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mda231 breast cancer cell line (ATCC)

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ATCC mda231 breast cancer cell line

Migration assays were performed using the Boyden chamber method. After transfection of each siRNA into the (A) A549 and (B) <t>MDA231</t> cells, the cells were incubated for 48 h before the migration assay. The cells that had migrated to the outer side of the membranes within 24 h were fixed and stained. A representative image of a triplicate analysis of each siRNA is shown. Scale bar, 20 µm. siRNA, small interfering RNA; Ctrl, control siRNA; SERF2, small EDRK-rich factor 2; PRKDC, DNA-dependent protein kinase catalytic subunit; S100A6, S100 calcium-binding protein A6; SH3GLB1, SH3-domain GRB2-like endophilin B1; CAPNS1, calpain, small subunit 1; PSMB4, proteasome subunit β type-4; RPL11, ribosomal protein L11; RPS7, ribosomal protein S7.

Mda231 Breast Cancer Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 24617 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mda231 breast cancer cell line - by Bioz Stars, 2026-09

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1) Product Images from "Exploration of genes related to the development of cancer of unknown primary"

Article Title: Exploration of genes related to the development of cancer of unknown primary

Journal: Oncology Reports

doi: 10.3892/or.2025.8905

Migration assays were performed using the Boyden chamber method. After transfection of each siRNA into the (A) A549 and (B) MDA231 cells, the cells were incubated for 48 h before the migration assay. The cells that had migrated to the outer side of the membranes within 24 h were fixed and stained. A representative image of a triplicate analysis of each siRNA is shown. Scale bar, 20 µm. siRNA, small interfering RNA; Ctrl, control siRNA; SERF2, small EDRK-rich factor 2; PRKDC, DNA-dependent protein kinase catalytic subunit; S100A6, S100 calcium-binding protein A6; SH3GLB1, SH3-domain GRB2-like endophilin B1; CAPNS1, calpain, small subunit 1; PSMB4, proteasome subunit β type-4; RPL11, ribosomal protein L11; RPS7, ribosomal protein S7.

Figure Legend Snippet: Migration assays were performed using the Boyden chamber method. After transfection of each siRNA into the (A) A549 and (B) MDA231 cells, the cells were incubated for 48 h before the migration assay. The cells that had migrated to the outer side of the membranes within 24 h were fixed and stained. A representative image of a triplicate analysis of each siRNA is shown. Scale bar, 20 µm. siRNA, small interfering RNA; Ctrl, control siRNA; SERF2, small EDRK-rich factor 2; PRKDC, DNA-dependent protein kinase catalytic subunit; S100A6, S100 calcium-binding protein A6; SH3GLB1, SH3-domain GRB2-like endophilin B1; CAPNS1, calpain, small subunit 1; PSMB4, proteasome subunit β type-4; RPL11, ribosomal protein L11; RPS7, ribosomal protein S7.

Techniques Used: Migration, Transfection, Incubation, Staining, Small Interfering RNA, Control, Binding Assay

Western blotting showing the reduction in protein expression following siRNA-induced knockdown of PRKDC and PSMB4. (Top) Protein expression was reduced after transfection of the cells with siRNA for PRKDC (left) and PSMB4 (right) in both the A549 and MDA231 cells. β-actin was used as the loading control, whereas si-NC was used as the negative control. (Bottom) Relative reductions in PRKDC or PSMB4 protein expression were determined using western blot analysis conducted in triplicate. Data are presented as the mean and standard deviation. *P<0.05; **P<0.01. siRNA/si, small interfering RNA; si-NC, siRNA universal negative control; PRKDC, DNA-dependent protein kinase catalytic subunit; PSMB4, proteasome subunit β type-4.

Figure Legend Snippet: Western blotting showing the reduction in protein expression following siRNA-induced knockdown of PRKDC and PSMB4. (Top) Protein expression was reduced after transfection of the cells with siRNA for PRKDC (left) and PSMB4 (right) in both the A549 and MDA231 cells. β-actin was used as the loading control, whereas si-NC was used as the negative control. (Bottom) Relative reductions in PRKDC or PSMB4 protein expression were determined using western blot analysis conducted in triplicate. Data are presented as the mean and standard deviation. *P<0.05; **P<0.01. siRNA/si, small interfering RNA; si-NC, siRNA universal negative control; PRKDC, DNA-dependent protein kinase catalytic subunit; PSMB4, proteasome subunit β type-4.

