mcf7 tam1 cells Search Results


mcf7 tam1 cells  (ATCC)
95
ATCC mcf7 tam1 cells
Mcf7 Tam1 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mcf7+tam1+cells/MCF-7+Tam1/pm40393248-64-11-16
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mcf7 tam1  (ATCC)
99
ATCC mcf7 tam1
Hsa_circ_0086735 sponged to miR-1296-5p, and miR-1296-5p targeted to STAT1. (A) Predicted complementary binding sites of hsa_circ_0086735 against miR-1296-5p. (B) The expression level of hsa_circ_0086735 was reversely related to that of miR-1296-5p. (C) Luciferase reporter assays confirm the binding between hsa_circ_0086735 and miR-1296-5p. The pmirGL3 reporter vectors were cloned with the wild-type hsa_circ_0086735 with the potential miR-1296-5p binding sites to construct WT-circ plasmids or mutant of these sites to construct MUT-circ plasmids, and then transfected into MCF-7 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (D) In vitro pull-down of hsa_circ_0086735 with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in ZR-75-1 cells. (E) Predicted complementary binding sites of miR-1296-5p against STAT1. (F) Luciferase reporter assays confirm the binding between miR-1296-5p and STAT1. The pmirGL3 reporter vectors were cloned with the wild-type STAT1 with the potential miR-1296-5p binding sites to construct WT-STAT1 plasmids or mutant of these sites to construct MUT-STATA1 plasmids, and then transfected into ZR-75-1 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (G) In vitro pull-down of STAT1 mRNA with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in <t>MCF7</t> cells. (H) The expression level of miR-1296-5p was reversely related to that of STAT1. *** p < 0.001.
Mcf7 Tam1, 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/product/mcf7+tam1+cells/MCF7/pmc10175596-79-10-17
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breast cancer cell line mda mb 231  (ATCC)
99
ATCC breast cancer cell line mda mb 231
Hsa_circ_0086735 sponged to miR-1296-5p, and miR-1296-5p targeted to STAT1. (A) Predicted complementary binding sites of hsa_circ_0086735 against miR-1296-5p. (B) The expression level of hsa_circ_0086735 was reversely related to that of miR-1296-5p. (C) Luciferase reporter assays confirm the binding between hsa_circ_0086735 and miR-1296-5p. The pmirGL3 reporter vectors were cloned with the wild-type hsa_circ_0086735 with the potential miR-1296-5p binding sites to construct WT-circ plasmids or mutant of these sites to construct MUT-circ plasmids, and then transfected into MCF-7 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (D) In vitro pull-down of hsa_circ_0086735 with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in ZR-75-1 cells. (E) Predicted complementary binding sites of miR-1296-5p against STAT1. (F) Luciferase reporter assays confirm the binding between miR-1296-5p and STAT1. The pmirGL3 reporter vectors were cloned with the wild-type STAT1 with the potential miR-1296-5p binding sites to construct WT-STAT1 plasmids or mutant of these sites to construct MUT-STATA1 plasmids, and then transfected into ZR-75-1 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (G) In vitro pull-down of STAT1 mRNA with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in <t>MCF7</t> cells. (H) The expression level of miR-1296-5p was reversely related to that of STAT1. *** p < 0.001.
Breast Cancer Cell Line 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/product/mcf7+tam1+cells/MDA-MB-231/pmc07885429-35-0-7
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atcc crl 3435 tm  (ATCC)
80
ATCC atcc crl 3435 tm
Hsa_circ_0086735 sponged to miR-1296-5p, and miR-1296-5p targeted to STAT1. (A) Predicted complementary binding sites of hsa_circ_0086735 against miR-1296-5p. (B) The expression level of hsa_circ_0086735 was reversely related to that of miR-1296-5p. (C) Luciferase reporter assays confirm the binding between hsa_circ_0086735 and miR-1296-5p. The pmirGL3 reporter vectors were cloned with the wild-type hsa_circ_0086735 with the potential miR-1296-5p binding sites to construct WT-circ plasmids or mutant of these sites to construct MUT-circ plasmids, and then transfected into MCF-7 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (D) In vitro pull-down of hsa_circ_0086735 with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in ZR-75-1 cells. (E) Predicted complementary binding sites of miR-1296-5p against STAT1. (F) Luciferase reporter assays confirm the binding between miR-1296-5p and STAT1. The pmirGL3 reporter vectors were cloned with the wild-type STAT1 with the potential miR-1296-5p binding sites to construct WT-STAT1 plasmids or mutant of these sites to construct MUT-STATA1 plasmids, and then transfected into ZR-75-1 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (G) In vitro pull-down of STAT1 mRNA with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in <t>MCF7</t> cells. (H) The expression level of miR-1296-5p was reversely related to that of STAT1. *** p < 0.001.
Atcc Crl 3435 Tm, supplied by ATCC, used in various techniques. Bioz Stars score: 80/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mcf7+tam1+cells/MCF-7+Tam1%3B+Breast+Ductal+Carcinoma%3B+Human/pmc10858355-1-6-6
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lentivirus  (Shanghai GenePharma)
90
Shanghai GenePharma lentivirus
