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human breast cancer cell lines bt20 (ATCC)

Name: human breast cancer cell lines bt20
Brand: ATCC
Rating: 86 (1 reviews)

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ATCC human breast cancer cell lines bt20

VGLL1 expression drives tumor cell proliferation and invasion. (A) Western blot analysis to assess VGLL1 protein expression in the cell lines PANC1, PANC10.05, Bewo, and PANC1 cells transduced to express either hVGLL1-MYC or empty vector (EV). (B) RT-qPCR analysis of VGLL1 mRNA expression in siScramble- (black) or siVGLL1- (red) treated cells after 48h. (C) RT-qPCR analysis of VGLL1 mRNA expression after retroviral transduction of PANC1 cells with hVGLL1-MYC MG-neo plasmid (blue) or empty MG-neo vector (black). (D, E) Cell proliferation analysis of siScramble- (black) or siVGLL1-treated PANC10.05, <t>BT20,</t> and Bewo cells (red), and PANC1 cells transduced with empty MG-neo vector (black) or hVGLL1-MYC MG-neo plasmid (blue). (F, G) Cell invasion assay results comparing siScramble (black) or siVGLL1-treated PANC10.05, BT20, and Bewo cells (red), and PANC1 cells transduced with empty MG-neo vector (black) or VGLL1-MYC MG-neo plasmid (blue). The indicated cells were plated onto the top of a transwell chamber and after 24 hr incubation, migrated invading cells were stained. Images were taken and quantified using ImageJ, with representative images displayed. *p<0.05, **p<0.01.

Human Breast Cancer Cell Lines Bt20, supplied by ATCC, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes"

Article Title: Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2024.1403052

Figure Legend Snippet: VGLL1 expression drives tumor cell proliferation and invasion. (A) Western blot analysis to assess VGLL1 protein expression in the cell lines PANC1, PANC10.05, Bewo, and PANC1 cells transduced to express either hVGLL1-MYC or empty vector (EV). (B) RT-qPCR analysis of VGLL1 mRNA expression in siScramble- (black) or siVGLL1- (red) treated cells after 48h. (C) RT-qPCR analysis of VGLL1 mRNA expression after retroviral transduction of PANC1 cells with hVGLL1-MYC MG-neo plasmid (blue) or empty MG-neo vector (black). (D, E) Cell proliferation analysis of siScramble- (black) or siVGLL1-treated PANC10.05, BT20, and Bewo cells (red), and PANC1 cells transduced with empty MG-neo vector (black) or hVGLL1-MYC MG-neo plasmid (blue). (F, G) Cell invasion assay results comparing siScramble (black) or siVGLL1-treated PANC10.05, BT20, and Bewo cells (red), and PANC1 cells transduced with empty MG-neo vector (black) or VGLL1-MYC MG-neo plasmid (blue). The indicated cells were plated onto the top of a transwell chamber and after 24 hr incubation, migrated invading cells were stained. Images were taken and quantified using ImageJ, with representative images displayed. *p<0.05, **p<0.01.

Techniques Used: Expressing, Western Blot, Plasmid Preparation, Quantitative RT-PCR, Retroviral, Transduction, Invasion Assay, Incubation, Staining

VGLL1 interacts with common and distinct transcription factors to regulate transcription in tumor cells. (A) Western blot analysis showing relative VGLL1 protein expression either in cell lysates or immunoprecipitated from PANC10.05 and Bewo cells expressing endogenous VGLL1, or PANC1 cells transduced with empty vector (EV) or hVGLL1-MYC plasmid (VGLL1-MYC). Samples without VGLL1 Ab (Beads no Ab) confirmed the specificity of the anti-VGLL1 Ab for IP applications. (B) VGLL1 ChIP-seq analysis was performed on native PANC10.05, BT20, and Bewo tumor cell lines. Homor Motif analysis of the VGLL1 chromatin binding regions revealed several transcription factors (TFs) likely to interact with VGLL1. The Venn diagram shows the common VGLL1 TFs between PANC10.05 (red), BT20 (green) and Bewo (blue) tumor cells. (C–E) ChIP-Atlas was used to compare our results with previously published ChIP-seq data. Each dot represents a different sample (cell line, tissue, etc.) used as a source to pull down individual TFs. Higher enrichment scores indicate higher similarity to the VGLL1 ChIP-seq results. Some samples demonstrated overlap in more than one tumor cell type (black) and others overlapped only with individual tumor cell lines PANC10.05 (red), BT20 (green), Bewo (blue). (F) Table of TFs that were identified in all three tumor cell types. The table contains the TF name and analyzed sample tissue, chromatin motif sequence recognized, percentage of overlapping targets compared to background and p-value. The same color scheme as above indicates the different tumor cell lines analyzed.

