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human tnbc cell lines hcc38 (ATCC)

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ATCC human tnbc cell lines hcc38
Human Tnbc Cell Lines Hcc38, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 498 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tnbc+cell+line+hcc38/pm38374113-43-0-14?v=ATCC
Average 96 stars, based on 498 article reviews

human tnbc cell lines hcc38 - by Bioz Stars, 2026-08

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A and B show the efficiency of the 18 drugs on eight TNBC cell lines (BT-549, CAL-148, HCC1806, HCC38, HCC70, MDA-MB-436, MDA-MB-453, and MDA-MB-468) and two controls (MCF-10A and MCF-7) using growth rate inhibition (GR 50 ) and area under the curve (AUC). Bortezomib, carfilzomib, cisplatin, delanzomib, docetaxel, epoxomicin, MLN-2238, MLN-9708 and nedaplatin were shown to be potent drugs (GR 50 < 1000 nM and AUC < 0.80). C Scatterplot illustrating cytotoxicity with GR max and GR 50 values. Topoisomerases were shown to be weak inhibitors, while proteasome inhibitors, mitosis inhibitors, and platinum agents had an adverse effect on cell viability. D and E show the cytotoxicity of all 18 drugs at the highest tested dose. The most cytotoxic drugs were celastrol, cisplatin, and nedaplatin, and the most sensitive cell lines to the highest dose were HCC38, HCC70, and MDA-MB-436. F show expression of AR in the 10 cell lines. Cell lines BT-549 (M), CAL-148 (LAR), HCC70 (BL1) and MDA-MB-453 (LAR) were AR-positive. Elevated AR expression was associated with high GR 50 values.

Journal: Cell Death Discovery

Article Title: Repurposing proteasome inhibitors for improved treatment of triple-negative breast cancer

doi: 10.1038/s41420-024-01819-5

Figure Lengend Snippet: A and B show the efficiency of the 18 drugs on eight TNBC cell lines (BT-549, CAL-148, HCC1806, HCC38, HCC70, MDA-MB-436, MDA-MB-453, and MDA-MB-468) and two controls (MCF-10A and MCF-7) using growth rate inhibition (GR 50 ) and area under the curve (AUC). Bortezomib, carfilzomib, cisplatin, delanzomib, docetaxel, epoxomicin, MLN-2238, MLN-9708 and nedaplatin were shown to be potent drugs (GR 50 < 1000 nM and AUC < 0.80). C Scatterplot illustrating cytotoxicity with GR max and GR 50 values. Topoisomerases were shown to be weak inhibitors, while proteasome inhibitors, mitosis inhibitors, and platinum agents had an adverse effect on cell viability. D and E show the cytotoxicity of all 18 drugs at the highest tested dose. The most cytotoxic drugs were celastrol, cisplatin, and nedaplatin, and the most sensitive cell lines to the highest dose were HCC38, HCC70, and MDA-MB-436. F show expression of AR in the 10 cell lines. Cell lines BT-549 (M), CAL-148 (LAR), HCC70 (BL1) and MDA-MB-453 (LAR) were AR-positive. Elevated AR expression was associated with high GR 50 values.

Article Snippet: Eight human TNBC cell lines (BT-549, CAL-148, HCC38, HCC70, HCC1806, MDA-MB-436, MDA-MB-453, and MDA-MB-468) and four control cell lines (BT-474, MCF-7, MCF-10A, and T47D) were purchased from American Type Culture Collection (ATCC) or German Collection of Microorganisms and Cell Cultures GmbH (DSMZ), and authenticated using the Eurofins Genomics Human Cell Line Authentication Service.

Techniques: Inhibition, Expressing

Figure 2. BLBC is sensitive to MLN2238. (A-D) The NGSEA analy sis of MLN2238 in the four subtypes of BRCA; (E) The IC50 values of MLN2238 from the GDSC database; (F) CCK-8 analysis at 24, 48, 72 hours after different concentrations of MLN2238 in HCC38 cells; G. ELISA-BrdU test to determine the cell proliferation ability of HCC38 cells (** P<0.01).

Journal: Cellular and molecular biology (Noisy-le-Grand, France)

Article Title: Inhibitory Effort of MLN2238 on Basal-Like Breast Cancer: An Investigation Based on the Gene Set Enrichment Analysis.

doi: 10.14715/cmb/2023.69.7.23

Figure Lengend Snippet: Figure 2. BLBC is sensitive to MLN2238. (A-D) The NGSEA analy sis of MLN2238 in the four subtypes of BRCA; (E) The IC50 values of MLN2238 from the GDSC database; (F) CCK-8 analysis at 24, 48, 72 hours after different concentrations of MLN2238 in HCC38 cells; G. ELISA-BrdU test to determine the cell proliferation ability of HCC38 cells (** P<0.01).