Hsa_circ_0086735 sponged to miR-1296-5p, and miR-1296-5p targeted to STAT1. (A) Predicted complementary binding sites of hsa_circ_0086735 against miR-1296-5p. (B) The expression level of hsa_circ_0086735 was reversely related to that of miR-1296-5p. (C) Luciferase reporter assays confirm the binding between hsa_circ_0086735 and miR-1296-5p. The pmirGL3 reporter vectors were cloned with the wild-type hsa_circ_0086735 with the potential miR-1296-5p binding sites to construct WT-circ plasmids or mutant of these sites to construct MUT-circ plasmids, and then transfected into MCF-7 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (D) In vitro pull-down of hsa_circ_0086735 with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in ZR-75-1 cells. (E) Predicted complementary binding sites of miR-1296-5p against STAT1. (F) Luciferase reporter assays confirm the binding between miR-1296-5p and STAT1. The pmirGL3 reporter vectors were cloned with the wild-type STAT1 with the potential miR-1296-5p binding sites to construct WT-STAT1 plasmids or mutant of these sites to construct MUT-STATA1 plasmids, and then transfected into ZR-75-1 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (G) In vitro pull-down of STAT1 mRNA with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in <t>MCF7</t> cells. (H) The expression level of miR-1296-5p was reversely related to that of STAT1. *** p < 0.001.
Lentivirus, supplied by Shanghai GenePharma, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mcf7+tam1+cells/lentivirus/pmc05260890-180-13-14
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mcf7 cells  (Korean Cell Line Bank)
86
Korean Cell Line Bank mcf7 cells
Tamoxifen-resistant luminal A breast cancer cells <t>(MCF7)</t> show increased hypoxia, lipid, and glutamine metabolism. (A) Expression heatmap of signature genes between MCF7(TamS) and tamoxifen-resistant MCF7(TamR) cell lines. ( B) Scatter plot showing the risk scores, survival time, and separation points of patients into risk groups. ( C) Volcano plot showing differentially expressed genes between MCF7(TamS) and tamoxifen-resistant MCF7(TamR). The FDR-corrected p value threshold was 0.05 (-Log10 =1.30). Orange: upregulated; purple: downregulated; grey: not significant. ( D) Hallmark gene set enrichment analysis shows different hallmark gene set expression between the two cell lines. ( E) GO and KEGG gene sets pathway analysis different gene set expression between two cell lines.
Mcf7 Cells, supplied by Korean Cell Line Bank, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mcf7+tam1+cells/7+mcf/pmc12148429-52-0-6
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mcf7 cells  (Selleck Chemicals)
96
Selleck Chemicals mcf7 cells
Characterization of tamoxifen resistant <t>MCF7</t> cells. (A) The cell proliferation assay indicated that the growth rate of MCF7-P was similar to that of MCF7/TAM1 and MCF7/TAM2. (B) Different from MCF7-P, the growth of MCF7/TAM1 and MCF7/TAM2 did not rely on the addition of E2. (C) The mRNA levels of ER target genes (PgR and pS2) were decreased in MCF7/TAM1 and MCF7/TAM2 cells compared with parental cells. (D) MCF7/TAM1 and MCF7/TAM2 were relatively insensitive towards tamoxifen treatment compared with MCF7-P cells. (E) Western blotting showed that the protein expression of TAZ and p-ERK1/2 was increased in MCF7/TAM1 and MCF7/TAM2 compared with MCF7-P, whereas the expression of ER and ERK1/2 was not altered. (F) Quantification analysis of TAZ, p-ERK1/2, ER and ERK1/2 expression in E was presented. *** P<0.001. MCF7-P, parental MCF7 cells; p-ERK1/2, phosphorylated-extracellular signal regulated kinase 1/2; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; ER, estrogen receptor.
Mcf7 Cells, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mcf7+tam1+cells/Tamoxifen/pmc06984795-73-0-9
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ici-resistant mcf-7/182r-6 cells  (European Collection of Authenticated Cell Cultures)
90
European Collection of Authenticated Cell Cultures ici-resistant mcf-7/182r-6 cells
Characterization of tamoxifen resistant <t>MCF7</t> cells. (A) The cell proliferation assay indicated that the growth rate of MCF7-P was similar to that of MCF7/TAM1 and MCF7/TAM2. (B) Different from MCF7-P, the growth of MCF7/TAM1 and MCF7/TAM2 did not rely on the addition of E2. (C) The mRNA levels of ER target genes (PgR and pS2) were decreased in MCF7/TAM1 and MCF7/TAM2 cells compared with parental cells. (D) MCF7/TAM1 and MCF7/TAM2 were relatively insensitive towards tamoxifen treatment compared with MCF7-P cells. (E) Western blotting showed that the protein expression of TAZ and p-ERK1/2 was increased in MCF7/TAM1 and MCF7/TAM2 compared with MCF7-P, whereas the expression of ER and ERK1/2 was not altered. (F) Quantification analysis of TAZ, p-ERK1/2, ER and ERK1/2 expression in E was presented. *** P<0.001. MCF7-P, parental MCF7 cells; p-ERK1/2, phosphorylated-extracellular signal regulated kinase 1/2; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; ER, estrogen receptor.
Ici Resistant Mcf 7/182r 6 Cells, supplied by European Collection of Authenticated Cell Cultures, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mcf7+tam1+cells/mcf+7+cell+line/pm35850772-76-28-36
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Image Search Results


