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Addgene inc negative control lentiviral construct

Negative Control Lentiviral Construct, supplied by Addgene inc, used in various techniques. Bioz Stars score: 96/100, based on 1473 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1473 article reviews

negative control lentiviral construct - by Bioz Stars, 2026-06

96/100 stars

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1) Product Images from "T3SS translocon induces pyroptosis by direct interaction with NLRC4/NAIP inflammasome"

Article Title: T3SS translocon induces pyroptosis by direct interaction with NLRC4/NAIP inflammasome

Journal: eLife

doi: 10.7554/eLife.100820

Figure Legend Snippet:

Techniques Used: Control, Knockdown, Knock-Out, Transfection, Construct, shRNA, Gene Knockout, Recombinant, Negative Control, Plasmid Preparation, Sequencing, Cytotoxicity Assay, Enzyme-linked Immunosorbent Assay, Software

Image Search Results

Journal: eLife

Article Title: T3SS translocon induces pyroptosis by direct interaction with NLRC4/NAIP inflammasome

doi: 10.7554/eLife.100820

Figure Lengend Snippet:

Article Snippet: Recombinant DNA reagent , pLKO.1 puro , Addgene , 8453, RRID: Addgene_8453 , Negative control lentiviral construct.

Techniques: Control, Knockdown, Knock-Out, Transfection, Construct, shRNA, Gene Knockout, Recombinant, Negative Control, Plasmid Preparation, Sequencing, Cytotoxicity Assay, Enzyme-linked Immunosorbent Assay, Software

The expression of SMARCAD1 is significantly higher in pancreatic cancer and positively correlated with poor prognosis. A. The mRNA expression level of SMARCAD1 in pancreatic cancer is much higher than that of normal tissues from GSE16515, GSE11838 and GSE15471. B-C. Expression levels of SMARCAD1 by immunohistochemistry performed with tissue microarray of PC (n=69) and adjacent normal tissues (n=68). Representative images showed positive expression of SMARCAD1 in PC and negative expression in paired normal tissues, respectively. Scale bars=50μm. D. Kaplan-Meier analysis shows the correlation between SMARCAD1 expression and overall survival in patients. Patients with high SMARCAD1 expression had poorer overall survival than those with low expression. *p<.05, **p<.01.

Journal: International Journal of Biological Sciences

Article Title: SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT

doi: 10.7150/ijbs.29562

Figure Lengend Snippet: The expression of SMARCAD1 is significantly higher in pancreatic cancer and positively correlated with poor prognosis. A. The mRNA expression level of SMARCAD1 in pancreatic cancer is much higher than that of normal tissues from GSE16515, GSE11838 and GSE15471. B-C. Expression levels of SMARCAD1 by immunohistochemistry performed with tissue microarray of PC (n=69) and adjacent normal tissues (n=68). Representative images showed positive expression of SMARCAD1 in PC and negative expression in paired normal tissues, respectively. Scale bars=50μm. D. Kaplan-Meier analysis shows the correlation between SMARCAD1 expression and overall survival in patients. Patients with high SMARCAD1 expression had poorer overall survival than those with low expression. *p<.05, **p<.01.

Article Snippet: Lentiviral constructs expressing SMARCAD1 shRNAs and negative control were obtained from Sigma.

Techniques: Expressing, Immunohistochemistry, Microarray

SMARCAD1 enhances proliferation of PANC-1 cells. A-B. The efficiency of SMARCAD1 knockdown (A) or overexpression (B) in PANC-1 cells was detected by western blotting. β-actin was used as an internal control. C-D. CCK8 assay was performed to determine the proliferation of PANC-1 cells with SMARCAD1 knockdown (C) or overexpression (D) at the indicated time points after plated. Cell viability was measured at 450nm. E-F. The effect of SMARCAD1 knockdown (E) or overexpression (F) on Colony-forming of PANC-1 cells was shown in the top panels. Number of foci was counted as shown in the bottom panels. All data were presented as mean ±SEM. *p<.05, **p<.01.

Journal: International Journal of Biological Sciences

Article Title: SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT

doi: 10.7150/ijbs.29562

Figure Lengend Snippet: SMARCAD1 enhances proliferation of PANC-1 cells. A-B. The efficiency of SMARCAD1 knockdown (A) or overexpression (B) in PANC-1 cells was detected by western blotting. β-actin was used as an internal control. C-D. CCK8 assay was performed to determine the proliferation of PANC-1 cells with SMARCAD1 knockdown (C) or overexpression (D) at the indicated time points after plated. Cell viability was measured at 450nm. E-F. The effect of SMARCAD1 knockdown (E) or overexpression (F) on Colony-forming of PANC-1 cells was shown in the top panels. Number of foci was counted as shown in the bottom panels. All data were presented as mean ±SEM. *p<.05, **p<.01.

Article Snippet: Lentiviral constructs expressing SMARCAD1 shRNAs and negative control were obtained from Sigma.

Techniques: Over Expression, Western Blot, CCK-8 Assay

SMARCAD1 promotes migration and invasion of PANC-1 cells. A-B. Effect of SMARCAD1 knockdown (A) or SMARCAD1 overexpression (B) on cell migration was detected by wound healing at indicated time points after scratching. The wound healing was measured by ImageJ software. C-D. Motility ability of PANC-1 cells with SMARCAD1 depletion (C) or overexpression (D) was assessed by transwell assay at 24h. Representative images of migration were photographed at 24h (Top panel). The number of migrated cells was counted from 5 randomly selected fields under microscope (Bottom panel). E-F. Invasion ability of PANC-1 cells with SMARCAD1 depletion (E) or overexpression (F) was assessed by transwell assay at 48h. Representative images of invasion were photographed at 48h (Top panel). The number of invaded cells was counted from 5 randomly selected fields under microscope (Bottom panel). Scale bars=150um. Data were presented as mean ±SEM. *p<.05, **p<.01.