Figure Legend Snippet: VGLL1 interacts with common and distinct transcription factors to regulate transcription in tumor cells. (A) Western blot analysis showing relative VGLL1 protein expression either in cell lysates or immunoprecipitated from PANC10.05 and Bewo cells expressing endogenous VGLL1, or PANC1 cells transduced with empty vector (EV) or hVGLL1-MYC plasmid (VGLL1-MYC). Samples without VGLL1 Ab (Beads no Ab) confirmed the specificity of the anti-VGLL1 Ab for IP applications. (B) VGLL1 ChIP-seq analysis was performed on native PANC10.05, BT20, and Bewo tumor cell lines. Homor Motif analysis of the VGLL1 chromatin binding regions revealed several transcription factors (TFs) likely to interact with VGLL1. The Venn diagram shows the common VGLL1 TFs between PANC10.05 (red), BT20 (green) and Bewo (blue) tumor cells. (C–E) ChIP-Atlas was used to compare our results with previously published ChIP-seq data. Each dot represents a different sample (cell line, tissue, etc.) used as a source to pull down individual TFs. Higher enrichment scores indicate higher similarity to the VGLL1 ChIP-seq results. Some samples demonstrated overlap in more than one tumor cell type (black) and others overlapped only with individual tumor cell lines PANC10.05 (red), BT20 (green), Bewo (blue). (F) Table of TFs that were identified in all three tumor cell types. The table contains the TF name and analyzed sample tissue, chromatin motif sequence recognized, percentage of overlapping targets compared to background and p-value. The same color scheme as above indicates the different tumor cell lines analyzed.

Techniques Used: Western Blot, Expressing, Immunoprecipitation, Transduction, Plasmid Preparation, ChIP-sequencing, Binding Assay, Sequencing

VGLL1 regulates transcription of common and unique genes in different tumor cell types. (A) A representative image of the ChIP-seq chromatin peaks detected for all tumor line samples comparing immunoprecipitated VGLL1 (VGLL1 IP) to input cell lysate. (B) Venn diagram shows the number of merged peaks detected and overlap between the 3 cell lines PANC10.05 (red), BT20 (green) and Bewo (blue). (C) Comparison of merged peak regions showing common and unique VGLL1 binding clusters for each tumor cell line. (D) RNA-seq analysis was performed on the indicated tumor cell lines treated with either siVGLL1 or siScramble. Changes in transcript expression for genes associated with VGLL1-binding regions identified in the merged peaks analysis are shown as Volcano plots for each tumor cell line, illustrating genes upregulated (orange) or downregulated (purple) by VGLL1 expression. (E) Representative images of the ChIP-seq chromatin peaks for each tumor cell line are shown for TRIM6-TRIM34, a read-through transcript upregulated by VGLL1 expression (top), NCOA2, a gene whose expression was upregulated by VGLL1 expression (bottom). Green boxes highlight examples of merged peaks present in all 3 tumor cell types and blue boxes indicate peaks not present in all cell lines. (F) GO-enrichment analysis was performed on VGLL1 ChIP-seq target genes modulated in response to VGLL1 knockdown. Upregulated pathways are shown in orange and downregulated pathways are in purple. .