Hsa_circ_0086735 sponged to miR-1296-5p, and miR-1296-5p targeted to STAT1. (A) Predicted complementary binding sites of hsa_circ_0086735 against miR-1296-5p. (B) The expression level of hsa_circ_0086735 was reversely related to that of miR-1296-5p. (C) Luciferase reporter assays confirm the binding between hsa_circ_0086735 and miR-1296-5p. The pmirGL3 reporter vectors were cloned with the wild-type hsa_circ_0086735 with the potential miR-1296-5p binding sites to construct WT-circ plasmids or mutant of these sites to construct MUT-circ plasmids, and then transfected into MCF-7 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (D) In vitro pull-down of hsa_circ_0086735 with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in ZR-75-1 cells. (E) Predicted complementary binding sites of miR-1296-5p against STAT1. (F) Luciferase reporter assays confirm the binding between miR-1296-5p and STAT1. The pmirGL3 reporter vectors were cloned with the wild-type STAT1 with the potential miR-1296-5p binding sites to construct WT-STAT1 plasmids or mutant of these sites to construct MUT-STATA1 plasmids, and then transfected into ZR-75-1 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (G) In vitro pull-down of STAT1 mRNA with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in MCF7 cells. (H) The expression level of miR-1296-5p was reversely related to that of STAT1. *** p < 0.001.

Journal: Frontiers in Molecular Biosciences

Article Title: Identification of circRNA-miRNA-mRNA network in luminal breast cancers by integrated analysis of microarray datasets

doi: 10.3389/fmolb.2023.1162259

Figure Lengend Snippet: Hsa_circ_0086735 sponged to miR-1296-5p, and miR-1296-5p targeted to STAT1. (A) Predicted complementary binding sites of hsa_circ_0086735 against miR-1296-5p. (B) The expression level of hsa_circ_0086735 was reversely related to that of miR-1296-5p. (C) Luciferase reporter assays confirm the binding between hsa_circ_0086735 and miR-1296-5p. The pmirGL3 reporter vectors were cloned with the wild-type hsa_circ_0086735 with the potential miR-1296-5p binding sites to construct WT-circ plasmids or mutant of these sites to construct MUT-circ plasmids, and then transfected into MCF-7 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (D) In vitro pull-down of hsa_circ_0086735 with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in ZR-75-1 cells. (E) Predicted complementary binding sites of miR-1296-5p against STAT1. (F) Luciferase reporter assays confirm the binding between miR-1296-5p and STAT1. The pmirGL3 reporter vectors were cloned with the wild-type STAT1 with the potential miR-1296-5p binding sites to construct WT-STAT1 plasmids or mutant of these sites to construct MUT-STATA1 plasmids, and then transfected into ZR-75-1 cells with miR-1296-5p mimic (mm-miR) or inhibitor (in-miR) or corresponding negative controls (mm-NC or in-NC). (G) In vitro pull-down of STAT1 mRNA with biotin-labeled miR-1296-5p (biotin-miR) or negative control (biotin-NC) in MCF7 cells. (H) The expression level of miR-1296-5p was reversely related to that of STAT1. *** p < 0.001.

Article Snippet: The cell lines used in the analysis include MCF7, ZR-75-1, MCF7 Tam1, and ZR-75-1 Tam1, purchased from American Type Culture Collection (Rockville, MD, United States).

Techniques: Binding Assay, Expressing, Luciferase, Clone Assay, Construct, Mutagenesis, Transfection, In Vitro, Labeling, Negative Control

The effect of hsa_circ_0086735-miR-1296-5p-STAT1 axis on proliferation and apoptosis of luminal-subtype cell lines. (A) and (B) The transfection efficiency was confirmed by qRT-PCR analysis. CCK8 was performed on MCF7 (C) and ZR-75-1 (D) cells. Apoptosis assay by AnnexinV-FITC/PI staining for MCF7 (E) and ZR-75-1 (F) cells. (G) Overall survival of 87 breast cancer patients whose tumors had high or low hsa_circ_0086735 expression. *** p < 0.001, compared with si-NC group. †† p < 0.01, ††† p < 0.001, compared with si-circ+in-NC group. && p < 0.01, &&& p < 0.001, compared with si-circ+in-miR + ctr-STAT1 group. si-NC: negative siRNA control for hsa_circ_0086735; si-circ: siRNA for hsa_circ_0086735; in-NC: inhibitor negative control; in-miR: miR-1296-5p inhibitor; ctr-STAT1: negative siRNA control for STAT1; si-STAT1: siRNA for STAT1.