Article Snippet: TNBC cell line HCC38 (ATCC, USA, CRL-2314D) was cultivated in RPMI-1640 medium (Hyclone, USA, SH30809.01B) complemented by 10% fetal bovine serum (FBS, Hyclone, USA, SH30070.03), and 1% streptomycin-penicillin at 37°C, 5% incubate in CO2 gas phase.

Techniques: CCK-8 Assay, Enzyme-linked Immunosorbent Assay

Figure 4. MLN2238 treatment induces cell cycle arrest in HCC38 cells. (A) Flow cytometry to determine the cell cycle distribution in cells with 0 and 250 nM MLN2238 for 24 h; (B) The proportion of each phase (G2/M, S and G0/G1) of the cell cycle in HCC38 cells with 0 and 250 nM MLN2238 for 24 h; (C-D) Western-blot analysis of p21 and p27 in HCC cells after treatment with 0 and 250 nM of MLN2238 for 24 h. (***P<0.001)

Journal: Cellular and molecular biology (Noisy-le-Grand, France)

Article Title: Inhibitory Effort of MLN2238 on Basal-Like Breast Cancer: An Investigation Based on the Gene Set Enrichment Analysis.

doi: 10.14715/cmb/2023.69.7.23

Figure Lengend Snippet: Figure 4. MLN2238 treatment induces cell cycle arrest in HCC38 cells. (A) Flow cytometry to determine the cell cycle distribution in cells with 0 and 250 nM MLN2238 for 24 h; (B) The proportion of each phase (G2/M, S and G0/G1) of the cell cycle in HCC38 cells with 0 and 250 nM MLN2238 for 24 h; (C-D) Western-blot analysis of p21 and p27 in HCC cells after treatment with 0 and 250 nM of MLN2238 for 24 h. (***P<0.001)

Techniques: Flow Cytometry, Western Blot

Figure 5.MLN2238 inhibits cell proliferation induced by PLK1 ove rexpression. (A) Volcano plot of DEGs related to BLBC; (B) The sur vival heat map of significantly upregulated targets of MLN2238; (C) TCGA database analysis of the relatively differential expression level (log2) of PLK1 in BRCA (P < 0.05); (D) K-M curves comparison between BRCA patients with PLK1 high-expression and PLK1 low- expression (P < 0.05, HR>1); (E) RT-PCR analysis of PLK1 expres sion in siPLK1 and PLK1-ov groups; (F) CCK-8 analysis in siPLK1 and PLK1-ov groups; G. ELISA-BrdU analysis in HCC38 cell with siPLK1, PLK1-ov, siPLK1-MLN2238 and PLK1-ov-MNL2238. (**P<0.01)

Journal: Cellular and molecular biology (Noisy-le-Grand, France)

Article Title: Inhibitory Effort of MLN2238 on Basal-Like Breast Cancer: An Investigation Based on the Gene Set Enrichment Analysis.

doi: 10.14715/cmb/2023.69.7.23

Figure Lengend Snippet: Figure 5.MLN2238 inhibits cell proliferation induced by PLK1 ove rexpression. (A) Volcano plot of DEGs related to BLBC; (B) The sur vival heat map of significantly upregulated targets of MLN2238; (C) TCGA database analysis of the relatively differential expression level (log2) of PLK1 in BRCA (P < 0.05); (D) K-M curves comparison between BRCA patients with PLK1 high-expression and PLK1 low- expression (P < 0.05, HR>1); (E) RT-PCR analysis of PLK1 expres sion in siPLK1 and PLK1-ov groups; (F) CCK-8 analysis in siPLK1 and PLK1-ov groups; G. ELISA-BrdU analysis in HCC38 cell with siPLK1, PLK1-ov, siPLK1-MLN2238 and PLK1-ov-MNL2238. (**P<0.01)

Techniques: Quantitative Proteomics, Comparison, Expressing, Reverse Transcription Polymerase Chain Reaction, CCK-8 Assay, Enzyme-linked Immunosorbent Assay