Figure Legend Snippet: VGLL1 regulates transcription of common and unique genes in different tumor cell types. (A) A representative image of the ChIP-seq chromatin peaks detected for all tumor line samples comparing immunoprecipitated VGLL1 (VGLL1 IP) to input cell lysate. (B) Venn diagram shows the number of merged peaks detected and overlap between the 3 cell lines PANC10.05 (red), BT20 (green) and Bewo (blue). (C) Comparison of merged peak regions showing common and unique VGLL1 binding clusters for each tumor cell line. (D) RNA-seq analysis was performed on the indicated tumor cell lines treated with either siVGLL1 or siScramble. Changes in transcript expression for genes associated with VGLL1-binding regions identified in the merged peaks analysis are shown as Volcano plots for each tumor cell line, illustrating genes upregulated (orange) or downregulated (purple) by VGLL1 expression. (E) Representative images of the ChIP-seq chromatin peaks for each tumor cell line are shown for TRIM6-TRIM34, a read-through transcript upregulated by VGLL1 expression (top), NCOA2, a gene whose expression was upregulated by VGLL1 expression (bottom). Green boxes highlight examples of merged peaks present in all 3 tumor cell types and blue boxes indicate peaks not present in all cell lines. (F) GO-enrichment analysis was performed on VGLL1 ChIP-seq target genes modulated in response to VGLL1 knockdown. Upregulated pathways are shown in orange and downregulated pathways are in purple. .

Techniques Used: ChIP-sequencing, Immunoprecipitation, Comparison, Binding Assay, RNA Sequencing Assay, Expressing, Knockdown

VGLL1 expression regulates transcription of genes involved in cellular proliferation and invasion. (A) Global heatmap showing all differentially expressed genes (DEGs) identified from RNAseq analysis of PANC10.05, BT20, and Bewo cells following treatment with either siScramble or siVGLL1. (B) Heatmap showing the top 20 upregulated or downregulated genes in response to VGLL1 knockdown that were common to all three tumor cell lines analyzed. (C) Volcano plots of DEGs identified in each tumor cell line. (D) Results of GO-pathway analysis using the DEGs identified for each tumor cell line. Upregulated genes and pathways are shown in orange and downregulated genes and pathways are indicated in purple.

Figure Legend Snippet: VGLL1 expression regulates transcription of genes involved in cellular proliferation and invasion. (A) Global heatmap showing all differentially expressed genes (DEGs) identified from RNAseq analysis of PANC10.05, BT20, and Bewo cells following treatment with either siScramble or siVGLL1. (B) Heatmap showing the top 20 upregulated or downregulated genes in response to VGLL1 knockdown that were common to all three tumor cell lines analyzed. (C) Volcano plots of DEGs identified in each tumor cell line. (D) Results of GO-pathway analysis using the DEGs identified for each tumor cell line. Upregulated genes and pathways are shown in orange and downregulated genes and pathways are indicated in purple.

Techniques Used: Expressing, Knockdown

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Journal: Frontiers in Oncology

Article Title: Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes

doi: 10.3389/fonc.2024.1403052

Figure Lengend Snippet: VGLL1 expression drives tumor cell proliferation and invasion. (A) Western blot analysis to assess VGLL1 protein expression in the cell lines PANC1, PANC10.05, Bewo, and PANC1 cells transduced to express either hVGLL1-MYC or empty vector (EV). (B) RT-qPCR analysis of VGLL1 mRNA expression in siScramble- (black) or siVGLL1- (red) treated cells after 48h. (C) RT-qPCR analysis of VGLL1 mRNA expression after retroviral transduction of PANC1 cells with hVGLL1-MYC MG-neo plasmid (blue) or empty MG-neo vector (black). (D, E) Cell proliferation analysis of siScramble- (black) or siVGLL1-treated PANC10.05, BT20, and Bewo cells (red), and PANC1 cells transduced with empty MG-neo vector (black) or hVGLL1-MYC MG-neo plasmid (blue). (F, G) Cell invasion assay results comparing siScramble (black) or siVGLL1-treated PANC10.05, BT20, and Bewo cells (red), and PANC1 cells transduced with empty MG-neo vector (black) or VGLL1-MYC MG-neo plasmid (blue). The indicated cells were plated onto the top of a transwell chamber and after 24 hr incubation, migrated invading cells were stained. Images were taken and quantified using ImageJ, with representative images displayed. *p<0.05, **p<0.01.