Journal: Frontiers in Molecular Biosciences

Article Title: Identification of circRNA-miRNA-mRNA network in luminal breast cancers by integrated analysis of microarray datasets

doi: 10.3389/fmolb.2023.1162259

Figure Lengend Snippet: The effect of hsa_circ_0086735-miR-1296-5p-STAT1 axis on proliferation and apoptosis of luminal-subtype cell lines. (A) and (B) The transfection efficiency was confirmed by qRT-PCR analysis. CCK8 was performed on MCF7 (C) and ZR-75-1 (D) cells. Apoptosis assay by AnnexinV-FITC/PI staining for MCF7 (E) and ZR-75-1 (F) cells. (G) Overall survival of 87 breast cancer patients whose tumors had high or low hsa_circ_0086735 expression. *** p < 0.001, compared with si-NC group. †† p < 0.01, ††† p < 0.001, compared with si-circ+in-NC group. && p < 0.01, &&& p < 0.001, compared with si-circ+in-miR + ctr-STAT1 group. si-NC: negative siRNA control for hsa_circ_0086735; si-circ: siRNA for hsa_circ_0086735; in-NC: inhibitor negative control; in-miR: miR-1296-5p inhibitor; ctr-STAT1: negative siRNA control for STAT1; si-STAT1: siRNA for STAT1.

Article Snippet: The cell lines used in the analysis include MCF7, ZR-75-1, MCF7 Tam1, and ZR-75-1 Tam1, purchased from American Type Culture Collection (Rockville, MD, United States).

Techniques: Transfection, Quantitative RT-PCR, Apoptosis Assay, Staining, Expressing, Control, Negative Control

Tamoxifen-resistant luminal A breast cancer cells (MCF7) show increased hypoxia, lipid, and glutamine metabolism. (A) Expression heatmap of signature genes between MCF7(TamS) and tamoxifen-resistant MCF7(TamR) cell lines. ( B) Scatter plot showing the risk scores, survival time, and separation points of patients into risk groups. ( C) Volcano plot showing differentially expressed genes between MCF7(TamS) and tamoxifen-resistant MCF7(TamR). The FDR-corrected p value threshold was 0.05 (-Log10 =1.30). Orange: upregulated; purple: downregulated; grey: not significant. ( D) Hallmark gene set enrichment analysis shows different hallmark gene set expression between the two cell lines. ( E) GO and KEGG gene sets pathway analysis different gene set expression between two cell lines.

Journal: Translational Oncology

Article Title: Targeting EPAS-1/HIF-2α Pathway to Address Endocrine Resistance in Luminal A Type Breast Cancer

doi: 10.1016/j.tranon.2025.102415

Figure Lengend Snippet: Tamoxifen-resistant luminal A breast cancer cells (MCF7) show increased hypoxia, lipid, and glutamine metabolism. (A) Expression heatmap of signature genes between MCF7(TamS) and tamoxifen-resistant MCF7(TamR) cell lines. ( B) Scatter plot showing the risk scores, survival time, and separation points of patients into risk groups. ( C) Volcano plot showing differentially expressed genes between MCF7(TamS) and tamoxifen-resistant MCF7(TamR). The FDR-corrected p value threshold was 0.05 (-Log10 =1.30). Orange: upregulated; purple: downregulated; grey: not significant. ( D) Hallmark gene set enrichment analysis shows different hallmark gene set expression between the two cell lines. ( E) GO and KEGG gene sets pathway analysis different gene set expression between two cell lines.

Article Snippet: MCF7 cells were obtained from the Korean Cell Line Bank, and MCF7/Tam1 cells were sourced from ATCC.

Techniques: Expressing

EPAS1 Inhibition by PT2977 Attenuates Drug Resistance in Tamoxifen-Resistant MCF7/Tam1 Cells MCF-7 and MCF-7 Tam1 cells were treated with tamoxifen and cultured for 24 h. ( A ) MCF-7, and MCF-7 Tam1 cells were treated with PT2977 and cultured for 24 h. CCK-8 assay was performed, and dose-response curves were obtained. ( B) Protein expression levels of EPAS1 in MCF-7 and MCF-7 Tam1 cells were detected using western blotting. β-Actin served as an internal control. ( C) The fluorescence intensity of the hypoxic probe was used for the analysis. ( D) MCF-7 cells were treated with PT2977 and cultured for 24h. A CCK-8 assay was performed, and dose-response curves were plotted. ( E) MCF-7 Tam1 cells were treated with PT2977 and cultured for 24 h. A CCK-8 assay was performed, and dose-response curves were plotted . (F) Protein expression level of EPAS1 in MCF-7 Tam1 cells treated with PT2977 as detected using western blotting. β-Actin served as an internal control.