Journal: International Journal of Biological Sciences

Article Title: SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT

doi: 10.7150/ijbs.29562

Figure Lengend Snippet: SMARCAD1 promotes migration and invasion of PANC-1 cells. A-B. Effect of SMARCAD1 knockdown (A) or SMARCAD1 overexpression (B) on cell migration was detected by wound healing at indicated time points after scratching. The wound healing was measured by ImageJ software. C-D. Motility ability of PANC-1 cells with SMARCAD1 depletion (C) or overexpression (D) was assessed by transwell assay at 24h. Representative images of migration were photographed at 24h (Top panel). The number of migrated cells was counted from 5 randomly selected fields under microscope (Bottom panel). E-F. Invasion ability of PANC-1 cells with SMARCAD1 depletion (E) or overexpression (F) was assessed by transwell assay at 48h. Representative images of invasion were photographed at 48h (Top panel). The number of invaded cells was counted from 5 randomly selected fields under microscope (Bottom panel). Scale bars=150um. Data were presented as mean ±SEM. *p<.05, **p<.01.

Article Snippet: Lentiviral constructs expressing SMARCAD1 shRNAs and negative control were obtained from Sigma.

Techniques: Migration, Over Expression, Software, Transwell Assay, Microscopy

SMARCAD1 induces EMT in PANC-1 cells. A-B. The morphology changes of PANC-1 cells: cells lose contact with each other with SMARCAD1 depletion (A) or gain more contact with SMARCAD1 overexpression (B), Scale bars=250μm. C-D. Changes in mRNA level of EMT relative markers were tested by Quantitative real-time PCR in SMARCAD1 knockdown (C) or overexpression (D) cells. The results were presented as mean ±SEM. All values were normalized to the level (=1) in NC or control cells. *p<.05, **p<.01. (D). E-F. The protein levels of EMT relative markers in SMARCAD1 knockdown (E) or overexpression (F) cells were assessed by western blotting. β-actin was used as an internal control.

Journal: International Journal of Biological Sciences

Article Title: SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT

doi: 10.7150/ijbs.29562

Figure Lengend Snippet: SMARCAD1 induces EMT in PANC-1 cells. A-B. The morphology changes of PANC-1 cells: cells lose contact with each other with SMARCAD1 depletion (A) or gain more contact with SMARCAD1 overexpression (B), Scale bars=250μm. C-D. Changes in mRNA level of EMT relative markers were tested by Quantitative real-time PCR in SMARCAD1 knockdown (C) or overexpression (D) cells. The results were presented as mean ±SEM. All values were normalized to the level (=1) in NC or control cells. *p<.05, **p<.01. (D). E-F. The protein levels of EMT relative markers in SMARCAD1 knockdown (E) or overexpression (F) cells were assessed by western blotting. β-actin was used as an internal control.

Article Snippet: Lentiviral constructs expressing SMARCAD1 shRNAs and negative control were obtained from Sigma.

Techniques: Over Expression, Real-time Polymerase Chain Reaction, Western Blot

SMARCAD1-induced EMT was regulated by Wnt/beta-catenin signaling pathway. A-B. The mRNA level of β-catenin was detected by Quantitative real-time PCR in PANC-1 cells with SMARCAD1 knockdown (A) or overexpression (B) respectively. The data were presented as mean ±SEM. All values were normalized to the level (=1) in NC or control cells. *p<.05, **p<.01. C-D. β-catenin, cyclin-D1, c-Myc and survivin protein levels were assayed by western blotting in PANC-1 cells with SMARCAD1 knockdown (C) or overexpression (D) respectively. E. PANC-1 cells with SMARCAD1 depletion were treated with CHIR99021 (6μM/ml) for 24h. The protein levels of EMT markers and Wnt/β-catenin target genes (β-catenin, cyclin-D1, c-Myc and survivin) were detected by western blotting. β-actin was used as an internal control.

Journal: International Journal of Biological Sciences

Article Title: SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT

doi: 10.7150/ijbs.29562

Figure Lengend Snippet: SMARCAD1-induced EMT was regulated by Wnt/beta-catenin signaling pathway. A-B. The mRNA level of β-catenin was detected by Quantitative real-time PCR in PANC-1 cells with SMARCAD1 knockdown (A) or overexpression (B) respectively. The data were presented as mean ±SEM. All values were normalized to the level (=1) in NC or control cells. *p<.05, **p<.01. C-D. β-catenin, cyclin-D1, c-Myc and survivin protein levels were assayed by western blotting in PANC-1 cells with SMARCAD1 knockdown (C) or overexpression (D) respectively. E. PANC-1 cells with SMARCAD1 depletion were treated with CHIR99021 (6μM/ml) for 24h. The protein levels of EMT markers and Wnt/β-catenin target genes (β-catenin, cyclin-D1, c-Myc and survivin) were detected by western blotting. β-actin was used as an internal control.

Article Snippet: Lentiviral constructs expressing SMARCAD1 shRNAs and negative control were obtained from Sigma.

Techniques: Real-time Polymerase Chain Reaction, Over Expression, Western Blot

c-Myc plays an important role in the synergistic antileukemic activity of AZD5991 and gilteritinib or MRX-2843 in FLT3 -mutated AML cells. ( A ) MOLM-13 cells were treated with AZD5991 (AZD), gilteritinib (gilt), or MRX-2843 (MRX), alone or in combination, for up to 24 h. Whole cell lysates were subjected to western blotting and probed with the indicated antibodies. Densitometry results (normalized to β-actin and compared to vehicle control at the matching time point) are shown below the corresponding blot. ( B ) MOLM-13 cells treated with AZD, gilt, or MRX, alone in combination, for up to 24 h, were stained with annexin V-FITC/PI and analyzed using a flow cytometer. *** indicates p < 0.001 compared to control and single-drug treatments. ( C , D ) MV4-11 and primary AML patient sample AML#262 cells were treated with AZD, gilt, MRX, or in combination for 3 h. Whole cell lysates were subjected to western blot analysis. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot in panel ( C ). After treatment, cells were stained with annexin V-FITC/PI and analyzed using a flow cytometer (panel ( D )). *** indicates p < 0.001 compared to control and single-drug treatments. ( E , F ) MV4-11 and MOLM-13 cells were treated with vehicle control, AZD, 10058-F4, or AZD + 10058-F4 for 3 h. Whole cell lysates were subjected to western blotting analysis. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot (panel ( E )). After treatment, cells were stained with annexin V-FITC/PI and analyzed using a flow cytometer (panel ( F )). *** indicates p < 0.001 compared to control and single-drug treatments. ( G ) Lentiviral CRISPR/Cas9 knockdown (KD) of c-Myc was performed in MV4-11 cells along with non-target control (NTC). Whole cell lysates were subjected to western blotting ( left panel). Cells were treated with vehicle control, AZD, gilt, MRX, or in combination for 3 h. Annexin V/PI staining and flow cytometry analysis results are shown in the ( right panel). ** indicates p < 0.01 and *** p < 0.001 compared to NTC for the same drug treatment.