Article Snippet: Human pancreatic cell lines PANC1 (cat#CRL-1469, RRID: CVCL_0480), PANC10.05 (RRID: CVCL_1639, cat#CRL-2547), Capan1 (RRID: CVCL_0237, cat#HTB-79), Capan2 (RRID: CVCL_0026, cat#HTB-80), SU8686 (RRID: CVCL_3881, cat#CRL-1837) and human breast cancer cell lines BT20 (RRID: CVCL_0178, cat#HTB-19), MDA-MB-468 (RRID: CVCL_0419, cat#HTB-25), MDA-MB-175-VII (RRID: CVCL_1400, cat#HTB-132), and human choriocarcinoma cells, Bewo (RRID: CVCL_0044, cat#CCL-98), were obtained from ATCC and tested negative for mycoplasma contamination.

Techniques: Expressing, Western Blot, Plasmid Preparation, Quantitative RT-PCR, Retroviral, Transduction, Invasion Assay, Incubation, Staining

Journal: Frontiers in Oncology

Article Title: Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes

doi: 10.3389/fonc.2024.1403052

Figure Lengend Snippet: VGLL1 interacts with common and distinct transcription factors to regulate transcription in tumor cells. (A) Western blot analysis showing relative VGLL1 protein expression either in cell lysates or immunoprecipitated from PANC10.05 and Bewo cells expressing endogenous VGLL1, or PANC1 cells transduced with empty vector (EV) or hVGLL1-MYC plasmid (VGLL1-MYC). Samples without VGLL1 Ab (Beads no Ab) confirmed the specificity of the anti-VGLL1 Ab for IP applications. (B) VGLL1 ChIP-seq analysis was performed on native PANC10.05, BT20, and Bewo tumor cell lines. Homor Motif analysis of the VGLL1 chromatin binding regions revealed several transcription factors (TFs) likely to interact with VGLL1. The Venn diagram shows the common VGLL1 TFs between PANC10.05 (red), BT20 (green) and Bewo (blue) tumor cells. (C–E) ChIP-Atlas was used to compare our results with previously published ChIP-seq data. Each dot represents a different sample (cell line, tissue, etc.) used as a source to pull down individual TFs. Higher enrichment scores indicate higher similarity to the VGLL1 ChIP-seq results. Some samples demonstrated overlap in more than one tumor cell type (black) and others overlapped only with individual tumor cell lines PANC10.05 (red), BT20 (green), Bewo (blue). (F) Table of TFs that were identified in all three tumor cell types. The table contains the TF name and analyzed sample tissue, chromatin motif sequence recognized, percentage of overlapping targets compared to background and p-value. The same color scheme as above indicates the different tumor cell lines analyzed.

Techniques: Western Blot, Expressing, Immunoprecipitation, Transduction, Plasmid Preparation, ChIP-sequencing, Binding Assay, Sequencing

Journal: Frontiers in Oncology

Article Title: Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes

doi: 10.3389/fonc.2024.1403052

Figure Lengend Snippet: VGLL1 regulates transcription of common and unique genes in different tumor cell types. (A) A representative image of the ChIP-seq chromatin peaks detected for all tumor line samples comparing immunoprecipitated VGLL1 (VGLL1 IP) to input cell lysate. (B) Venn diagram shows the number of merged peaks detected and overlap between the 3 cell lines PANC10.05 (red), BT20 (green) and Bewo (blue). (C) Comparison of merged peak regions showing common and unique VGLL1 binding clusters for each tumor cell line. (D) RNA-seq analysis was performed on the indicated tumor cell lines treated with either siVGLL1 or siScramble. Changes in transcript expression for genes associated with VGLL1-binding regions identified in the merged peaks analysis are shown as Volcano plots for each tumor cell line, illustrating genes upregulated (orange) or downregulated (purple) by VGLL1 expression. (E) Representative images of the ChIP-seq chromatin peaks for each tumor cell line are shown for TRIM6-TRIM34, a read-through transcript upregulated by VGLL1 expression (top), NCOA2, a gene whose expression was upregulated by VGLL1 expression (bottom). Green boxes highlight examples of merged peaks present in all 3 tumor cell types and blue boxes indicate peaks not present in all cell lines. (F) GO-enrichment analysis was performed on VGLL1 ChIP-seq target genes modulated in response to VGLL1 knockdown. Upregulated pathways are shown in orange and downregulated pathways are in purple. .

