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Santa Cruz Biotechnology shrna targeting glut1

<t>GLUT1</t> Expression and Clinical Importance in EC. (A) The mRNA expression of GLUT1 (cancer versus normal tissues) in pan-cancers was analyzed with the Oncomine database. The graphic demonstrates the number of datasets that meet our threshold for each cancer type. Red: up-regulation; blue: down-regulation. (B) The heatmap was generated by the ImaGEO database using two EC data sets (GSE17025 and GSE56026). (C) Up- or down-regulated genes in EC tissues compared to normal tissues (ImaGEO). (D) The GEO dataset was analyzed for GLUT1 expression in stage I EC samples and normal endometrium samples. (E) The expression of GLUT1 protein was examined in EC tissue and adjacent normal tissues (Human Protein Atlas database; scale bar: 100 μm). (F) The probability of overall survival in EC patients expressing high or low GLUT1 levels was assessed using the KM plotter database.

Shrna Targeting Glut1, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 17 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/shrna+targeting+glut1/Glut1+siRNA/pmc09195630-52-10-13
Average 93 stars, based on 17 article reviews

shrna targeting glut1 - by Bioz Stars, 2026-10

93/100 stars

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1) Product Images from "Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143"

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

Journal: Frontiers in Oncology

doi: 10.3389/fonc.2022.912935

GLUT1 Expression and Clinical Importance in EC. (A) The mRNA expression of GLUT1 (cancer versus normal tissues) in pan-cancers was analyzed with the Oncomine database. The graphic demonstrates the number of datasets that meet our threshold for each cancer type. Red: up-regulation; blue: down-regulation. (B) The heatmap was generated by the ImaGEO database using two EC data sets (GSE17025 and GSE56026). (C) Up- or down-regulated genes in EC tissues compared to normal tissues (ImaGEO). (D) The GEO dataset was analyzed for GLUT1 expression in stage I EC samples and normal endometrium samples. (E) The expression of GLUT1 protein was examined in EC tissue and adjacent normal tissues (Human Protein Atlas database; scale bar: 100 μm). (F) The probability of overall survival in EC patients expressing high or low GLUT1 levels was assessed using the KM plotter database.

Figure Legend Snippet: GLUT1 Expression and Clinical Importance in EC. (A) The mRNA expression of GLUT1 (cancer versus normal tissues) in pan-cancers was analyzed with the Oncomine database. The graphic demonstrates the number of datasets that meet our threshold for each cancer type. Red: up-regulation; blue: down-regulation. (B) The heatmap was generated by the ImaGEO database using two EC data sets (GSE17025 and GSE56026). (C) Up- or down-regulated genes in EC tissues compared to normal tissues (ImaGEO). (D) The GEO dataset was analyzed for GLUT1 expression in stage I EC samples and normal endometrium samples. (E) The expression of GLUT1 protein was examined in EC tissue and adjacent normal tissues (Human Protein Atlas database; scale bar: 100 μm). (F) The probability of overall survival in EC patients expressing high or low GLUT1 levels was assessed using the KM plotter database.

Techniques Used: Expressing, Generated

Critical Roles of GLUT1 in Promoting EC Cell Phenotypes. (A) Western blotting analysis of GLUT1 protein expression in a normal endometrial cell line (EM) and human EC cell lines. (B) Western blotting analysis of GLUT1 expression in GLUT1-overexpressing HHUA cells and Ishikawa cells with GLUT1 silencing. (C–F) EC cell proliferation (C) , invasion (D) , glucose consumption (E) , and lactate production (F) assays following GLUT1 overexpression or knockdown. (G, H) GLUT1-overexpressing HHUA cells (G) and Ishikawa cells after knockdown of GLUT1 (H) were treated with different concentrations of paclitaxel, and cell viability was examined using the CCK-8 assay. Vec: vector. *** P < 0.001.

Figure Legend Snippet: Critical Roles of GLUT1 in Promoting EC Cell Phenotypes. (A) Western blotting analysis of GLUT1 protein expression in a normal endometrial cell line (EM) and human EC cell lines. (B) Western blotting analysis of GLUT1 expression in GLUT1-overexpressing HHUA cells and Ishikawa cells with GLUT1 silencing. (C–F) EC cell proliferation (C) , invasion (D) , glucose consumption (E) , and lactate production (F) assays following GLUT1 overexpression or knockdown. (G, H) GLUT1-overexpressing HHUA cells (G) and Ishikawa cells after knockdown of GLUT1 (H) were treated with different concentrations of paclitaxel, and cell viability was examined using the CCK-8 assay. Vec: vector. *** P < 0.001.