Journal: Cells

Article Title: Inhibition of Mcl-1 Synergistically Enhances the Antileukemic Activity of Gilteritinib and MRX-2843 in Preclinical Models of FLT3 -Mutated Acute Myeloid Leukemia

doi: 10.3390/cells11172752

Figure Lengend Snippet: c-Myc plays an important role in the synergistic antileukemic activity of AZD5991 and gilteritinib or MRX-2843 in FLT3 -mutated AML cells. ( A ) MOLM-13 cells were treated with AZD5991 (AZD), gilteritinib (gilt), or MRX-2843 (MRX), alone or in combination, for up to 24 h. Whole cell lysates were subjected to western blotting and probed with the indicated antibodies. Densitometry results (normalized to β-actin and compared to vehicle control at the matching time point) are shown below the corresponding blot. ( B ) MOLM-13 cells treated with AZD, gilt, or MRX, alone in combination, for up to 24 h, were stained with annexin V-FITC/PI and analyzed using a flow cytometer. *** indicates p < 0.001 compared to control and single-drug treatments. ( C , D ) MV4-11 and primary AML patient sample AML#262 cells were treated with AZD, gilt, MRX, or in combination for 3 h. Whole cell lysates were subjected to western blot analysis. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot in panel ( C ). After treatment, cells were stained with annexin V-FITC/PI and analyzed using a flow cytometer (panel ( D )). *** indicates p < 0.001 compared to control and single-drug treatments. ( E , F ) MV4-11 and MOLM-13 cells were treated with vehicle control, AZD, 10058-F4, or AZD + 10058-F4 for 3 h. Whole cell lysates were subjected to western blotting analysis. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot (panel ( E )). After treatment, cells were stained with annexin V-FITC/PI and analyzed using a flow cytometer (panel ( F )). *** indicates p < 0.001 compared to control and single-drug treatments. ( G ) Lentiviral CRISPR/Cas9 knockdown (KD) of c-Myc was performed in MV4-11 cells along with non-target control (NTC). Whole cell lysates were subjected to western blotting ( left panel). Cells were treated with vehicle control, AZD, gilt, MRX, or in combination for 3 h. Annexin V/PI staining and flow cytometry analysis results are shown in the ( right panel). ** indicates p < 0.01 and *** p < 0.001 compared to NTC for the same drug treatment.

Article Snippet: Bak, Bax, and non-target negative control (NTC) shRNA lentiviral constructs were purchased from Sigma Aldrich.

Techniques: Activity Assay, Western Blot, Staining, Flow Cytometry, CRISPR

$FLT3 inhibition enhances AZD5991-induced cytochrome c release. ( A ) Proposed mechanism of action of gilteritinib/MXR-2843 in combination with AZD5991. ( B , C ) MV4-11 cells were treated with vehicle control, AZD5991 (AZD), gilteritinib (gilt), MRX-2843 (MRX), or in combination for 3 h. Cellular fractionation was performed. Mitochondrial and cytosolic fractions were subjected to western blotting analysis. This experiment was performed two independent times in triplicate. One representative image is shown. Relative densitometry measurements were determined, normalized to β-actin or VDAC1, and compared to the vehicle control. Results from one representative experiment are graphed as mean ± SEM in panel ( C ). * indicates p < 0.05, ** indicates p < 0.01, and *** indicates p < 0.001 compared to vehicle control. # indicates p < 0.05 compared to single-drug treatment. ( D ) MV4-11 cells were treated with vehicle control, AZD, gilt, MRX, or in combination for 3 h. Western blots were generated utilizing whole cell lysates. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot. ( E , F ) MV4-11 cells were treated with vehicle control, AZD, 10058-F4, or in combination for 3 h. Cellular fractionation was performed as described in panel ( B ). * indicates p < 0.05, ** indicates p < 0.01 and *** indicates p < 0.001 compared to vehicle control. ## indicates p < 0.01 compared to single-drug treatment. ( G ) MV4-11 cells were treated with vehicle control, AZD, 10058-F4, or in combination for 3 h. Western blots were generated utilizing whole cell lysates. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot. ( H , I ) shRNA knockdown of Bak and Bax was performed in MV4-11 cells with non-template control (NTC) as the negative control. Whole cell lysates were subjected to western blotting (panel ( H )). Cells were treated with vehicle control, AZD, gilt, MRX, or in combination for 3 h. Annexin V/PI staining and flow cytometry analysis results are shown in panel ( I ). *** p < 0.001 compared to NTC for the same drug treatment.$