Journal: Translational Oncology

Article Title: Targeting EPAS-1/HIF-2α Pathway to Address Endocrine Resistance in Luminal A Type Breast Cancer

doi: 10.1016/j.tranon.2025.102415

Figure Lengend Snippet: EPAS1 Inhibition by PT2977 Attenuates Drug Resistance in Tamoxifen-Resistant MCF7/Tam1 Cells MCF-7 and MCF-7 Tam1 cells were treated with tamoxifen and cultured for 24 h. ( A ) MCF-7, and MCF-7 Tam1 cells were treated with PT2977 and cultured for 24 h. CCK-8 assay was performed, and dose-response curves were obtained. ( B) Protein expression levels of EPAS1 in MCF-7 and MCF-7 Tam1 cells were detected using western blotting. β-Actin served as an internal control. ( C) The fluorescence intensity of the hypoxic probe was used for the analysis. ( D) MCF-7 cells were treated with PT2977 and cultured for 24h. A CCK-8 assay was performed, and dose-response curves were plotted. ( E) MCF-7 Tam1 cells were treated with PT2977 and cultured for 24 h. A CCK-8 assay was performed, and dose-response curves were plotted . (F) Protein expression level of EPAS1 in MCF-7 Tam1 cells treated with PT2977 as detected using western blotting. β-Actin served as an internal control.

Article Snippet: MCF7 cells were obtained from the Korean Cell Line Bank, and MCF7/Tam1 cells were sourced from ATCC.

Techniques: Inhibition, Cell Culture, CCK-8 Assay, Expressing, Western Blot, Control, Fluorescence

Characterization of tamoxifen resistant MCF7 cells. (A) The cell proliferation assay indicated that the growth rate of MCF7-P was similar to that of MCF7/TAM1 and MCF7/TAM2. (B) Different from MCF7-P, the growth of MCF7/TAM1 and MCF7/TAM2 did not rely on the addition of E2. (C) The mRNA levels of ER target genes (PgR and pS2) were decreased in MCF7/TAM1 and MCF7/TAM2 cells compared with parental cells. (D) MCF7/TAM1 and MCF7/TAM2 were relatively insensitive towards tamoxifen treatment compared with MCF7-P cells. (E) Western blotting showed that the protein expression of TAZ and p-ERK1/2 was increased in MCF7/TAM1 and MCF7/TAM2 compared with MCF7-P, whereas the expression of ER and ERK1/2 was not altered. (F) Quantification analysis of TAZ, p-ERK1/2, ER and ERK1/2 expression in E was presented. *** P<0.001. MCF7-P, parental MCF7 cells; p-ERK1/2, phosphorylated-extracellular signal regulated kinase 1/2; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; ER, estrogen receptor.

Journal: International Journal of Molecular Medicine

Article Title: lncRNA CYTOR promotes tamoxifen resistance in breast cancer cells via sponging miR-125a-5p

doi: 10.3892/ijmm.2019.4428

Figure Lengend Snippet: Characterization of tamoxifen resistant MCF7 cells. (A) The cell proliferation assay indicated that the growth rate of MCF7-P was similar to that of MCF7/TAM1 and MCF7/TAM2. (B) Different from MCF7-P, the growth of MCF7/TAM1 and MCF7/TAM2 did not rely on the addition of E2. (C) The mRNA levels of ER target genes (PgR and pS2) were decreased in MCF7/TAM1 and MCF7/TAM2 cells compared with parental cells. (D) MCF7/TAM1 and MCF7/TAM2 were relatively insensitive towards tamoxifen treatment compared with MCF7-P cells. (E) Western blotting showed that the protein expression of TAZ and p-ERK1/2 was increased in MCF7/TAM1 and MCF7/TAM2 compared with MCF7-P, whereas the expression of ER and ERK1/2 was not altered. (F) Quantification analysis of TAZ, p-ERK1/2, ER and ERK1/2 expression in E was presented. *** P<0.001. MCF7-P, parental MCF7 cells; p-ERK1/2, phosphorylated-extracellular signal regulated kinase 1/2; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; ER, estrogen receptor.

Article Snippet: MCF7 cells were exposed to tamoxifen (1 μ M; Selleck Chemicals) for over 12 months and two colonies were picked and cultured as MCF7/TAM1 and MCF7/TAM2 cells.