Journal: International Journal of Molecular Sciences

Article Title: Multi-Level Control of the ATM/ATR-CHK1 Axis by the Transcription Factor E4F1 in Triple-Negative Breast Cancer

doi: 10.3390/ijms23169217

Figure Lengend Snippet: Depletion of the transcription factor E4F1 sensitizes SUM159 Human Triple-Negative Breast Cancer (TNBC) cell line to the chemotherapy drugs Gemcitabine and Cisplatin. ( A )—Depletion of E4F1 in SUM159. Immunoblot analysis of E4F1 protein level in protein extracts prepared from SUM159 cells treated with either a control shRNA (sh Ctrl ) or a shRNA directed against E4F1 (sh E4F1 ), or with a combination of the latter sh E4F1 with an expression vector encoding an E4F1 cDNA resistant to this sh E4F1 (pE4F1*). Extracts were prepared 4 days after cell infection with lentiviral vectors expressing shRNAs. shRNA directed against human E4F1 have been previously validated ; ( B , C )—E4F1-depleted SUM159 cells fail to arrest in S-Phase upon Gemcitabine treatment. Three days after sh Ctrl or sh E4F1 treatment, cells were exposed to sub-lethal dose of Gemcitabine (140 nM, IC30) for 24 h; ( B ) Representative flow cytometry analysis (PI staining) of cell cycle distribution in populations of cells collected at 24 h after start of Gemcitabine treatment. Of note FACScan gating settings were meant to exclude sub-G1 cells; ( C ) Quantitation of the distribution of cells in G2/M, S and G0/G1 cell cycle phases was performed with the FlowJo software. Results are expressed as mean values ± SD of three independent experiments. ** p < 0.01, by a one way ANOVA test performed on GraphPad Prism; ( D – F) —shRNA-mediated depletion of E4F1 sensitizes TNBC SUM159 cells to cytotoxic drugs, an effect rescued by the co-expression of the sh E4F1 -resistant pE4F1* construct (see also on another TNBC cell line, HCC38). Three days after sh Ctrl , sh E4F1 or sh E4F1 + pE4F1* transduction, cells were exposed to sub-lethal doses of Gemcitabine (140 nM, IC30) or Cisplatin (1.5 mM) for 24 h and assessed for cell death by ( D ) Phase contrast microscopy, ( E , F ) Flow cytometry analysis for apoptosis /necrosis by staining dying cells with annexin V/7-AAD and propidium Iodide (PI). ( E ) Representative flow cytometry profile of annexin V/7-AAD/PI –positive cells, and ( F ) quantitation (FlowJo software) of three independent experiments expressed as mean values ± SD of three independent experiments. ** p < 0.01, *** p < 0.001 as determined by a one way ANOVA test performed on GraphPad Prism.

Article Snippet: The HCC38 TNBC cell line (ATCC-CRL-2314) was obtained from American Type Culture Collection and was grown in RPMI medium (Gibco), supplemented with 10% fetal bovine serum, 100 μg/mL streptomycin and 100 units/mL penicillin and treated 24 h with Gemcitabine (IC30, 180 nM; Sandoz), or Cisplatin (950 nM; Sigma Aldrich).

Techniques: Western Blot, Control, shRNA, Expressing, Plasmid Preparation, Infection, Flow Cytometry, Staining, Quantitation Assay, Software, Construct, Transduction, Microscopy

E4F1-depletion impacts on ATM/ATR-CHK1 signaling in response to CT drugs Gemcitabine and Cisplatin. ( A )—ShRNA-mediated depletion of E4F1 in SUM159 TNBC cells impacts on CHK1 protein level and on the S 345 phosphorylation of CHK1 by ATM/ATR in response to Gemcitabine and Cisplatin. This effect was reversed by the co-expression of the shRNA resistant pE4F1* cDNA. Immunoblot analysis of indicated proteins or phosphor-proteins (CHK1 P ) in total extracts prepared from SUM159 cells transduced with either control shRNA (sh Ctrl ), sh E4F1 , or sh E4F1 + pE4F1*, and treated for 24 h with Gemcitabine or Cisplatin. See also immunoblots in showing a similar experiment in another TNBC cell line, HCC38; ( B , C ) Immunofluorescence staining of DNA (blue), phospho (S139)- γH2AX (green) and ATR (red) in SUM159 cells transduced with either sh Ctrl , sh E4F1 , or sh E4F1 + pE4F1*, and upon antibiotics selection, treated for 24 h with Gemcitabine; ( B ) Representative experiment; ( C ) Quantitation of three independent experiments expressed as mean values ± SD. *** p < 0.001 as determined by two-tailed unpaired t -test performed on Graph Pad Prism. See also for immunoblotting analysis of γH2AX phosphorylation in cell lysates.