Journal: Cells

Article Title: Inhibition of Mcl-1 Synergistically Enhances the Antileukemic Activity of Gilteritinib and MRX-2843 in Preclinical Models of FLT3 -Mutated Acute Myeloid Leukemia

doi: 10.3390/cells11172752

Figure Lengend Snippet: FLT3 inhibition enhances AZD5991-induced cytochrome c release. ( A ) Proposed mechanism of action of gilteritinib/MXR-2843 in combination with AZD5991. ( B , C ) MV4-11 cells were treated with vehicle control, AZD5991 (AZD), gilteritinib (gilt), MRX-2843 (MRX), or in combination for 3 h. Cellular fractionation was performed. Mitochondrial and cytosolic fractions were subjected to western blotting analysis. This experiment was performed two independent times in triplicate. One representative image is shown. Relative densitometry measurements were determined, normalized to β-actin or VDAC1, and compared to the vehicle control. Results from one representative experiment are graphed as mean ± SEM in panel ( C ). * indicates p < 0.05, ** indicates p < 0.01, and *** indicates p < 0.001 compared to vehicle control. # indicates p < 0.05 compared to single-drug treatment. ( D ) MV4-11 cells were treated with vehicle control, AZD, gilt, MRX, or in combination for 3 h. Western blots were generated utilizing whole cell lysates. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot. ( E , F ) MV4-11 cells were treated with vehicle control, AZD, 10058-F4, or in combination for 3 h. Cellular fractionation was performed as described in panel ( B ). * indicates p < 0.05, ** indicates p < 0.01 and *** indicates p < 0.001 compared to vehicle control. ## indicates p < 0.01 compared to single-drug treatment. ( G ) MV4-11 cells were treated with vehicle control, AZD, 10058-F4, or in combination for 3 h. Western blots were generated utilizing whole cell lysates. Densitometry results (normalized to β-actin and compared to vehicle control) are shown below the corresponding blot. ( H , I ) shRNA knockdown of Bak and Bax was performed in MV4-11 cells with non-template control (NTC) as the negative control. Whole cell lysates were subjected to western blotting (panel ( H )). Cells were treated with vehicle control, AZD, gilt, MRX, or in combination for 3 h. Annexin V/PI staining and flow cytometry analysis results are shown in panel ( I ). *** p < 0.001 compared to NTC for the same drug treatment.

Article Snippet: Bak, Bax, and non-target negative control (NTC) shRNA lentiviral constructs were purchased from Sigma Aldrich.

Techniques: Inhibition, Cell Fractionation, Western Blot, Generated, shRNA, Negative Control, Staining, Flow Cytometry

Journal: Cell Death & Disease

Article Title: Oxidative stress activates NORAD expression by H3K27ac and promotes oxaliplatin resistance in gastric cancer by enhancing autophagy flux via targeting the miR-433-3p

doi: 10.1038/s41419-020-03368-y

Figure Lengend Snippet: A WGCNA for the relationship between gene modules and clinical traits. B WGCNA for the relationship between microRNA modules and clinical traits. C Top five genes ranked by importance based on random-forest model. D GO biological process pathways involved for differentially expressed genes after NORAD knockdown using TMT-based quantitative proteomic analysis in SGC-7901 and SGC-7901-R cell lines. E The influence of NORAD knockdown on ATG12 abundance using TMT-based quantitative proteomic analysis between SGC-7901 and SGC-7901-R cell line ( t = 6.721, P < 0.000). F The influence of NORAD knockdown on ATG5 abundance using TMT-based quantitative proteomic analysis between SGC-7901 and SGC-7901-R cell line ( t = 4.032, P < 0.000). G The association between NORAD and ATG5 based on TCGA and GTEx data. H The association between NORAD and ATG12 based on TCGA and GTEx data. I The expression of NORAD ( t = 6.538, P < 0.000) and miR-433-3p ( t = 4.276, P < 0.000) in 379 gastric cancer patients. J The expression profile of NORAD ( t = 2.817, P = 0.003) and miR-433-3p ( t = 2.175, P = 0.008) in nonrecurrent and recurrent gastric cancer patients. K – N The overall survival and cancer-specific survival for NORAD (OS, χ 2 = 65.28, P < 0.000, 2K; CSS, χ 2 = 61.06, P < 0.000, 2M) and miR-433-3p (OS, χ 2 = 20.56, P < 0.000, 2L; CSS, χ 2 = 16.92, P < 0.000, 2N) in 379 gastric cancer patients.

Article Snippet: Lentiviral constructs for NORAD and miR-433-3p knockdown, miR-433-3p overexpression, and respective negative controls (NCs) were synthesized by Genechem (Shanghai, China).