Techniques: Proliferation Assay, Western Blot, Expressing

lncRNA CYTOR promoted tamoxifen resistance in breast cancer cells. (A) Screen of breast cancer-associated lncRNA (from LncRNADisease database) showed that several lncRNAs were differentially expressed between MCF7-P and MCF7/TAM1. (B) Screen of breast cancer-associated lncRNA (from LncRNADisease database) showed that several lncRNAs were differentially expressed between MCF7-P and MCF7/TAM2. (C) CYTOR siRNA decreased CYTOR expression in MCF7/TAM1 cells and MCF7/TAM2 cells. (D) Silencing of CYTOR re-sensitized MCF7/TAM1 cells to tamoxifen treatment. (E) Silencing of CYTOR re-sensitized MCF7/TAM2 cells to tamoxifen treatment. (F) Silencing of CYTOR showed no effect on the proliferation of MCF7/TAM1 without treatment of tamoxifen. (G) Silencing of CYTOR showed no effect on the proliferation of MCF7/TAM2 without treatment of tamoxifen. * P<0.05, *** P<0.001. CYTOR, cytoskeleton regulator RNA; lnc, long noncoding; si, small interfering; RT-q, reverse transcription; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2.

Journal: International Journal of Molecular Medicine

Article Title: lncRNA CYTOR promotes tamoxifen resistance in breast cancer cells via sponging miR-125a-5p

doi: 10.3892/ijmm.2019.4428

Figure Lengend Snippet: lncRNA CYTOR promoted tamoxifen resistance in breast cancer cells. (A) Screen of breast cancer-associated lncRNA (from LncRNADisease database) showed that several lncRNAs were differentially expressed between MCF7-P and MCF7/TAM1. (B) Screen of breast cancer-associated lncRNA (from LncRNADisease database) showed that several lncRNAs were differentially expressed between MCF7-P and MCF7/TAM2. (C) CYTOR siRNA decreased CYTOR expression in MCF7/TAM1 cells and MCF7/TAM2 cells. (D) Silencing of CYTOR re-sensitized MCF7/TAM1 cells to tamoxifen treatment. (E) Silencing of CYTOR re-sensitized MCF7/TAM2 cells to tamoxifen treatment. (F) Silencing of CYTOR showed no effect on the proliferation of MCF7/TAM1 without treatment of tamoxifen. (G) Silencing of CYTOR showed no effect on the proliferation of MCF7/TAM2 without treatment of tamoxifen. * P<0.05, *** P<0.001. CYTOR, cytoskeleton regulator RNA; lnc, long noncoding; si, small interfering; RT-q, reverse transcription; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2.

Article Snippet: MCF7 cells were exposed to tamoxifen (1 μ M; Selleck Chemicals) for over 12 months and two colonies were picked and cultured as MCF7/TAM1 and MCF7/TAM2 cells.

Techniques: Expressing, Reverse Transcription

CYTOR directly regulates miR-125a-5p in breast cancer cells. (A) Bioinformatic analysis showed that miR-125a-5p harbored a putative binding site for CYTOR. (B) Bioinformatic analysis of The Cancer Genome Atlas data suggested that expression of CYTOR was negatively correlated with miR-125-5p in breast cancer. (C) miR-125a-5p expression was decreased in MCF7/TAM1 and MCF7/TAM2 compared with parental cells. (D) Silencing of CYTOR increased miR-125a-5p expression in MCF7/TAM1 and MCF7/TAM2 cells. (E) Transfection of miR-125a-5p mimic increased miR-125a-5p levels in MCF7/TAM1 cells. (F) Dual luciferase reporter assay indicated that miR-125a-5p could directly bind to CYTOR in MCF7/TAM1 cells. ** P<0.01 and *** P<0.001. CYTOR, cytoskeleton regulator RNA; miR, microRNA; Mut, mutant; NC, negative control.

Journal: International Journal of Molecular Medicine

Article Title: lncRNA CYTOR promotes tamoxifen resistance in breast cancer cells via sponging miR-125a-5p

doi: 10.3892/ijmm.2019.4428

Figure Lengend Snippet: CYTOR directly regulates miR-125a-5p in breast cancer cells. (A) Bioinformatic analysis showed that miR-125a-5p harbored a putative binding site for CYTOR. (B) Bioinformatic analysis of The Cancer Genome Atlas data suggested that expression of CYTOR was negatively correlated with miR-125-5p in breast cancer. (C) miR-125a-5p expression was decreased in MCF7/TAM1 and MCF7/TAM2 compared with parental cells. (D) Silencing of CYTOR increased miR-125a-5p expression in MCF7/TAM1 and MCF7/TAM2 cells. (E) Transfection of miR-125a-5p mimic increased miR-125a-5p levels in MCF7/TAM1 cells. (F) Dual luciferase reporter assay indicated that miR-125a-5p could directly bind to CYTOR in MCF7/TAM1 cells. ** P<0.01 and *** P<0.001. CYTOR, cytoskeleton regulator RNA; miR, microRNA; Mut, mutant; NC, negative control.

Article Snippet: MCF7 cells were exposed to tamoxifen (1 μ M; Selleck Chemicals) for over 12 months and two colonies were picked and cultured as MCF7/TAM1 and MCF7/TAM2 cells.