Journal: International Journal of Molecular Sciences

Article Title: Multi-Level Control of the ATM/ATR-CHK1 Axis by the Transcription Factor E4F1 in Triple-Negative Breast Cancer

doi: 10.3390/ijms23169217

Figure Lengend Snippet: E4F1-depletion impacts on ATM/ATR-CHK1 signaling in response to CT drugs Gemcitabine and Cisplatin. ( A )—ShRNA-mediated depletion of E4F1 in SUM159 TNBC cells impacts on CHK1 protein level and on the S 345 phosphorylation of CHK1 by ATM/ATR in response to Gemcitabine and Cisplatin. This effect was reversed by the co-expression of the shRNA resistant pE4F1* cDNA. Immunoblot analysis of indicated proteins or phosphor-proteins (CHK1 P ) in total extracts prepared from SUM159 cells transduced with either control shRNA (sh Ctrl ), sh E4F1 , or sh E4F1 + pE4F1*, and treated for 24 h with Gemcitabine or Cisplatin. See also immunoblots in showing a similar experiment in another TNBC cell line, HCC38; ( B , C ) Immunofluorescence staining of DNA (blue), phospho (S139)- γH2AX (green) and ATR (red) in SUM159 cells transduced with either sh Ctrl , sh E4F1 , or sh E4F1 + pE4F1*, and upon antibiotics selection, treated for 24 h with Gemcitabine; ( B ) Representative experiment; ( C ) Quantitation of three independent experiments expressed as mean values ± SD. *** p < 0.001 as determined by two-tailed unpaired t -test performed on Graph Pad Prism. See also for immunoblotting analysis of γH2AX phosphorylation in cell lysates.

Techniques: shRNA, Phospho-proteomics, Expressing, Western Blot, Transduction, Control, Immunofluorescence, Staining, Selection, Quantitation Assay, Two Tailed Test

EME1 is a direct target of epigenetically regulated tumor suppressive miR-449a in TNBC cell lines. ( A ) Identification of significantly upregulated miRNAs after TSA treatment for 24 h by intersection using one-way ANOVA followed by Dunnett’s multiple comparison test. p < 0.1; FC ≥ 4. ( B ) Cell viability analyzed by WST-1 assay in TNBC cells transfected with miR-449-mimics normalized to control (Allstars Negative Control) transfected cells. ( C ) Apoptosis analyzed by caspase3/7 activity in TNBC cells transfected with miR-449-mimics normalized to cell viability and the control. Bar graphs show mean ± SD. N = 3, * p < 0.1, ** p < 0.01, *** p < 0.001. ( D ) Expression of EME1 measured by RT-PCR 48 h after transfection with miR-449a-mimics or control. ( E ) Expression of EME1 protein in HCC38 cells using Western blotting. Actin was used as a loading control on the same blot but on a different part of the gel. ( F ) Ago2 immunoprecipitation was performed and the enrichment of EME1 vs input was detected by RT-PCR. ( G ) Firefly luciferase activity measurements in HEK293 cells of miRNA-mimics in relation to renilla luciferase activity. 3′UTR: untranslated region of EME1, 3′UTR-MUT: untranslated region of EME1 with mutations in the predicted target site for miR-449a. Bar graphs show mean ± SD ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test for ( D ), one-way ANOVA/Dunnett’s multiple comparison test for ( B , C ).

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-449a Inhibits Triple Negative Breast Cancer by Disturbing DNA Repair and Chromatid Separation

doi: 10.3390/ijms23095131

Figure Lengend Snippet: EME1 is a direct target of epigenetically regulated tumor suppressive miR-449a in TNBC cell lines. ( A ) Identification of significantly upregulated miRNAs after TSA treatment for 24 h by intersection using one-way ANOVA followed by Dunnett’s multiple comparison test. p < 0.1; FC ≥ 4. ( B ) Cell viability analyzed by WST-1 assay in TNBC cells transfected with miR-449-mimics normalized to control (Allstars Negative Control) transfected cells. ( C ) Apoptosis analyzed by caspase3/7 activity in TNBC cells transfected with miR-449-mimics normalized to cell viability and the control. Bar graphs show mean ± SD. N = 3, * p < 0.1, ** p < 0.01, *** p < 0.001. ( D ) Expression of EME1 measured by RT-PCR 48 h after transfection with miR-449a-mimics or control. ( E ) Expression of EME1 protein in HCC38 cells using Western blotting. Actin was used as a loading control on the same blot but on a different part of the gel. ( F ) Ago2 immunoprecipitation was performed and the enrichment of EME1 vs input was detected by RT-PCR. ( G ) Firefly luciferase activity measurements in HEK293 cells of miRNA-mimics in relation to renilla luciferase activity. 3′UTR: untranslated region of EME1, 3′UTR-MUT: untranslated region of EME1 with mutations in the predicted target site for miR-449a. Bar graphs show mean ± SD ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test for ( D ), one-way ANOVA/Dunnett’s multiple comparison test for ( B , C ).