Techniques Used: Western Blot, Expressing, Over Expression, Knockdown, CCK-8 Assay, Plasmid Preparation

KEGG Pathway and Wiki Pathway Enrichment Analysis of GLUT1 -Associated Genes in EC. (A) Genes that were found to be highly co-expressed with GLUT1 in the TCGA EC dataset from the LinkedOmics database were chosen. (B, C) Gene set enrichment analysis for positively correlated genes of GLUT1 in TCGA EC tissues. Enrichment analysis for KEGG pathways (B) and Wikipathway cancer (C) was performed using the LinkedOmics database.

Figure Legend Snippet: KEGG Pathway and Wiki Pathway Enrichment Analysis of GLUT1 -Associated Genes in EC. (A) Genes that were found to be highly co-expressed with GLUT1 in the TCGA EC dataset from the LinkedOmics database were chosen. (B, C) Gene set enrichment analysis for positively correlated genes of GLUT1 in TCGA EC tissues. Enrichment analysis for KEGG pathways (B) and Wikipathway cancer (C) was performed using the LinkedOmics database.

Techniques Used:

GLUT1 is a Positive Upstream Regulator of MMP1, MMP14, and Cyclin D1. (A) The expression of GLUT1 was positively correlated with the expression of MMP1, MMP14 , and Cyclin D1 in EC tissues from the TCGA dataset. (B) qRT-PCR analysis of the indicated genes in EC cells after overexpression or knockdown of GLUT1. (C) The expression of MMP1, MMP14 , and Cyclin D1 in TCGA EC and normal tissues (ENCORI database). *** P < 0.001.

Figure Legend Snippet: GLUT1 is a Positive Upstream Regulator of MMP1, MMP14, and Cyclin D1. (A) The expression of GLUT1 was positively correlated with the expression of MMP1, MMP14 , and Cyclin D1 in EC tissues from the TCGA dataset. (B) qRT-PCR analysis of the indicated genes in EC cells after overexpression or knockdown of GLUT1. (C) The expression of MMP1, MMP14 , and Cyclin D1 in TCGA EC and normal tissues (ENCORI database). *** P < 0.001.

Techniques Used: Expressing, Quantitative RT-PCR, Over Expression, Knockdown

GLUT1 is a Target Gene of MiR-140 and MiR-143. (A) Venn diagram showing the overlapping miRNAs predicted by three online databases. (B) Computational prediction of duplex formation between miR-140/miR-143 and the GLUT1 3′-UTR region. (C) The expression of miR-140/miR-143 in TCGA EC tissues and normal tissues (miR-TV database). (D) qRT-PCR analysis of miR-140/miR-143 in EC and EM cells. (E) GLUT1 protein expression was examined using western blotting assays in EC cells transfected as indicated. (F) Luciferase reporter assays in Ishikawa cells transfected with the wild-type (WT) or mutant (MUT) GLUT1 3′-UTR, as well as miR-140/miR-143 mimic or a control mimic. *** P < 0.001.

Figure Legend Snippet: GLUT1 is a Target Gene of MiR-140 and MiR-143. (A) Venn diagram showing the overlapping miRNAs predicted by three online databases. (B) Computational prediction of duplex formation between miR-140/miR-143 and the GLUT1 3′-UTR region. (C) The expression of miR-140/miR-143 in TCGA EC tissues and normal tissues (miR-TV database). (D) qRT-PCR analysis of miR-140/miR-143 in EC and EM cells. (E) GLUT1 protein expression was examined using western blotting assays in EC cells transfected as indicated. (F) Luciferase reporter assays in Ishikawa cells transfected with the wild-type (WT) or mutant (MUT) GLUT1 3′-UTR, as well as miR-140/miR-143 mimic or a control mimic. *** P < 0.001.

Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Luciferase, Mutagenesis, Control

TMPO-AS1 Induces GLUT1 Expression by Repressing MiR-140 and MiR-143 Levels. (A) GLUT1 protein expression was measured in Ishikawa and HHUA cells transfected with (or without) TMPO-AS1 siRNA, along with (or without) miR-140/miR-143 inhibitor. (B) Examination of MMP1 , MMP14 , and Cyclin D1 expression in Ishikawa cells transfected as indicated. (C) Correlation analysis between TMPO-AS1 and GLUT1 or between TMPO-AS1 and miR-140/miR-143. *** P < 0.001.

Figure Legend Snippet: TMPO-AS1 Induces GLUT1 Expression by Repressing MiR-140 and MiR-143 Levels. (A) GLUT1 protein expression was measured in Ishikawa and HHUA cells transfected with (or without) TMPO-AS1 siRNA, along with (or without) miR-140/miR-143 inhibitor. (B) Examination of MMP1 , MMP14 , and Cyclin D1 expression in Ishikawa cells transfected as indicated. (C) Correlation analysis between TMPO-AS1 and GLUT1 or between TMPO-AS1 and miR-140/miR-143. *** P < 0.001.

Techniques Used: Expressing, Transfection

Graphical Abstract showing that the LncRNA TMPO-AS1 Regulates Glycolysis and Paclitaxel Resistance in EC Cells by Affecting the MiR-140/MiR-143-GLUT1 Pathway.

Figure Legend Snippet: Graphical Abstract showing that the LncRNA TMPO-AS1 Regulates Glycolysis and Paclitaxel Resistance in EC Cells by Affecting the MiR-140/MiR-143-GLUT1 Pathway.

Techniques Used:

shRNA:

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143
Article Snippet: The resulting cell lines were expanded after 14 days of selection with G418 (500 μg per ml, Sigma-Aldrich, St. Louis, MO). .. GLUT1 silencing was conducted in the Ishikawa cell line using shRNA targeting GLUT1 (Santa Cruz Biotechnologies, Santa Cruz, CA) or control shRNA (Santa Cruz Biotechnologies) and Lipofectamine 3000 reagent. .. The transfected cells were expanded after being selected with puromycin (1 μg per ml, Sigma-Aldrich, St. Louis, MO) for 14 days.

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143.
Article Snippet: The resulting cell lines were expanded after 14 days of selection with G418 (500 mg per ml, Sigma-Aldrich, St. Louis, MO). .. May 2022 | Volume 12 | Article 912935 GLUT1 silencing was conducted in the Ishikawa cell line using shRNA targeting GLUT1 (Santa Cruz Biotechnologies, Santa Cruz, CA) or control shRNA (Santa Cruz Biotechnologies) and Lipofectamine 3000 reagent. .. The transfected cells were expanded after being selected with puromycin (1 mg per ml, Sigma-Aldrich, St. Louis, MO) for 14 days.

Control:

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143.
Article Snippet: The resulting cell lines were expanded after 14 days of selection with G418 (500 mg per ml, Sigma-Aldrich, St. Louis, MO). .. May 2022 | Volume 12 | Article 912935 GLUT1 silencing was conducted in the Ishikawa cell line using shRNA targeting GLUT1 (Santa Cruz Biotechnologies, Santa Cruz, CA) or control shRNA (Santa Cruz Biotechnologies) and Lipofectamine 3000 reagent. .. The transfected cells were expanded after being selected with puromycin (1 mg per ml, Sigma-Aldrich, St. Louis, MO) for 14 days.

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Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: GLUT1 Expression and Clinical Importance in EC. (A) The mRNA expression of GLUT1 (cancer versus normal tissues) in pan-cancers was analyzed with the Oncomine database. The graphic demonstrates the number of datasets that meet our threshold for each cancer type. Red: up-regulation; blue: down-regulation. (B) The heatmap was generated by the ImaGEO database using two EC data sets (GSE17025 and GSE56026). (C) Up- or down-regulated genes in EC tissues compared to normal tissues (ImaGEO). (D) The GEO dataset was analyzed for GLUT1 expression in stage I EC samples and normal endometrium samples. (E) The expression of GLUT1 protein was examined in EC tissue and adjacent normal tissues (Human Protein Atlas database; scale bar: 100 μm). (F) The probability of overall survival in EC patients expressing high or low GLUT1 levels was assessed using the KM plotter database.

Article Snippet: GLUT1 silencing was conducted in the Ishikawa cell line using shRNA targeting GLUT1 (Santa Cruz Biotechnologies, Santa Cruz, CA) or control shRNA (Santa Cruz Biotechnologies) and Lipofectamine 3000 reagent.