Techniques: Knockdown, Expressing

A qRT-PCR to test the expression of NORAD in gastric cancer cells compared with gastric normal cell, GES-1. One-way ANOVA test was used to test the difference of NORAD expression. GES-1 vs SGC-7901, q = 19.97, P < 0.000; GES-1 vs AGS, q = 4.28, P < 0.004; GES-1 vs SNU-1, q = 2.21, P = 0.174; GES-1 vs HGC-27, q = 6.35, P = 0.864; GES-1 vs KATO III, q = 0.916, P < 0.000. B qRT-PCR to test the expression of NORAD in SGC-7901-R (SGC-7901-R vs. SGC-7901, t = 28.20, P < 0.000) and KATO III-R (KATO III-R vs. KATO III, t = 18.51, P < 0.000) compared with parental cells. C qRT-PCR to test the expression of NORAD in SGC-7901-R and KATO III-R when treated with 2 μg/ml L-OHP (NC vs L-OHP: SGC-7901, t = 7.645, P = 0.001; SGC-7901-R, t = 20.08, P = 0.000;KATO III, t = 9.547, P = 0.001, KATO III-R, t = 48.13, P = 0.000. NC vs NAC: SGC-7901, t = 2.946, P = 0.011; SGC-7901-R, t = 6.752, P = 0.001; KATO III, t = 5.110, P = 0.002, KATO III-R, t = 20.87, P = 0.000. NC vs NAC + L-OHP: SGC-7901, t = 2.535, P = 0.032; SGC-7901-R, t = 2.868, P = 0.031; KATO III, t = 10.62, P = 0.000, KATO III-R, t = 26.71, P = 0.000). D NORAD expression after NORAD knockdown in SGC-7901, SGC-7901-R, KATO III and KATO III-R (SGC-7901, t = 60.73, P = 0.000; SGC-7901-R, t = 45.19, P = 0.000; KATO III, t = 119.1, P = 0.000; KATO III-R, t = 124.6, P = 0.000). E CCK-8 test for NORAD knockdown SGC-7901 and SGC-7901-R to evaluate the IC50 Tukey’s multiple comparisons test was used to evaluate the statistical significance of cell survival rate treated with different concentration of L-OHP. SGC-7901 vs SGC-7901-R: 0 μg/ml vs 1 μg/ml, P < 0.000; 0 μg/ml vs 1.5 μg/ml, P < 0.000; 0 μg/ml vs 2.0 μg/ml, P < 0.000; 0 μg/ml vs 2.5 μg/ml, P < 0.000. KATO III vs KATO III-R: 0 μg/ml vs 1 μg/ml, P < 0.000; 0 μg/ml vs 1.5 μg/ml, P < 0.000; 0 μg/ml vs 2.0 μg/ml, P < 0.000; 0 μg/ml vs 2.5 μg/ml, P < 0.000. F Flow cytometry apoptosis assay and the quantification result for NORAD knockdown in SGC-7901-R ( t = 13.23, P = 0.000) and KATO III-R ( t = 11.78, P = 0.000). G Transwell assay to evaluate the migration and invasion ability of NORAD knockdown in SGC-7901-R (Migration, t = 8.263, P = 0.002; Invasion, t = 8.046, P = 0.002) and KATO III-R (Migration, t = 8.695, P = 0.001; Invasion, t = 9.979, P = 0.001). H DHE method to test the ROS production in NORAD knockdown cells treated with 2 μg/ml L-OHP. (SGC-7901, t = 12.08, P = 0.001; SGC-7901-R, t = 6.191, P = 0.006; KATO III, t = 9.455, P = 0.002, KATO III-R, t = 6.379, P = 0.006) I – K SOD, GSH and MDA expression in NORAD knockdown cells when treated with 2 μg/ml L-OHP. 2I, SOD: SGC-7901, t = 4.067, P = 0.002; SGC-7901-R, t = 5.917, P = 0.002; KATO III, t = 15.87, P = 0.004, KATO III-R, t = 12.36, P = 0.001. 2J, GSH: SGC-7901, t = 4.228, P = 0.027; SGC-7901-R, t = 8.982, P = 0.002; KATO III, t = 3.830, P = 0.027, KATO III-R, t = 24.80, P = 0.000. 2K, MDA: SGC-7901, t = 5.364, P = 0.006; SGC-7901-R, t = 28.08, P = 0.000; KATO III, t = 16.61, P = 0.000, KATO III-R, t = 12.49, P = 0.000.

Journal: Cell Death & Disease

Article Title: Oxidative stress activates NORAD expression by H3K27ac and promotes oxaliplatin resistance in gastric cancer by enhancing autophagy flux via targeting the miR-433-3p

doi: 10.1038/s41419-020-03368-y

Figure Lengend Snippet: A qRT-PCR to test the expression of NORAD in gastric cancer cells compared with gastric normal cell, GES-1. One-way ANOVA test was used to test the difference of NORAD expression. GES-1 vs SGC-7901, q = 19.97, P < 0.000; GES-1 vs AGS, q = 4.28, P < 0.004; GES-1 vs SNU-1, q = 2.21, P = 0.174; GES-1 vs HGC-27, q = 6.35, P = 0.864; GES-1 vs KATO III, q = 0.916, P < 0.000. B qRT-PCR to test the expression of NORAD in SGC-7901-R (SGC-7901-R vs. SGC-7901, t = 28.20, P < 0.000) and KATO III-R (KATO III-R vs. KATO III, t = 18.51, P < 0.000) compared with parental cells. C qRT-PCR to test the expression of NORAD in SGC-7901-R and KATO III-R when treated with 2 μg/ml L-OHP (NC vs L-OHP: SGC-7901, t = 7.645, P = 0.001; SGC-7901-R, t = 20.08, P = 0.000;KATO III, t = 9.547, P = 0.001, KATO III-R, t = 48.13, P = 0.000. NC vs NAC: SGC-7901, t = 2.946, P = 0.011; SGC-7901-R, t = 6.752, P = 0.001; KATO III, t = 5.110, P = 0.002, KATO III-R, t = 20.87, P = 0.000. NC vs NAC + L-OHP: SGC-7901, t = 2.535, P = 0.032; SGC-7901-R, t = 2.868, P = 0.031; KATO III, t = 10.62, P = 0.000, KATO III-R, t = 26.71, P = 0.000). D NORAD expression after NORAD knockdown in SGC-7901, SGC-7901-R, KATO III and KATO III-R (SGC-7901, t = 60.73, P = 0.000; SGC-7901-R, t = 45.19, P = 0.000; KATO III, t = 119.1, P = 0.000; KATO III-R, t = 124.6, P = 0.000). E CCK-8 test for NORAD knockdown SGC-7901 and SGC-7901-R to evaluate the IC50 Tukey’s multiple comparisons test was used to evaluate the statistical significance of cell survival rate treated with different concentration of L-OHP. SGC-7901 vs SGC-7901-R: 0 μg/ml vs 1 μg/ml, P < 0.000; 0 μg/ml vs 1.5 μg/ml, P < 0.000; 0 μg/ml vs 2.0 μg/ml, P < 0.000; 0 μg/ml vs 2.5 μg/ml, P < 0.000. KATO III vs KATO III-R: 0 μg/ml vs 1 μg/ml, P < 0.000; 0 μg/ml vs 1.5 μg/ml, P < 0.000; 0 μg/ml vs 2.0 μg/ml, P < 0.000; 0 μg/ml vs 2.5 μg/ml, P < 0.000. F Flow cytometry apoptosis assay and the quantification result for NORAD knockdown in SGC-7901-R ( t = 13.23, P = 0.000) and KATO III-R ( t = 11.78, P = 0.000). G Transwell assay to evaluate the migration and invasion ability of NORAD knockdown in SGC-7901-R (Migration, t = 8.263, P = 0.002; Invasion, t = 8.046, P = 0.002) and KATO III-R (Migration, t = 8.695, P = 0.001; Invasion, t = 9.979, P = 0.001). H DHE method to test the ROS production in NORAD knockdown cells treated with 2 μg/ml L-OHP. (SGC-7901, t = 12.08, P = 0.001; SGC-7901-R, t = 6.191, P = 0.006; KATO III, t = 9.455, P = 0.002, KATO III-R, t = 6.379, P = 0.006) I – K SOD, GSH and MDA expression in NORAD knockdown cells when treated with 2 μg/ml L-OHP. 2I, SOD: SGC-7901, t = 4.067, P = 0.002; SGC-7901-R, t = 5.917, P = 0.002; KATO III, t = 15.87, P = 0.004, KATO III-R, t = 12.36, P = 0.001. 2J, GSH: SGC-7901, t = 4.228, P = 0.027; SGC-7901-R, t = 8.982, P = 0.002; KATO III, t = 3.830, P = 0.027, KATO III-R, t = 24.80, P = 0.000. 2K, MDA: SGC-7901, t = 5.364, P = 0.006; SGC-7901-R, t = 28.08, P = 0.000; KATO III, t = 16.61, P = 0.000, KATO III-R, t = 12.49, P = 0.000.

