 Gy)-treated TP53-wild type A549, HCT116, and TP53null HCT116 cells (5 × 10 5 in a 6-well plate) post 24 h culture. n = 2. B - C qPCR was used to validate the 13 irradiation-mediated genes from RNAseq (Table S3 and Table S4), including the increased MDM2, CYFIP2, STOM, and the decreased MKI67, CENPE, ARGHGAP11A, BRCA1, ASPM, ALAN, TOP2A, FANCI, TOPBP1, and ECT2, in (B) A549 treated with 8 Gy (24 h post-irradiation), C A549 treated with MDM2 inhibitor Nutlin-3a (10 µg/mL for 24 h). D and E qPCR was also used to detect p53-downstream CDKN1A and the selected 13 genes in TP53-wild type and TP53null HCT116 treated with 8 Gy of irradiation (24 h post-irradiation). n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Radiotherapy enhances M1 macrophage immunogenic activity through IFNs induction and stimulation in TP53-wild type tumors

    doi: 10.1007/s00262-026-04300-7

    Figure Lengend Snippet: Radiotherapy specifically suppresses TP53-wild type tumors. A Flow cytometry based on fluorescent Annexin V staining was used to detect apoptosis in the irradiation (0, 4, and 8 Gy)-treated TP53-wild type A549, HCT116, and TP53null HCT116 cells (5 × 10 5 in a 6-well plate) post 24 h culture. n = 2. B - C qPCR was used to validate the 13 irradiation-mediated genes from RNAseq (Table S3 and Table S4), including the increased MDM2, CYFIP2, STOM, and the decreased MKI67, CENPE, ARGHGAP11A, BRCA1, ASPM, ALAN, TOP2A, FANCI, TOPBP1, and ECT2, in (B) A549 treated with 8 Gy (24 h post-irradiation), C A549 treated with MDM2 inhibitor Nutlin-3a (10 µg/mL for 24 h). D and E qPCR was also used to detect p53-downstream CDKN1A and the selected 13 genes in TP53-wild type and TP53null HCT116 treated with 8 Gy of irradiation (24 h post-irradiation). n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The human lung cancer cell lines A549, HepG2, and PLC5 used in this study were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Flow Cytometry, Staining, Irradiation, RNA sequencing, Two Tailed Test

    Radiotherapy induces IFNs in TP53-wild type tumors. A qPCR was used to detect the expression of IFNs in TP53-wild type HepG2, HCT116, TP53-mutant PLC5, and TP53null HCT116 (5 × 10 5 in a 6-well plate) treated with 0, 4, 8 Gy of irradiation (24 h post-irradiation). B The IFNγ-mediated up-regulated genes from RNAseq analysis (Table S2), including PD-L1, ICAM1, BATF, IRF1, SOCS1, HAPLN3, TAP1, PSMB9, and MAFF, were investigated by qPCR in TP53-wild type and TP53null HCT116 (5 × 10 5 in a 6-well plate) treated with 8 Gy of irradiation (24 h post-irradiation). C The cultured medium from the irradiated A549 (0, 4, 8 Gy, post 24 h) was collected to treat parental A549 (5 × 10 5 in a 6-well plate) for 2 h. qPCR was used to measure the selected gene expression. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Cancer Immunology, Immunotherapy : CII

    Article Title: Radiotherapy enhances M1 macrophage immunogenic activity through IFNs induction and stimulation in TP53-wild type tumors

    doi: 10.1007/s00262-026-04300-7

    Figure Lengend Snippet: Radiotherapy induces IFNs in TP53-wild type tumors. A qPCR was used to detect the expression of IFNs in TP53-wild type HepG2, HCT116, TP53-mutant PLC5, and TP53null HCT116 (5 × 10 5 in a 6-well plate) treated with 0, 4, 8 Gy of irradiation (24 h post-irradiation). B The IFNγ-mediated up-regulated genes from RNAseq analysis (Table S2), including PD-L1, ICAM1, BATF, IRF1, SOCS1, HAPLN3, TAP1, PSMB9, and MAFF, were investigated by qPCR in TP53-wild type and TP53null HCT116 (5 × 10 5 in a 6-well plate) treated with 8 Gy of irradiation (24 h post-irradiation). C The cultured medium from the irradiated A549 (0, 4, 8 Gy, post 24 h) was collected to treat parental A549 (5 × 10 5 in a 6-well plate) for 2 h. qPCR was used to measure the selected gene expression. n = 3 and error bars were presented by SD in qPCR analysis. Statistical analysis was achieved by an unpaired two-tailed Student’s t-test. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: The human lung cancer cell lines A549, HepG2, and PLC5 used in this study were purchased from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Expressing, Mutagenesis, Irradiation, RNA sequencing, Cell Culture, Gene Expression, Two Tailed Test

    Ongoing copy number alterations in model systems. A, Schematic of the method used to obtain and sequence single cells from cultured colorectal cancer cell line SW620 and patient-derived organoid (PDO) 3994-1117. Cell line SW620 underwent single-cell dispensing using the cellenONE system, followed by direct library prep (DLP) while the 10× Genomics Chromium was used to prepare single-cell libraries from the patient-derived organoid 3994-1117. B, Heatmap showing CNAs in single cells from colorectal cancer cell line SW620 and ( C ) from patient-derived organoid 3994-1117. Red = gain, blue = loss. D, Phylogenetic tree constructed using CNAs in the colorectal cancer cell line SW620. E, Frequency of copy number gains and losses at the tips of the SW620 phylogenetic tree. F, Phylogenetic tree constructed using CNAs in the colorectal cancer organoid 3994-117. G, Frequency of copy number gains and losses at the tips of the 3994-117 phylogenetic tree (as in E ).

    Journal: Cancer Discovery

    Article Title: Negative Selection Maintains Grossly Altered but Broadly Stable Karyotypes in Metastatic Colorectal Cancer

    doi: 10.1158/2159-8290.CD-24-0813

    Figure Lengend Snippet: Ongoing copy number alterations in model systems. A, Schematic of the method used to obtain and sequence single cells from cultured colorectal cancer cell line SW620 and patient-derived organoid (PDO) 3994-1117. Cell line SW620 underwent single-cell dispensing using the cellenONE system, followed by direct library prep (DLP) while the 10× Genomics Chromium was used to prepare single-cell libraries from the patient-derived organoid 3994-1117. B, Heatmap showing CNAs in single cells from colorectal cancer cell line SW620 and ( C ) from patient-derived organoid 3994-1117. Red = gain, blue = loss. D, Phylogenetic tree constructed using CNAs in the colorectal cancer cell line SW620. E, Frequency of copy number gains and losses at the tips of the SW620 phylogenetic tree. F, Phylogenetic tree constructed using CNAs in the colorectal cancer organoid 3994-117. G, Frequency of copy number gains and losses at the tips of the 3994-117 phylogenetic tree (as in E ).

    Article Snippet: The colorectal cancer cell line SW620 was obtained from the ATCC (CCL-227) and cultured in high-glucose DMEM with 10% FBS and 2% penicillin–streptomycin.

    Techniques: Sequencing, Cell Culture, Derivative Assay, Single Cell, Cellenone, Construct