Techniques: Expressing, Generated

Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: Critical Roles of GLUT1 in Promoting EC Cell Phenotypes. (A) Western blotting analysis of GLUT1 protein expression in a normal endometrial cell line (EM) and human EC cell lines. (B) Western blotting analysis of GLUT1 expression in GLUT1-overexpressing HHUA cells and Ishikawa cells with GLUT1 silencing. (C–F) EC cell proliferation (C) , invasion (D) , glucose consumption (E) , and lactate production (F) assays following GLUT1 overexpression or knockdown. (G, H) GLUT1-overexpressing HHUA cells (G) and Ishikawa cells after knockdown of GLUT1 (H) were treated with different concentrations of paclitaxel, and cell viability was examined using the CCK-8 assay. Vec: vector. *** P < 0.001.

Techniques: Western Blot, Expressing, Over Expression, Knockdown, CCK-8 Assay, Plasmid Preparation

Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: KEGG Pathway and Wiki Pathway Enrichment Analysis of GLUT1 -Associated Genes in EC. (A) Genes that were found to be highly co-expressed with GLUT1 in the TCGA EC dataset from the LinkedOmics database were chosen. (B, C) Gene set enrichment analysis for positively correlated genes of GLUT1 in TCGA EC tissues. Enrichment analysis for KEGG pathways (B) and Wikipathway cancer (C) was performed using the LinkedOmics database.

Techniques:

Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: GLUT1 is a Positive Upstream Regulator of MMP1, MMP14, and Cyclin D1. (A) The expression of GLUT1 was positively correlated with the expression of MMP1, MMP14 , and Cyclin D1 in EC tissues from the TCGA dataset. (B) qRT-PCR analysis of the indicated genes in EC cells after overexpression or knockdown of GLUT1. (C) The expression of MMP1, MMP14 , and Cyclin D1 in TCGA EC and normal tissues (ENCORI database). *** P < 0.001.

Techniques: Expressing, Quantitative RT-PCR, Over Expression, Knockdown

Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: GLUT1 is a Target Gene of MiR-140 and MiR-143. (A) Venn diagram showing the overlapping miRNAs predicted by three online databases. (B) Computational prediction of duplex formation between miR-140/miR-143 and the GLUT1 3′-UTR region. (C) The expression of miR-140/miR-143 in TCGA EC tissues and normal tissues (miR-TV database). (D) qRT-PCR analysis of miR-140/miR-143 in EC and EM cells. (E) GLUT1 protein expression was examined using western blotting assays in EC cells transfected as indicated. (F) Luciferase reporter assays in Ishikawa cells transfected with the wild-type (WT) or mutant (MUT) GLUT1 3′-UTR, as well as miR-140/miR-143 mimic or a control mimic. *** P < 0.001.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Transfection, Luciferase, Mutagenesis, Control

Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: TMPO-AS1 Induces GLUT1 Expression by Repressing MiR-140 and MiR-143 Levels. (A) GLUT1 protein expression was measured in Ishikawa and HHUA cells transfected with (or without) TMPO-AS1 siRNA, along with (or without) miR-140/miR-143 inhibitor. (B) Examination of MMP1 , MMP14 , and Cyclin D1 expression in Ishikawa cells transfected as indicated. (C) Correlation analysis between TMPO-AS1 and GLUT1 or between TMPO-AS1 and miR-140/miR-143. *** P < 0.001.

Techniques: Expressing, Transfection

Journal: Frontiers in Oncology

Article Title: Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143

doi: 10.3389/fonc.2022.912935

Figure Lengend Snippet: Graphical Abstract showing that the LncRNA TMPO-AS1 Regulates Glycolysis and Paclitaxel Resistance in EC Cells by Affecting the MiR-140/MiR-143-GLUT1 Pathway.