Techniques: ChIP-sequencing, Immunoprecipitation, Comparison, Binding Assay, RNA Sequencing Assay, Expressing, Knockdown

Journal: Frontiers in Oncology

Article Title: Placental co-transcriptional activator Vestigial-like 1 (VGLL1) drives tumorigenesis via increasing transcription of proliferation and invasion genes

doi: 10.3389/fonc.2024.1403052

Figure Lengend Snippet: VGLL1 expression regulates transcription of genes involved in cellular proliferation and invasion. (A) Global heatmap showing all differentially expressed genes (DEGs) identified from RNAseq analysis of PANC10.05, BT20, and Bewo cells following treatment with either siScramble or siVGLL1. (B) Heatmap showing the top 20 upregulated or downregulated genes in response to VGLL1 knockdown that were common to all three tumor cell lines analyzed. (C) Volcano plots of DEGs identified in each tumor cell line. (D) Results of GO-pathway analysis using the DEGs identified for each tumor cell line. Upregulated genes and pathways are shown in orange and downregulated genes and pathways are indicated in purple.

Techniques: Expressing, Knockdown

A and B: Effects of WA on MDA-MB-231 (a) and BT20 (b) cell apoptosis as measured by Annexin V-FITC-propidium iodide flow cytometry. Cells were treated with indicated concentrations of WA for 24 h. Results were presented as mean ( n = 3) SD. ∗, P < 0.05, significantly different from control by one-way ANOVA. (C) Western analysis of the expression of PARP and caspase-3 in MDA-MB-231 and BT20 cells. Cells were treated with indicated concentrations of WA for 24 h. Western for β -actin was conducted to confirm equal loading of proteins.

Journal: ISRN Biochemistry

Article Title: Withaferin A Induces Proteasome-Dependent Degradation of Breast Cancer Susceptibility Gene 1 and Heat Shock Factor 1 Proteins in Breast Cancer Cells

doi: 10.5402/2012/707586

Figure Lengend Snippet: A and B: Effects of WA on MDA-MB-231 (a) and BT20 (b) cell apoptosis as measured by Annexin V-FITC-propidium iodide flow cytometry. Cells were treated with indicated concentrations of WA for 24 h. Results were presented as mean ( n = 3) SD. ∗, P < 0.05, significantly different from control by one-way ANOVA. (C) Western analysis of the expression of PARP and caspase-3 in MDA-MB-231 and BT20 cells. Cells were treated with indicated concentrations of WA for 24 h. Western for β -actin was conducted to confirm equal loading of proteins.

Article Snippet: Triple negative MDA-MB-231 and BT20 human breast cancer cell lines were purchased from the American Type Culture Collection (ATCC; Manassas, VA) and cultured in DMEM containing 5% fetal bovine serum (FBS), 100 units/Ml penicillin, 100 μ g/mL streptomycin, and 2 mM glutamine.

Techniques: Flow Cytometry, Western Blot, Expressing

A. Western analysis of the expression of HSF1 and BRCA1 proteins in MDA-MB-231 and BT20 cells. Cells were treated with indicated concentrations of WA for 24 h.

Journal: ISRN Biochemistry

Article Title: Withaferin A Induces Proteasome-Dependent Degradation of Breast Cancer Susceptibility Gene 1 and Heat Shock Factor 1 Proteins in Breast Cancer Cells

doi: 10.5402/2012/707586

Figure Lengend Snippet: A. Western analysis of the expression of HSF1 and BRCA1 proteins in MDA-MB-231 and BT20 cells. Cells were treated with indicated concentrations of WA for 24 h.

Techniques: Western Blot, Expressing

The Effects of CBX on growth inhibition of MCF7 and BT20 cells. Cells were exposed to the indicated concentration (50-1000µM) for 24 h (♦) and 48 h (□) in the case of MCF7 as well as for 24 h (▲) and 48 h (■) in the case of BT20. The number of viable cells was determined by Trypan blue exclusion test. Growth inhibition in each treatment was expressed as a percentage of the control. Each value represents the mean ± SE of at least five independent experiments.