Article Snippet: Lentiviral constructs for NORAD and miR-433-3p knockdown, miR-433-3p overexpression, and respective negative controls (NCs) were synthesized by Genechem (Shanghai, China).

Techniques: Quantitative RT-PCR, Expressing, Knockdown, CCK-8 Assay, Concentration Assay, Flow Cytometry, Apoptosis Assay, Transwell Assay, Migration

A , B Western blot to test the DNA damage repair related genes expression in SGC-7901 and KATO III: DNA-PKcs 450 kDa, ATR 300 kDa, Phospho-ATR (Ser428) 300 kDa, ATM 350kDA, Phospho-ATM (Ser1981) 350 kDa, H2AX 15 kDa, Phospho-Histone H2AX (Ser139) 15 kDa, β-Tubulin 55 kDa, GAPDH 37 kDa. C UCSC genome browser prediction about the enrichment of H3K27ac at the promoter region of NORAD in different cell lines. D NORAD location in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by FISH tests. E H3K27ac expression in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by western blot: H3K27ac 17 kDa, Histone H3 17 kDa. F H3K27ac location in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by FISH tests. G CREBBP expression in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by western blot: CREBBP 300 kDa, β-Actin 45 kDa. H CREBBP location in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by FISH tests. I C646 can decrease the expression of NORAD in SGC-7901, SGC-7901-R, KATO III, and KATO III-R (SGC-7901, t = 11.52, P = 0.000; SGC-7901-R, t = 18.28, P = 0.000; KATO III, t = 17.64, P = 0.000, KATO III-R, t = 33.85, P = 0.000). J ChIP results to test the enrichment of H3K27ac at the promoter region of NORAD in SGC-7901, SGC-7901-R, KATO III, and KATO III-R. anti-H3k27ac vs anti IgG: SGC-7901, t = 17.19, P = 0.000; SGC-7901-R, t = 21.03, P = 0.000; KATO III, t = 31.22, P = 0.000, KATO III-R, t = 20.82, P = 0.000. K ChIP results to test the enrichment of CREBBP at the promoter region of NORAD in SGC-7901, SGC-7901-R, KATO III, and KATO III-R. anti-H3k27ac vs anti IgG: SGC-7901, t = 9.83, P = 0.000; SGC-7901-R, t = 15.83, P = 0.000; KATO III, t = 7.99, P = 0.000, KATO III-R, t = 19.92, P = 0.000. L Downregulation of CREBBP in SGC-7901-R and KATO III-R: CREBBP 300 kDa, β-Tubulin 55 kDa. M CREBBP knockdown can inhibit the enrichment of H3K27ac at the promoter region of NORAD in SGC-7901-R and KATO III-R. anti-H3k27ac: SGC-7901 vs SGC-7901-R, t = 16.23, P = 0.000; KATO III vs KATO III-R, t = 13.79, P = 0.000.

Journal: Cell Death & Disease

Article Title: Oxidative stress activates NORAD expression by H3K27ac and promotes oxaliplatin resistance in gastric cancer by enhancing autophagy flux via targeting the miR-433-3p

doi: 10.1038/s41419-020-03368-y

Figure Lengend Snippet: A , B Western blot to test the DNA damage repair related genes expression in SGC-7901 and KATO III: DNA-PKcs 450 kDa, ATR 300 kDa, Phospho-ATR (Ser428) 300 kDa, ATM 350kDA, Phospho-ATM (Ser1981) 350 kDa, H2AX 15 kDa, Phospho-Histone H2AX (Ser139) 15 kDa, β-Tubulin 55 kDa, GAPDH 37 kDa. C UCSC genome browser prediction about the enrichment of H3K27ac at the promoter region of NORAD in different cell lines. D NORAD location in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by FISH tests. E H3K27ac expression in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by western blot: H3K27ac 17 kDa, Histone H3 17 kDa. F H3K27ac location in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by FISH tests. G CREBBP expression in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by western blot: CREBBP 300 kDa, β-Actin 45 kDa. H CREBBP location in SGC-7901, SGC-7901-R, KATO III, and KATO III-R by FISH tests. I C646 can decrease the expression of NORAD in SGC-7901, SGC-7901-R, KATO III, and KATO III-R (SGC-7901, t = 11.52, P = 0.000; SGC-7901-R, t = 18.28, P = 0.000; KATO III, t = 17.64, P = 0.000, KATO III-R, t = 33.85, P = 0.000). J ChIP results to test the enrichment of H3K27ac at the promoter region of NORAD in SGC-7901, SGC-7901-R, KATO III, and KATO III-R. anti-H3k27ac vs anti IgG: SGC-7901, t = 17.19, P = 0.000; SGC-7901-R, t = 21.03, P = 0.000; KATO III, t = 31.22, P = 0.000, KATO III-R, t = 20.82, P = 0.000. K ChIP results to test the enrichment of CREBBP at the promoter region of NORAD in SGC-7901, SGC-7901-R, KATO III, and KATO III-R. anti-H3k27ac vs anti IgG: SGC-7901, t = 9.83, P = 0.000; SGC-7901-R, t = 15.83, P = 0.000; KATO III, t = 7.99, P = 0.000, KATO III-R, t = 19.92, P = 0.000. L Downregulation of CREBBP in SGC-7901-R and KATO III-R: CREBBP 300 kDa, β-Tubulin 55 kDa. M CREBBP knockdown can inhibit the enrichment of H3K27ac at the promoter region of NORAD in SGC-7901-R and KATO III-R. anti-H3k27ac: SGC-7901 vs SGC-7901-R, t = 16.23, P = 0.000; KATO III vs KATO III-R, t = 13.79, P = 0.000.