Techniques:

GLUT1 affects antitumor activity of ascorbate in gastric cancer cells. (A) Immunoblotting of GLUT1 in the indicated cells. β-Actin was used as a loading control. (B) Attenuation of elevated intracellular ROS level induced by ascorbate (2mM, 1h) after GLUT1 knockdown in the indicated cells. (C) Effect of GLUT1 knockdown on sensitivity of the indicated cells to ascorbate detected by colony formation assays. Gastric cancer cells with GLUT1 knockdown or control cells were plated and treated with ascorbate at 50μM. (D) Growth curve of xenografts after ascorbate treatment in AGS cells with GLUT1 knockdown. (E) Intracellular ROS level after ascorbate treatment (2mM, 1h) in HGC27 cells with enforced GLUT1 expression. (F) Growth curve of xenografts after ascorbate treatment in HGC27 cells with enforced GLUT1 expression. (G) Apoptosis analysis of AGS and SGC7901 cells treated with DHA or stabilized ascorbate. (H-J) Mass spectra analysis of intracellular ascorbate or DHA in gastric cancer cells after manipulation of GLUT1 expression. Cells were treated with 4mM vitamin C for 2h before measurement of ascorbate or DHA. Data in B, C, D, E, F, G, H, I and J are presented as mean ±S.D. (n = 3 in B, C, E, G, H, I, J and n=6 in D, F). * P < 0.05 versus control; NS, non-significant.

Journal: Theranostics

Article Title: Pharmacological Ascorbate Suppresses Growth of Gastric Cancer Cells with GLUT1 Overexpression and Enhances the Efficacy of Oxaliplatin Through Redox Modulation

doi: 10.7150/thno.21745

Figure Lengend Snippet: GLUT1 affects antitumor activity of ascorbate in gastric cancer cells. (A) Immunoblotting of GLUT1 in the indicated cells. β-Actin was used as a loading control. (B) Attenuation of elevated intracellular ROS level induced by ascorbate (2mM, 1h) after GLUT1 knockdown in the indicated cells. (C) Effect of GLUT1 knockdown on sensitivity of the indicated cells to ascorbate detected by colony formation assays. Gastric cancer cells with GLUT1 knockdown or control cells were plated and treated with ascorbate at 50μM. (D) Growth curve of xenografts after ascorbate treatment in AGS cells with GLUT1 knockdown. (E) Intracellular ROS level after ascorbate treatment (2mM, 1h) in HGC27 cells with enforced GLUT1 expression. (F) Growth curve of xenografts after ascorbate treatment in HGC27 cells with enforced GLUT1 expression. (G) Apoptosis analysis of AGS and SGC7901 cells treated with DHA or stabilized ascorbate. (H-J) Mass spectra analysis of intracellular ascorbate or DHA in gastric cancer cells after manipulation of GLUT1 expression. Cells were treated with 4mM vitamin C for 2h before measurement of ascorbate or DHA. Data in B, C, D, E, F, G, H, I and J are presented as mean ±S.D. (n = 3 in B, C, E, G, H, I, J and n=6 in D, F). * P < 0.05 versus control; NS, non-significant.

Article Snippet: The shRNA targeting GLUT1 and lentivirus expressing human cDNA encoding GLUT1 were purchased from GenePharma (Shanghai, China).

Techniques: Activity Assay, Western Blot, Control, Knockdown, Expressing

GLUT1 is overexpressed in gastric cancer tissues and predicts poor prognosis. (A) GLUT1 mRNA expression levels in gastric cancer tissues compared with paired normal gastric tissues and expression in multiple cancer microarray data sets available from online database ( https://www.oncomine.com/ /). (B) GLUT1 expression in 10 pairs of human gastric cancer tissues (T) and matched adjacent non-tumor tissues (N). (C) Representative staining showing negative, weak, moderate and strong expression of GLUT1 protein in gastric cancer tissues. GLUT1 was located in the cell membrane (left panel). The expression of GLUT1 is significantly different between tumor and normal tissues (right panel). (D) Scoring of GLUT1 in paired tumor tissues and lymph node metastasis. (E) Representative staining (left panel) and scoring (right panel) of GLUT1 in paired adjacent normal tissues, primary tumor tissues and distant metastasis. (F) Kaplan-Meier analysis of overall survival and disease free survival based on GLUT1 expression in all 209 patients. Data in C, D and E are presented as mean ±S.D. Scale bar: 100μm.