Journal: BioImpacts : BI

Article Title: Gap Junctions: The Claymore for Cancerous Cells

doi: 10.5681/bi.2011.015

Figure Lengend Snippet: The Effects of CBX on growth inhibition of MCF7 and BT20 cells. Cells were exposed to the indicated concentration (50-1000µM) for 24 h (♦) and 48 h (□) in the case of MCF7 as well as for 24 h (▲) and 48 h (■) in the case of BT20. The number of viable cells was determined by Trypan blue exclusion test. Growth inhibition in each treatment was expressed as a percentage of the control. Each value represents the mean ± SE of at least five independent experiments.

Article Snippet: The MCF7 and BT20 human breast cancer cell lines, Cell culture plates and flasks were obtained from National cell bank of Iran (Pasteur institute, Iran) and IWAKI, Japan respectively.

Techniques: Inhibition, Concentration Assay

Photomicrographs of MCF7 and BT20 cells were taken by a light microscope at a magnification of 40×. MCF7 and BT20 cells were treated by 150 µM of CBX. The death cells are shown by black arrows. Panel A represent untreated MCF7 cells versus CBX treated MCF7 cells in panels B and C at exposure times of 24h and 48h respectively. Panel D represent untreated BT20 cells versus CBX treated BT20 cells in panels E and F at exposure times of 24h and 48h respectively.

Journal: BioImpacts : BI

Article Title: Gap Junctions: The Claymore for Cancerous Cells

doi: 10.5681/bi.2011.015

Figure Lengend Snippet: Photomicrographs of MCF7 and BT20 cells were taken by a light microscope at a magnification of 40×. MCF7 and BT20 cells were treated by 150 µM of CBX. The death cells are shown by black arrows. Panel A represent untreated MCF7 cells versus CBX treated MCF7 cells in panels B and C at exposure times of 24h and 48h respectively. Panel D represent untreated BT20 cells versus CBX treated BT20 cells in panels E and F at exposure times of 24h and 48h respectively.

Techniques: Light Microscopy

Results of MTT assay for evaluation of cell viability. Cells were exposed to the indicated concentration of CBX (50-1000µM) at exposure time of 24 h (♦) and 48 h (□) and also are repeated in the case of BT20 for mentioned concentrations and exposure times. As shown in this diagram, CBX in 150 µM of concentration could significantly suppress the production of formazan as reductive metabolite of MTT (3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) in both cell lines. Each value represents the mean ± SE of at least five independent experiments.

Journal: BioImpacts : BI

Article Title: Gap Junctions: The Claymore for Cancerous Cells

doi: 10.5681/bi.2011.015

Figure Lengend Snippet: Results of MTT assay for evaluation of cell viability. Cells were exposed to the indicated concentration of CBX (50-1000µM) at exposure time of 24 h (♦) and 48 h (□) and also are repeated in the case of BT20 for mentioned concentrations and exposure times. As shown in this diagram, CBX in 150 µM of concentration could significantly suppress the production of formazan as reductive metabolite of MTT (3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) in both cell lines. Each value represents the mean ± SE of at least five independent experiments.

Techniques: MTT Assay, Concentration Assay

Quantitative real time PCR assessments of CBX on MCF7 cells (Panel A) and BT20 cells (Panel B). Normalized relative expressions intensity ratio of the genes upon the expression of housekeeping GAPDH gene. All of the genes expressions are significant statistically upon GAPDH. The values were obtained as a view of SYBR Green emitted fluorescent intensity in triplicate experiments statistically (mean ± SEM).

Journal: BioImpacts : BI

Article Title: Gap Junctions: The Claymore for Cancerous Cells

doi: 10.5681/bi.2011.015

Figure Lengend Snippet: Quantitative real time PCR assessments of CBX on MCF7 cells (Panel A) and BT20 cells (Panel B). Normalized relative expressions intensity ratio of the genes upon the expression of housekeeping GAPDH gene. All of the genes expressions are significant statistically upon GAPDH. The values were obtained as a view of SYBR Green emitted fluorescent intensity in triplicate experiments statistically (mean ± SEM).

Techniques: Real-time Polymerase Chain Reaction, Expressing, SYBR Green Assay

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