Techniques: Binding Assay, Expressing, Transfection, Luciferase, Reporter Assay, Mutagenesis, Negative Control

SRF is upregulated and acts as a target gene of miR-125a-5p in tamoxifen resistant MCF7 cells. (A) There was a putative binding site for miR-125a-5p on the 3′UTR of SRF. (B) Transfection of recombinant SRF increased SRF protein expression in MCF7 cells. (C) Quantification analysis of SRF protein expression in B was presented. (D) Overexpression of SRF decreased sensitivity of MCF7 cells towards tamoxifen treatment. (E) RT-qPCR showed that SRF was overexpressed in MCF7/TAM1 and MCF7/TAM2 compared with parental cells. (F) Western blotting showed that SRF protein levels were increased in MCF7/TAM1 and MCF7/TAM2. (G) Quantification analysis of SRF protein expression in F was presented. (H) RT-qPCR suggested that SRF mRNA levels were decreased towards miR-125a-5p overexpression in MCF7/TAM1 and MCF7/TAM2 cells. ** P<0.01 and *** P<0.001. SRF is upregulated and acts as a target gene of miR-125a-5p in tamoxifen resistant MCF7 cells. (I) Western blotting showed that SRF protein levels were decreased towards miR-125a-5p overexpression in MCF7/TAM1 and MCF7/TAM2 cells. (J) Quantification analysis of SRF protein expression in I was presented. (K) Dual luciferase reporter assay showed that SRF was a target gene of miR-125a-5p in MCF7/TAM1 cells. ** P<0.01. SRF, serum response factor; RT-q, reverse transcription-quantitative; UTR, untranslated region; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; NC, negative control; miR, microRNA; WTT, wild-type; Mut, mutant.

Journal: International Journal of Molecular Medicine

Article Title: lncRNA CYTOR promotes tamoxifen resistance in breast cancer cells via sponging miR-125a-5p

doi: 10.3892/ijmm.2019.4428

Figure Lengend Snippet: SRF is upregulated and acts as a target gene of miR-125a-5p in tamoxifen resistant MCF7 cells. (A) There was a putative binding site for miR-125a-5p on the 3′UTR of SRF. (B) Transfection of recombinant SRF increased SRF protein expression in MCF7 cells. (C) Quantification analysis of SRF protein expression in B was presented. (D) Overexpression of SRF decreased sensitivity of MCF7 cells towards tamoxifen treatment. (E) RT-qPCR showed that SRF was overexpressed in MCF7/TAM1 and MCF7/TAM2 compared with parental cells. (F) Western blotting showed that SRF protein levels were increased in MCF7/TAM1 and MCF7/TAM2. (G) Quantification analysis of SRF protein expression in F was presented. (H) RT-qPCR suggested that SRF mRNA levels were decreased towards miR-125a-5p overexpression in MCF7/TAM1 and MCF7/TAM2 cells. ** P<0.01 and *** P<0.001. SRF is upregulated and acts as a target gene of miR-125a-5p in tamoxifen resistant MCF7 cells. (I) Western blotting showed that SRF protein levels were decreased towards miR-125a-5p overexpression in MCF7/TAM1 and MCF7/TAM2 cells. (J) Quantification analysis of SRF protein expression in I was presented. (K) Dual luciferase reporter assay showed that SRF was a target gene of miR-125a-5p in MCF7/TAM1 cells. ** P<0.01. SRF, serum response factor; RT-q, reverse transcription-quantitative; UTR, untranslated region; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; NC, negative control; miR, microRNA; WTT, wild-type; Mut, mutant.

Article Snippet: MCF7 cells were exposed to tamoxifen (1 μ M; Selleck Chemicals) for over 12 months and two colonies were picked and cultured as MCF7/TAM1 and MCF7/TAM2 cells.

Techniques: Binding Assay, Transfection, Recombinant, Expressing, Over Expression, Quantitative RT-PCR, Western Blot, Luciferase, Reporter Assay, Reverse Transcription, Negative Control, Mutagenesis

CYTOR regulates SRF expression in a miR-125a-5p dependent manner. (A) Transfection of miR-125a-5p inhibitor decreased miR-125a-5p levels in MCF7/TAM1 and MCF7/TAM2 cells. (B) Silencing of CYTOR decreased SRF mRNA levels in MCF7/TAM1 and MCF7/TAM2 cells, which was reversed upon miR-125a-5p inhibition. (C) Silencing of CYTOR decreased SRF, TAZ and p-ERK1/2 protein levels in MCF7/TAM1 cells, which was reversed upon miR-125a-5p inhibition. (D) Quantification of SRF, p-ERK1/2, ERK1/2 and TAZ expression in C was exhibited. (E) Silencing of CYTOR decreased SRF and p-ERK1/2 protein levels in MCF7/TAM2 cells, which was reversed upon miR-125a-5p inhibition. (F) Quantification of SRF, p-ERK1/2, ERK1/2 and TAZ expression in E was exhibited. (G) Silencing of CYTOR decreased TAZ mRNA levels in MCF7/TAM1 and MCF7/TAM2 cells, which was reversed upon miR-125a-5p inhibition. * P<0.05; ** P<0.01 and *** P<0.001. SRF, serum response factor; CYTOR, cytoskeleton regulator RNA; miR, microRNA; p-ERK1/2, phosphorylated-extracellular signal regulated kinase; NC, negative control.