Journal: Theranostics

Article Title: Pharmacological Ascorbate Suppresses Growth of Gastric Cancer Cells with GLUT1 Overexpression and Enhances the Efficacy of Oxaliplatin Through Redox Modulation

doi: 10.7150/thno.21745

Figure Lengend Snippet: GLUT1 is overexpressed in gastric cancer tissues and predicts poor prognosis. (A) GLUT1 mRNA expression levels in gastric cancer tissues compared with paired normal gastric tissues and expression in multiple cancer microarray data sets available from online database ( https://www.oncomine.com/ /). (B) GLUT1 expression in 10 pairs of human gastric cancer tissues (T) and matched adjacent non-tumor tissues (N). (C) Representative staining showing negative, weak, moderate and strong expression of GLUT1 protein in gastric cancer tissues. GLUT1 was located in the cell membrane (left panel). The expression of GLUT1 is significantly different between tumor and normal tissues (right panel). (D) Scoring of GLUT1 in paired tumor tissues and lymph node metastasis. (E) Representative staining (left panel) and scoring (right panel) of GLUT1 in paired adjacent normal tissues, primary tumor tissues and distant metastasis. (F) Kaplan-Meier analysis of overall survival and disease free survival based on GLUT1 expression in all 209 patients. Data in C, D and E are presented as mean ±S.D. Scale bar: 100μm.

Article Snippet: The shRNA targeting GLUT1 and lentivirus expressing human cDNA encoding GLUT1 were purchased from GenePharma (Shanghai, China).

Techniques: Expressing, Microarray, Staining, Membrane

Combination of ascorbate and oxaliplatin is efficacious in gastric PDX models. (A) Schematic illustration of PDX model generation and subsequent in vivo analysis. (B) Immunoblotting of GLUT1 in the tumor tissues from two PDX models. β-Actin was used as a loading control. (C, F) The volume of the tumors was monitored and a tumor growth curve was created for each group. (D, G) Weight of dissected tumors was recorded. (E, H) Photographs of dissected tumors in each group. (I) Immuno-staining of Ki67 and cleaved caspase 3 in the paraffin-embedded tumor sections of PDX models were shown and evaluated (scale bar: 50μm). Data in C, D, F, G and I are presented as mean ±S.D. (n = 4). *P < 0.05 versus corresponding control. NS, non-significant.

Journal: Theranostics

Article Title: Pharmacological Ascorbate Suppresses Growth of Gastric Cancer Cells with GLUT1 Overexpression and Enhances the Efficacy of Oxaliplatin Through Redox Modulation

doi: 10.7150/thno.21745

Figure Lengend Snippet: Combination of ascorbate and oxaliplatin is efficacious in gastric PDX models. (A) Schematic illustration of PDX model generation and subsequent in vivo analysis. (B) Immunoblotting of GLUT1 in the tumor tissues from two PDX models. β-Actin was used as a loading control. (C, F) The volume of the tumors was monitored and a tumor growth curve was created for each group. (D, G) Weight of dissected tumors was recorded. (E, H) Photographs of dissected tumors in each group. (I) Immuno-staining of Ki67 and cleaved caspase 3 in the paraffin-embedded tumor sections of PDX models were shown and evaluated (scale bar: 50μm). Data in C, D, F, G and I are presented as mean ±S.D. (n = 4). *P < 0.05 versus corresponding control. NS, non-significant.

Article Snippet: The shRNA targeting GLUT1 and lentivirus expressing human cDNA encoding GLUT1 were purchased from GenePharma (Shanghai, China).

Techniques: In Vivo, Western Blot, Control, Immunostaining

Proposed working model of our study: Ascorbate transported into cytoplasm via GLUT1 disrupts redox homeostasis and enhances sensitivity to chemotherapy in gastric cancer.

Journal: Theranostics

Article Title: Pharmacological Ascorbate Suppresses Growth of Gastric Cancer Cells with GLUT1 Overexpression and Enhances the Efficacy of Oxaliplatin Through Redox Modulation

doi: 10.7150/thno.21745

Figure Lengend Snippet: Proposed working model of our study: Ascorbate transported into cytoplasm via GLUT1 disrupts redox homeostasis and enhances sensitivity to chemotherapy in gastric cancer.

Article Snippet: The shRNA targeting GLUT1 and lentivirus expressing human cDNA encoding GLUT1 were purchased from GenePharma (Shanghai, China).

Techniques:

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shrna targeting glut1 (Santa Cruz Biotechnology)

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1) Product Images from "Long Non-Coding RNA TMPO-AS1 Promotes GLUT1-Mediated Glycolysis and Paclitaxel Resistance in Endometrial Cancer Cells by Interacting With miR-140 and miR-143"

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