Techniques Used: Western Blot, Expressing, Knockdown, Transfection, Control, Negative Control, Standard Deviation, Small Interfering RNA

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Article Title: Extracellular Vesicles Secreted by Cancer‐Associated Fibroblasts Drive Non‐Invasive Cancer Cell Progression to Metastasis via TGF‐β Signalling Hyperactivation
Article Snippet: .. Human MCF7 and MDA‐MB‐231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC). ..

Article Title: Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.
Article Snippet: .. Human MCF7 and MDA-MB-231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC). ..

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Journal: Oncology Reports

Article Title: Exploration of genes related to the development of cancer of unknown primary

doi: 10.3892/or.2025.8905

Figure Lengend Snippet: Migration assays were performed using the Boyden chamber method. After transfection of each siRNA into the (A) A549 and (B) MDA231 cells, the cells were incubated for 48 h before the migration assay. The cells that had migrated to the outer side of the membranes within 24 h were fixed and stained. A representative image of a triplicate analysis of each siRNA is shown. Scale bar, 20 µm. siRNA, small interfering RNA; Ctrl, control siRNA; SERF2, small EDRK-rich factor 2; PRKDC, DNA-dependent protein kinase catalytic subunit; S100A6, S100 calcium-binding protein A6; SH3GLB1, SH3-domain GRB2-like endophilin B1; CAPNS1, calpain, small subunit 1; PSMB4, proteasome subunit β type-4; RPL11, ribosomal protein L11; RPS7, ribosomal protein S7.

Article Snippet: The A549 human lung cancer cell line (cat. no. CCL-185) and the MDA231 breast cancer cell line (cat. no. HTB-26) were procured from American Type Culture Collection, and cultured in DMEM (Thermo Fisher Scientific, Inc.) with 10% FBS (MilliporeSigma) in accordance with the instructions provided by the suppliers.

Techniques: Migration, Transfection, Incubation, Staining, Small Interfering RNA, Control, Binding Assay

Journal: Oncology Reports

Article Title: Exploration of genes related to the development of cancer of unknown primary

doi: 10.3892/or.2025.8905

Figure Lengend Snippet: Western blotting showing the reduction in protein expression following siRNA-induced knockdown of PRKDC and PSMB4. (Top) Protein expression was reduced after transfection of the cells with siRNA for PRKDC (left) and PSMB4 (right) in both the A549 and MDA231 cells. β-actin was used as the loading control, whereas si-NC was used as the negative control. (Bottom) Relative reductions in PRKDC or PSMB4 protein expression were determined using western blot analysis conducted in triplicate. Data are presented as the mean and standard deviation. *P<0.05; **P<0.01. siRNA/si, small interfering RNA; si-NC, siRNA universal negative control; PRKDC, DNA-dependent protein kinase catalytic subunit; PSMB4, proteasome subunit β type-4.

Techniques: Western Blot, Expressing, Knockdown, Transfection, Control, Negative Control, Standard Deviation, Small Interfering RNA

FIGURE 1 CAF-sEVs transport TGF-β signalling components and activate the TGF-β signalling in breast cancer cells in vitro. (a) 19TT- sEV morphology was analysed by cryogenic electron microscopy. (b) TGF-β/SMAD signalling reporter (Ad-CAGA-Gluc) activity was quantified in MDA231 cells treated for 24 h ± 19TT-large EVs (10K pellet), EV-depleted conditioned medium (100K supernatant), or small EVs (100K pellet). Fractions corresponding to 10K pellet and 100K pellet were resuspended in 100 µL serum-free medium (SFM) during isolation and before use in this analysis. Five microliters per well 10K pellet, 100K supernatant, and 100K pellet were used in this analysis. Treatment with rhTGF-β1 was used as positive control. (c) 19TT-sEV protein extracts were tested for the expression of extracellular vesicle markers and TGF-β signalling components by western blot. Whole cell lysates (WCL) were used as positive control. Twenty micrograms of protein extracts were loaded to each lane. (d) Nanoparticle tracking analysis (NTA) was used to determine the particle size distribution of sEVs secreted by 19TT CAFs treated ± 5 ng/mL rhTGF-β1 for 2 h. (e) Luciferase assay was used to quantify the TGF-β/SMAD signalling reporter (Ad-CAGA-Gluc) activity in MDA231 cells as in (b). Cells were treated ± 19TT-sEVs (1 µg/well total protein) isolated from 19TT cells treated ± 5 ng/mL rhTGF-β1 for 2 h. Results represent mean ± SD of at least three independent experiments (n = 3). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data in (b & e). ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: Journal of extracellular vesicles