Article Snippet: Lentiviral constructs for NORAD and miR-433-3p knockdown, miR-433-3p overexpression, and respective negative controls (NCs) were synthesized by Genechem (Shanghai, China).

Techniques: Western Blot, Expressing, Knockdown

A LC3B I/II expression in NORAD knockdown SGC-7901-R and KATO III-R cells: LC3B I/II 16/14 kDa, p62 62 kDa, GAPDH 37 kDa. B Autophagy flux was decreased by knocking down NORAD (SGC-7901-R, t = 4.241, P = 0.043; KATO III-R, t = 3.992, P = 0.036) C Expression of autophagy-related genes in NORAD knockdown SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa, ATG10 25 kDa, β-Tubulin 55 kDa. D Starbase prediction for the binding site of NORAD to miR-433-3p; and Starbase prediction for the binding site of miR-433-3p to ATG5 and ATG12. E qRT-PCR to detect the expression of miR-433-3p in gastric cancer compared with GES-1. One-way ANOVA: GES-1 vs SGC-7901, q = 10.37, P < 0.000; GES-1 vs AGS, q = 10.26, P < 0.000; GES-1 vs SNU-1, q = 6.274, P = 0.000; GES-1 vs HGC-27, q = 5.816, P = 0.000; GES-1 vs KATO III, q = 12.27, P < 0.000. F qRT-PCR to detect the expression of miR-433-3p in SGC-7901-R compared with SGC-7901 and KATO III-R compared with KATO III (SGC-7901 vs SGC-7901-R, t = 40.75, P = 0.000; KATO III vs KATO III-R, t = 23.00, P = 0.000). G qRT-PCR to detect the influence of NORAD knockdown on the expression of miR-433-3p in SGC-7901, SGC-7901-R, KATO III, and KATO III-R. (SGC-7901, t = 10.72, P < 0.000; SGC-7901-R, t = 17.31, P < 0.000; KATO III, t = 6.778, P < 0.000; KATO III-R, t = 12.98, P < 0.000). H Dual-luciferase reporter gene assay for NORAD and miR-433-3p (NORAD-Wt vs NORAD-Mut in miR-433-3p group: SGC-7901, t = 10.76, P < 0.000; SGC-7901-R, t = 7.986, P < 0.000; KATO III, t = 6.778, P < 0.000; KATO III-R, t = 12.98, P < 0.000). I RNA pull-down assay for the expression of NORAD in miR-433-3p-Wt and miR-433-3p-Mut group in SGC-7901, SGC-7901-R, KATO III, and KATO III-R (miR-433-3p-Wt vs miR-433-3p -Mut: SGC-7901, t = 9.321, P = 0.001; SGC-7901-R, t = 8.962, P = 0.001; KATO III, t = 10.60, P = 0.000; KATO III-R, t = 19.07, P = 0.000). J RIP assay to detect the enrichment of miR-433-3p (NORAD-Wt vs NORAD-Mut: SGC-7901, t = 32.111, P = 0.000; SGC-7901-R, t = 15.12, P = 0.000; KATO III, t = 24.21, P = 0.000; KATO III-R, t = 13.22, P = 0.000).

Journal: Cell Death & Disease

Article Title: Oxidative stress activates NORAD expression by H3K27ac and promotes oxaliplatin resistance in gastric cancer by enhancing autophagy flux via targeting the miR-433-3p

doi: 10.1038/s41419-020-03368-y

Figure Lengend Snippet: A LC3B I/II expression in NORAD knockdown SGC-7901-R and KATO III-R cells: LC3B I/II 16/14 kDa, p62 62 kDa, GAPDH 37 kDa. B Autophagy flux was decreased by knocking down NORAD (SGC-7901-R, t = 4.241, P = 0.043; KATO III-R, t = 3.992, P = 0.036) C Expression of autophagy-related genes in NORAD knockdown SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa, ATG10 25 kDa, β-Tubulin 55 kDa. D Starbase prediction for the binding site of NORAD to miR-433-3p; and Starbase prediction for the binding site of miR-433-3p to ATG5 and ATG12. E qRT-PCR to detect the expression of miR-433-3p in gastric cancer compared with GES-1. One-way ANOVA: GES-1 vs SGC-7901, q = 10.37, P < 0.000; GES-1 vs AGS, q = 10.26, P < 0.000; GES-1 vs SNU-1, q = 6.274, P = 0.000; GES-1 vs HGC-27, q = 5.816, P = 0.000; GES-1 vs KATO III, q = 12.27, P < 0.000. F qRT-PCR to detect the expression of miR-433-3p in SGC-7901-R compared with SGC-7901 and KATO III-R compared with KATO III (SGC-7901 vs SGC-7901-R, t = 40.75, P = 0.000; KATO III vs KATO III-R, t = 23.00, P = 0.000). G qRT-PCR to detect the influence of NORAD knockdown on the expression of miR-433-3p in SGC-7901, SGC-7901-R, KATO III, and KATO III-R. (SGC-7901, t = 10.72, P < 0.000; SGC-7901-R, t = 17.31, P < 0.000; KATO III, t = 6.778, P < 0.000; KATO III-R, t = 12.98, P < 0.000). H Dual-luciferase reporter gene assay for NORAD and miR-433-3p (NORAD-Wt vs NORAD-Mut in miR-433-3p group: SGC-7901, t = 10.76, P < 0.000; SGC-7901-R, t = 7.986, P < 0.000; KATO III, t = 6.778, P < 0.000; KATO III-R, t = 12.98, P < 0.000). I RNA pull-down assay for the expression of NORAD in miR-433-3p-Wt and miR-433-3p-Mut group in SGC-7901, SGC-7901-R, KATO III, and KATO III-R (miR-433-3p-Wt vs miR-433-3p -Mut: SGC-7901, t = 9.321, P = 0.001; SGC-7901-R, t = 8.962, P = 0.001; KATO III, t = 10.60, P = 0.000; KATO III-R, t = 19.07, P = 0.000). J RIP assay to detect the enrichment of miR-433-3p (NORAD-Wt vs NORAD-Mut: SGC-7901, t = 32.111, P = 0.000; SGC-7901-R, t = 15.12, P = 0.000; KATO III, t = 24.21, P = 0.000; KATO III-R, t = 13.22, P = 0.000).