Article Snippet: Cell culture und transfection: TNBC cell lines HCC38 (RRID:CVCL_1267), HCC1395 (RRID:CVCL_1249), HCC1937 (RRID:CVCL_0290), their corresponding lymphoblastic cell lines HCC38 BL (RRID:CRL_2346) and HCC1937 BL (RRID:CRL_2337), and immortalized normal breast cell line MCF12A (RRID:CVCL_3744) (all obtained from American Type Culture Collection (ATCC), Manassas, VA, USA) were cultured as recommended by ATCC.

Techniques: Comparison, WST-1 Assay, Transfection, Control, Negative Control, Activity Assay, Expressing, Reverse Transcription Polymerase Chain Reaction, Western Blot, Immunoprecipitation, Luciferase

Induction of miR-449a expression and EME1 silencing both increase the frequency of ultrafine bridges, 53BP1 foci, and micronuclei. ( A ) Representative IF images and quantification ( B , C ) of PICH positive ultrafine bridges (green) in HCC38 cells transfected with miRNA mimics or control or with an EME1 siRNA. DNA was stained using DAPI (4′,6-Diamidin-2-phenylindol) (blue). N = 150. ( D ) Representative IF images and quantification ( E , F ) of 53BP1 positive foci (green) in HCC38 cells transfected with miRNA-mimics or control, or with an EME1 siRNA. DNA was stained using DAPI (blue). N = 150 ( G ) Representative images of micronuclei stained using DAPI and quantification ( H , I ). N = 150. Bar graphs show mean ± SEM. Error bars represent SEM. N = 3. ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test. Scale bars = 10 µm.

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-449a Inhibits Triple Negative Breast Cancer by Disturbing DNA Repair and Chromatid Separation

doi: 10.3390/ijms23095131

Figure Lengend Snippet: Induction of miR-449a expression and EME1 silencing both increase the frequency of ultrafine bridges, 53BP1 foci, and micronuclei. ( A ) Representative IF images and quantification ( B , C ) of PICH positive ultrafine bridges (green) in HCC38 cells transfected with miRNA mimics or control or with an EME1 siRNA. DNA was stained using DAPI (4′,6-Diamidin-2-phenylindol) (blue). N = 150. ( D ) Representative IF images and quantification ( E , F ) of 53BP1 positive foci (green) in HCC38 cells transfected with miRNA-mimics or control, or with an EME1 siRNA. DNA was stained using DAPI (blue). N = 150 ( G ) Representative images of micronuclei stained using DAPI and quantification ( H , I ). N = 150. Bar graphs show mean ± SEM. Error bars represent SEM. N = 3. ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test. Scale bars = 10 µm.

Techniques: Expressing, Transfection, Control, Staining

MiR-449a decreases expression of Survivin indirectly by targeting E2F3. ( A ) Expression of E2F3 mRNA measured by RT-PCR 48 h after transfection with miR-449a-mimics or control. ( B ) Expression of E2F3 protein using Western blotting in HCC38 cells. Actin was used as a loading control on the same blot but on a different part of the gel. ( C ) Expression of Survivin mRNA measured by RT-PCR 48 h after transfection with miR-449a-mimics or control on mRNA level. ( D ) Expression of Survivin protein using Western blot in HCC38 cells. Actin was used as a loading control on the same blot but on a different part of the gel. ( E ) Expression of Survivin mRNA measured by RT-PCR 48 h after transfection with siE2F3 or si-control. ( F ) Expression of Survivin protein using Western blot in HCC38 cells after transfection with siE2F3 or si-control. Actin was used as a loading control on the same blot but on a different part of the gel. Error bars represent SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test.