Article Title: Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.

doi: 10.1002/jev2.70055

Figure Lengend Snippet: FIGURE 1 CAF-sEVs transport TGF-β signalling components and activate the TGF-β signalling in breast cancer cells in vitro. (a) 19TT- sEV morphology was analysed by cryogenic electron microscopy. (b) TGF-β/SMAD signalling reporter (Ad-CAGA-Gluc) activity was quantified in MDA231 cells treated for 24 h ± 19TT-large EVs (10K pellet), EV-depleted conditioned medium (100K supernatant), or small EVs (100K pellet). Fractions corresponding to 10K pellet and 100K pellet were resuspended in 100 µL serum-free medium (SFM) during isolation and before use in this analysis. Five microliters per well 10K pellet, 100K supernatant, and 100K pellet were used in this analysis. Treatment with rhTGF-β1 was used as positive control. (c) 19TT-sEV protein extracts were tested for the expression of extracellular vesicle markers and TGF-β signalling components by western blot. Whole cell lysates (WCL) were used as positive control. Twenty micrograms of protein extracts were loaded to each lane. (d) Nanoparticle tracking analysis (NTA) was used to determine the particle size distribution of sEVs secreted by 19TT CAFs treated ± 5 ng/mL rhTGF-β1 for 2 h. (e) Luciferase assay was used to quantify the TGF-β/SMAD signalling reporter (Ad-CAGA-Gluc) activity in MDA231 cells as in (b). Cells were treated ± 19TT-sEVs (1 µg/well total protein) isolated from 19TT cells treated ± 5 ng/mL rhTGF-β1 for 2 h. Results represent mean ± SD of at least three independent experiments (n = 3). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data in (b & e). ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: Human MCF7 and MDA-MB-231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC).

Techniques: In Vitro, Electron Microscopy, Activity Assay, Isolation, Positive Control, Expressing, Western Blot, Luciferase, Comparison

FIGURE 2 CAF-sEVs hyperactivate TGF-β signalling in breast cancer cells in vitro. (a) TGF/SMAD3 signalling reporter (Ad-CAGA- Fluc) activity was quantified in MDA231 cells treated with recombinant human (rh)TGF-β1 or 19TT-sEVs at increasing concentrations for 24 h. (b) Phosphorylated (p)SMAD2 levels analysed in MDA231 cells treated for 1 h. (c) TGF/SMAD3 signalling reporter (Ad-CAGA-Fluc) activity was quantified in MCF7 cells treated with rhTGF-β1 or 19TT-sEVs at increasing concentrations for 24 h. (d) pSMAD2 levels analysed in MCF7 cells treated for 1 h. (e–f) TGF/SMAD3 signalling reporter (Ad-CAGA-Fluc) activity was quantified in (e) MDA231 and (f) MCF7 cells infected with Ad-CMV-GFP (control adenovirus) or Ad-CMV-Flag-SMAD7 treated for 24 h. (g, h) TGF/SMAD3 signalling reporter (Ad-CAGA-Fluc) activity was quantified in (g) MDA231 or (h) MCF7 cells challenged with SB431542 and treated with rhTGF-β1 or 19TT-sEVs for 24 h. (i, j) pSMAD2 levels in (i) MDA231 and (j) MCF7 challenged with SB431542 and treated with rhTGF-β1 or 19TT-sEVs for 1 h. DMSO was used as a vehicle for SB431542. The concentration of 19TT-sEVs used to treat breast cancer cells in (b) and (d–j) was equivalent to 5 ng/mL TGF-β activity. Results represent mean ± SD (n ≥3). Unpaired Student’s t-test was used to analyse data in (a & c). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data in (e–h). ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: Journal of extracellular vesicles

Article Title: Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.