Journal: International Journal of Molecular Medicine

Article Title: lncRNA CYTOR promotes tamoxifen resistance in breast cancer cells via sponging miR-125a-5p

doi: 10.3892/ijmm.2019.4428

Figure Lengend Snippet: CYTOR regulates SRF expression in a miR-125a-5p dependent manner. (A) Transfection of miR-125a-5p inhibitor decreased miR-125a-5p levels in MCF7/TAM1 and MCF7/TAM2 cells. (B) Silencing of CYTOR decreased SRF mRNA levels in MCF7/TAM1 and MCF7/TAM2 cells, which was reversed upon miR-125a-5p inhibition. (C) Silencing of CYTOR decreased SRF, TAZ and p-ERK1/2 protein levels in MCF7/TAM1 cells, which was reversed upon miR-125a-5p inhibition. (D) Quantification of SRF, p-ERK1/2, ERK1/2 and TAZ expression in C was exhibited. (E) Silencing of CYTOR decreased SRF and p-ERK1/2 protein levels in MCF7/TAM2 cells, which was reversed upon miR-125a-5p inhibition. (F) Quantification of SRF, p-ERK1/2, ERK1/2 and TAZ expression in E was exhibited. (G) Silencing of CYTOR decreased TAZ mRNA levels in MCF7/TAM1 and MCF7/TAM2 cells, which was reversed upon miR-125a-5p inhibition. * P<0.05; ** P<0.01 and *** P<0.001. SRF, serum response factor; CYTOR, cytoskeleton regulator RNA; miR, microRNA; p-ERK1/2, phosphorylated-extracellular signal regulated kinase; NC, negative control.

Article Snippet: MCF7 cells were exposed to tamoxifen (1 μ M; Selleck Chemicals) for over 12 months and two colonies were picked and cultured as MCF7/TAM1 and MCF7/TAM2 cells.

Techniques: Expressing, Transfection, Inhibition, Negative Control

CYTOR regulates tamoxifen sensitivity via targeting SRF. (A) Transfection of recombinant SRF increased SRF protein expression in MCF7/TAM1 and MCF7/TAM2 cells. (B) Quantification analysis of SRF protein expression in A was exhibited. (C) In MCF7/TAM1 and MCF7/TAM2 cells, silencing of CYTOR decreased TAZ and p-ERK1/2 expression, which was reversed upon transfection of recombinant SRF. (D) Quantification of protein expression in C was exhibited. (E) Overexpression of SRF attenuated CYTOR siRNA induced elevation of tamoxifen sensitivity in MCF7/TAM1 cells. (F) Overexpression of SRF attenuated CYTOR siRNA induced elevation of tamoxifen sensitivity in MCF7/TAM2 cells. * P<0.05; ** P<0.01 and *** P<0.001. SRF, serum response factor; CYTOR, cytoskeleton regulator RNA; si, small interfering; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; p-ERK 1/2, phosphorylated-extracellular protein kinase 1/2.

Journal: International Journal of Molecular Medicine

Article Title: lncRNA CYTOR promotes tamoxifen resistance in breast cancer cells via sponging miR-125a-5p

doi: 10.3892/ijmm.2019.4428

Figure Lengend Snippet: CYTOR regulates tamoxifen sensitivity via targeting SRF. (A) Transfection of recombinant SRF increased SRF protein expression in MCF7/TAM1 and MCF7/TAM2 cells. (B) Quantification analysis of SRF protein expression in A was exhibited. (C) In MCF7/TAM1 and MCF7/TAM2 cells, silencing of CYTOR decreased TAZ and p-ERK1/2 expression, which was reversed upon transfection of recombinant SRF. (D) Quantification of protein expression in C was exhibited. (E) Overexpression of SRF attenuated CYTOR siRNA induced elevation of tamoxifen sensitivity in MCF7/TAM1 cells. (F) Overexpression of SRF attenuated CYTOR siRNA induced elevation of tamoxifen sensitivity in MCF7/TAM2 cells. * P<0.05; ** P<0.01 and *** P<0.001. SRF, serum response factor; CYTOR, cytoskeleton regulator RNA; si, small interfering; MCF7/TAM1, tamoxifen-resistant MCF7 subline1; MCF7/TAM2, tamoxifen-resistant MCF7 subline2; p-ERK 1/2, phosphorylated-extracellular protein kinase 1/2.

Article Snippet: MCF7 cells were exposed to tamoxifen (1 μ M; Selleck Chemicals) for over 12 months and two colonies were picked and cultured as MCF7/TAM1 and MCF7/TAM2 cells.

Techniques: Transfection, Recombinant, Expressing, Over Expression