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-449a Inhibits Triple Negative Breast Cancer by Disturbing DNA Repair and Chromatid Separation

doi: 10.3390/ijms23095131

Figure Lengend Snippet: MiR-449a decreases expression of Survivin indirectly by targeting E2F3. ( A ) Expression of E2F3 mRNA measured by RT-PCR 48 h after transfection with miR-449a-mimics or control. ( B ) Expression of E2F3 protein using Western blotting in HCC38 cells. Actin was used as a loading control on the same blot but on a different part of the gel. ( C ) Expression of Survivin mRNA measured by RT-PCR 48 h after transfection with miR-449a-mimics or control on mRNA level. ( D ) Expression of Survivin protein using Western blot in HCC38 cells. Actin was used as a loading control on the same blot but on a different part of the gel. ( E ) Expression of Survivin mRNA measured by RT-PCR 48 h after transfection with siE2F3 or si-control. ( F ) Expression of Survivin protein using Western blot in HCC38 cells after transfection with siE2F3 or si-control. Actin was used as a loading control on the same blot but on a different part of the gel. Error bars represent SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Western Blot

MiR-449a decreases expression of RAD51 and BRCA2 leading to increased yH2AX signals. ( A ) Expression of BRCA2 and RAD51 mRNA measured by RT-PCR 48 h after transfection with miR-449a-mimics/control or with siE2F3/si-control. ( B ) Expression of BRCA2 and RAD51 proteins using Western blotting in HCC38 cells. Actin was used as a loading control on the same blot but on a different part of the gel. ( C ) Representative IF images and quantification ( D ) of yH2AX positive foci (green) after transfection with miR-449a-mimics, siSurvivin or siE2F3 compared to control or si-control respectively. DNA was stained using DAPI (blue). ( E ) Representative IF images and quantification ( F ) of PICH positive ultrafine bridges (green) after transfection with siE2F3 or si-control in HCC38 cells. ( G ) Quantification of 53BP1 positive foci (green) or micronuclei ( H ) stained using DAPI. Error bars represent SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test. Scale bars = 10 µm.

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-449a Inhibits Triple Negative Breast Cancer by Disturbing DNA Repair and Chromatid Separation

doi: 10.3390/ijms23095131

Figure Lengend Snippet: MiR-449a decreases expression of RAD51 and BRCA2 leading to increased yH2AX signals. ( A ) Expression of BRCA2 and RAD51 mRNA measured by RT-PCR 48 h after transfection with miR-449a-mimics/control or with siE2F3/si-control. ( B ) Expression of BRCA2 and RAD51 proteins using Western blotting in HCC38 cells. Actin was used as a loading control on the same blot but on a different part of the gel. ( C ) Representative IF images and quantification ( D ) of yH2AX positive foci (green) after transfection with miR-449a-mimics, siSurvivin or siE2F3 compared to control or si-control respectively. DNA was stained using DAPI (blue). ( E ) Representative IF images and quantification ( F ) of PICH positive ultrafine bridges (green) after transfection with siE2F3 or si-control in HCC38 cells. ( G ) Quantification of 53BP1 positive foci (green) or micronuclei ( H ) stained using DAPI. Error bars represent SEM. N = 3. * p < 0.05, ** p < 0.01, *** p < 0.001, 2-tailed Student’s t -test. Scale bars = 10 µm.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Western Blot, Staining

Induced expression of miR-449a in combination with Olaparib strongly decreased the amount of viable HCC1937 cells with a pathogenic variant in BRCA1. HCC38 ( A ) and HCC1937 ( B ) cells were treated with Olaparib (DMSO as control) and transfected with miR-449a (or control). Apoptosis analyzed by caspase3/7 activity in TNBC cells transfected with miR-449-mimics normalized to cell viability. Bar graphs show mean ± SD * p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant; 2-way Anova with Tukey’s multiple comparisons.

Journal: International Journal of Molecular Sciences

Article Title: MicroRNA-449a Inhibits Triple Negative Breast Cancer by Disturbing DNA Repair and Chromatid Separation

doi: 10.3390/ijms23095131

Figure Lengend Snippet: Induced expression of miR-449a in combination with Olaparib strongly decreased the amount of viable HCC1937 cells with a pathogenic variant in BRCA1. HCC38 ( A ) and HCC1937 ( B ) cells were treated with Olaparib (DMSO as control) and transfected with miR-449a (or control). Apoptosis analyzed by caspase3/7 activity in TNBC cells transfected with miR-449-mimics normalized to cell viability. Bar graphs show mean ± SD * p < 0.05, ** p < 0.01, *** p < 0.001, ns: not significant; 2-way Anova with Tukey’s multiple comparisons.

Techniques: Expressing, Variant Assay, Control, Transfection, Activity Assay

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