doi: 10.1002/jev2.70055

Figure Lengend Snippet: FIGURE 2 CAF-sEVs hyperactivate TGF-β signalling in breast cancer cells in vitro. (a) TGF/SMAD3 signalling reporter (Ad-CAGA- Fluc) activity was quantified in MDA231 cells treated with recombinant human (rh)TGF-β1 or 19TT-sEVs at increasing concentrations for 24 h. (b) Phosphorylated (p)SMAD2 levels analysed in MDA231 cells treated for 1 h. (c) TGF/SMAD3 signalling reporter (Ad-CAGA-Fluc) activity was quantified in MCF7 cells treated with rhTGF-β1 or 19TT-sEVs at increasing concentrations for 24 h. (d) pSMAD2 levels analysed in MCF7 cells treated for 1 h. (e–f) TGF/SMAD3 signalling reporter (Ad-CAGA-Fluc) activity was quantified in (e) MDA231 and (f) MCF7 cells infected with Ad-CMV-GFP (control adenovirus) or Ad-CMV-Flag-SMAD7 treated for 24 h. (g, h) TGF/SMAD3 signalling reporter (Ad-CAGA-Fluc) activity was quantified in (g) MDA231 or (h) MCF7 cells challenged with SB431542 and treated with rhTGF-β1 or 19TT-sEVs for 24 h. (i, j) pSMAD2 levels in (i) MDA231 and (j) MCF7 challenged with SB431542 and treated with rhTGF-β1 or 19TT-sEVs for 1 h. DMSO was used as a vehicle for SB431542. The concentration of 19TT-sEVs used to treat breast cancer cells in (b) and (d–j) was equivalent to 5 ng/mL TGF-β activity. Results represent mean ± SD (n ≥3). Unpaired Student’s t-test was used to analyse data in (a & c). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data in (e–h). ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: Human MCF7 and MDA-MB-231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC).

Techniques: In Vitro, Activity Assay, Recombinant, Infection, Control, Concentration Assay, Comparison

FIGURE 3 Heparin and PNP-Xyl treatment inhibit TGF-β signalling activity induced by CAF-sEVs in breast cancer cells in vitro. (a–c) Effects caused by Heparin on cells treated with 1 ng/mL recombinant human (rh)TGF-β1 or 19TT-sEVs. (a) Phosphorylated (p)SMAD2 levels in MDA231 cells treated for 1 h. TGF-β/SMAD signalling reporter (Ad-CAGA-Fluc) activity in (b) MDA231 or (c) MCF7 cells treated for 24 h. (d-f) Effects caused by PNP-Xyl on cells treated with 1 ng/mL rhTGF-β1 or 19TT-sEVs. (d) pSMAD2 levels in MDA231 cells treated for 1 h. TGF-β/SMAD signalling reporter (Ad- CAGA-Fluc) activity in (e) MDA231 or (f) MCF7 cells treated for 24 h. The concentration of 19TT-sEVs used to treat breast cancer cells was equivalent to 1 ng/mL TGF-β activity. Results represent mean ± SD (n = 3). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data. ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: Journal of extracellular vesicles

Article Title: Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.

doi: 10.1002/jev2.70055

Figure Lengend Snippet: FIGURE 3 Heparin and PNP-Xyl treatment inhibit TGF-β signalling activity induced by CAF-sEVs in breast cancer cells in vitro. (a–c) Effects caused by Heparin on cells treated with 1 ng/mL recombinant human (rh)TGF-β1 or 19TT-sEVs. (a) Phosphorylated (p)SMAD2 levels in MDA231 cells treated for 1 h. TGF-β/SMAD signalling reporter (Ad-CAGA-Fluc) activity in (b) MDA231 or (c) MCF7 cells treated for 24 h. (d-f) Effects caused by PNP-Xyl on cells treated with 1 ng/mL rhTGF-β1 or 19TT-sEVs. (d) pSMAD2 levels in MDA231 cells treated for 1 h. TGF-β/SMAD signalling reporter (Ad- CAGA-Fluc) activity in (e) MDA231 or (f) MCF7 cells treated for 24 h. The concentration of 19TT-sEVs used to treat breast cancer cells was equivalent to 1 ng/mL TGF-β activity. Results represent mean ± SD (n = 3). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data. ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: Human MCF7 and MDA-MB-231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC).

Techniques: Activity Assay, In Vitro, Recombinant, Concentration Assay, Comparison

FIGURE 4 CAF-sEVs rely on TGF-β signalling activation to induce breast cancer cell aggressiveness in vitro. (a) MCF7 cell morphology analysed by bright field microscopy in cells treated with recombinant human (rh)TGF-β1 or 19TT-sEvs over 5 days. (20× magnification). Cell cultures were treated thrice (0, 48, and 96 h). Images obtained in cell cultures fixed and permeabilized. (b) E-cadherin and ZO-1 localization in MCF7 cells treated as in (a). (c) E-cadherin and ZO-1 expression in MCF7 cells treated as in (a). (d) MDA231 cell invasion in transwell inserts. (e–f) Wound healing assay for MDA231 cells challenged with (e) SMAD7 overexpression or (f) Heparin treatment. Ad-CMV-GFP: control adenovirus. The concentration of 19TT- sEVs used to treat breast cancer cells was equivalent to 5 ng/mL TGF-β activity. Results represent mean ± SD (n = 3). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data. ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: Journal of extracellular vesicles