Article Snippet: Lentiviral constructs for NORAD and miR-433-3p knockdown, miR-433-3p overexpression, and respective negative controls (NCs) were synthesized by Genechem (Shanghai, China).

Techniques: Expressing, Knockdown, Binding Assay, Quantitative RT-PCR, Luciferase, Reporter Gene Assay, Pull Down Assay

A Expression of ATG5 and ATG12 in miR-433-3p upregulated SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, GAPDH 37 kDa. B Expression of ATG5 and ATG12 in miR-433-3p knockdown SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa. C Dual-luciferase reporter gene assay for miR-433-3p and ATG12 in SGC-7901-R ( t = 8.789, P < 0.000) and KATO III-R ( t = 15.29, P < 0.000). D Dual-luciferase reporter gene assay for miR-433-3p and ATG5 in SGC-7901-R ( t = 2.260, P = 0.105) and KATO III-R ( t = 7.296, P = 0.002). E Expression of ATG5 and ATG12 in NORAD-Wt(containing the binding site for miR-433-3p) upregulated SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa. F Expression of ATG5 and ATG12 in NORAD-Mut (containing the binding site for miR-433-3p) upregulated SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa. G miR-433-3p knockdown could reverse the downregulation of ATG12 and ATG5 that was induced by NORAD knockdown. Group A: NORAD knockdown + miR-433-3p knockdown; Group B: NORAD knockdown; Group C: miR-433-3p knockdown.

Journal: Cell Death & Disease

Article Title: Oxidative stress activates NORAD expression by H3K27ac and promotes oxaliplatin resistance in gastric cancer by enhancing autophagy flux via targeting the miR-433-3p

doi: 10.1038/s41419-020-03368-y

Figure Lengend Snippet: A Expression of ATG5 and ATG12 in miR-433-3p upregulated SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, GAPDH 37 kDa. B Expression of ATG5 and ATG12 in miR-433-3p knockdown SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa. C Dual-luciferase reporter gene assay for miR-433-3p and ATG12 in SGC-7901-R ( t = 8.789, P < 0.000) and KATO III-R ( t = 15.29, P < 0.000). D Dual-luciferase reporter gene assay for miR-433-3p and ATG5 in SGC-7901-R ( t = 2.260, P = 0.105) and KATO III-R ( t = 7.296, P = 0.002). E Expression of ATG5 and ATG12 in NORAD-Wt(containing the binding site for miR-433-3p) upregulated SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa. F Expression of ATG5 and ATG12 in NORAD-Mut (containing the binding site for miR-433-3p) upregulated SGC-7901-R and KATO III-R cell line: ATG5(ATG5-ATG12 complex) 55 kDa, ATG12(free ATG12) 16 kDa, ATG 78 kDa, GAPDH 37 kDa. G miR-433-3p knockdown could reverse the downregulation of ATG12 and ATG5 that was induced by NORAD knockdown. Group A: NORAD knockdown + miR-433-3p knockdown; Group B: NORAD knockdown; Group C: miR-433-3p knockdown.

Article Snippet: Lentiviral constructs for NORAD and miR-433-3p knockdown, miR-433-3p overexpression, and respective negative controls (NCs) were synthesized by Genechem (Shanghai, China).

Techniques: Expressing, Knockdown, Luciferase, Reporter Gene Assay, Binding Assay

A Xenograft tumors from 10 nude mice’ right flank. SGC-7901 and SGC-7901-R was used to produce the xenograft tumors. B Estimated volumes of xenograft tumors: volume = π/6 × width 2 × length ( t = 4.383, P = 0.002). C NORAD ( t = 14.52, P = 0.001) and miR-433-3p ( t = 4.98, P = 0.031) expression in SGC-7901 and SGC-7901-R generated xenograft tumors. D Xenograft tumors from 10 nude mice’ right flank. SGC-7901-R transduced with NORAD knockdown lentivirus and relevant NC cells were used to produce the xenograft tumors. E Estimated volumes of xenograft tumors: volume = π/6 × width 2 × length ( t = 5.489, P = 0.007).

Journal: Cell Death & Disease

Article Title: Oxidative stress activates NORAD expression by H3K27ac and promotes oxaliplatin resistance in gastric cancer by enhancing autophagy flux via targeting the miR-433-3p

doi: 10.1038/s41419-020-03368-y

Figure Lengend Snippet: A Xenograft tumors from 10 nude mice’ right flank. SGC-7901 and SGC-7901-R was used to produce the xenograft tumors. B Estimated volumes of xenograft tumors: volume = π/6 × width 2 × length ( t = 4.383, P = 0.002). C NORAD ( t = 14.52, P = 0.001) and miR-433-3p ( t = 4.98, P = 0.031) expression in SGC-7901 and SGC-7901-R generated xenograft tumors. D Xenograft tumors from 10 nude mice’ right flank. SGC-7901-R transduced with NORAD knockdown lentivirus and relevant NC cells were used to produce the xenograft tumors. E Estimated volumes of xenograft tumors: volume = π/6 × width 2 × length ( t = 5.489, P = 0.007).

Article Snippet: Lentiviral constructs for NORAD and miR-433-3p knockdown, miR-433-3p overexpression, and respective negative controls (NCs) were synthesized by Genechem (Shanghai, China).

Techniques: Expressing, Generated, Transduction, Knockdown

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