Article Title: Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.

doi: 10.1002/jev2.70055

Figure Lengend Snippet: FIGURE 4 CAF-sEVs rely on TGF-β signalling activation to induce breast cancer cell aggressiveness in vitro. (a) MCF7 cell morphology analysed by bright field microscopy in cells treated with recombinant human (rh)TGF-β1 or 19TT-sEvs over 5 days. (20× magnification). Cell cultures were treated thrice (0, 48, and 96 h). Images obtained in cell cultures fixed and permeabilized. (b) E-cadherin and ZO-1 localization in MCF7 cells treated as in (a). (c) E-cadherin and ZO-1 expression in MCF7 cells treated as in (a). (d) MDA231 cell invasion in transwell inserts. (e–f) Wound healing assay for MDA231 cells challenged with (e) SMAD7 overexpression or (f) Heparin treatment. Ad-CMV-GFP: control adenovirus. The concentration of 19TT- sEVs used to treat breast cancer cells was equivalent to 5 ng/mL TGF-β activity. Results represent mean ± SD (n = 3). One-way ANOVA test followed by Dunn’s Multiple Comparison test were used to analyse data. ns: statistically non-significant, *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: Human MCF7 and MDA-MB-231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC).

Techniques: Activation Assay, In Vitro, Microscopy, Recombinant, Expressing, Wound Healing Assay, Over Expression, Control, Concentration Assay, Activity Assay, Comparison

FIGURE 7 CAF-sEVs enhance TGF-β signalling activity in MDA231 cells in vivo and increase CTCs, metastasis, and tumour self-seeding. (a) Schematic illustration and timeline for NOD-SCID mice implanted with unlabelled MDA231 and Gaussia luciferase-labelled MDA231 (MDA.Gluc) cells and treated ±19TT-sEVs. (b, c) Quantification of TGF-β/SMAD signalling reporter (Ad-CAGA-Fluc) activity in MDA.Gluc tumours by In Vivo Imaging System (n = 3 mice). (d–g) Gaussia luciferase activity in (d) blood, (e) lung, (f) bone, and (g) unlabelled MDA231 tumour samples (n = 5 mice). Animals are color-coded. Black dashed lines indicate the background activity for the Gaussia luciferase quantified in samples from non-implanted mice (n = 2 mice). Results represent mean ± SEM. Unpaired Student’s t-test (c), One-Way ANOVA followed by Tukey’s Multiple Comparison Test (d–g), *p < 0.05, **p<0.01, ***p<0.001, ns: statistically non-significant.

Journal: Journal of extracellular vesicles

Article Title: Extracellular Vesicles Secreted by Cancer-Associated Fibroblasts Drive Non-Invasive Cancer Cell Progression to Metastasis via TGF-β Signalling Hyperactivation.

doi: 10.1002/jev2.70055

Figure Lengend Snippet: FIGURE 7 CAF-sEVs enhance TGF-β signalling activity in MDA231 cells in vivo and increase CTCs, metastasis, and tumour self-seeding. (a) Schematic illustration and timeline for NOD-SCID mice implanted with unlabelled MDA231 and Gaussia luciferase-labelled MDA231 (MDA.Gluc) cells and treated ±19TT-sEVs. (b, c) Quantification of TGF-β/SMAD signalling reporter (Ad-CAGA-Fluc) activity in MDA.Gluc tumours by In Vivo Imaging System (n = 3 mice). (d–g) Gaussia luciferase activity in (d) blood, (e) lung, (f) bone, and (g) unlabelled MDA231 tumour samples (n = 5 mice). Animals are color-coded. Black dashed lines indicate the background activity for the Gaussia luciferase quantified in samples from non-implanted mice (n = 2 mice). Results represent mean ± SEM. Unpaired Student’s t-test (c), One-Way ANOVA followed by Tukey’s Multiple Comparison Test (d–g), *p < 0.05, **p<0.01, ***p<0.001, ns: statistically non-significant.

Article Snippet: Human MCF7 and MDA-MB-231 (MDA231) breast cancer cell lines were purchased from American Type Culture Collection (ATCC).

Techniques: Activity Assay, In Vivo, Luciferase, In Vivo Imaging, Comparison

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mda231 breast cancer cell line (ATCC)

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