human acute t lymphocytic leukemia cell line  (ATCC)


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    ATCC human acute t lymphocytic leukemia cell line
    Niclosamide induces <t>T-ALL</t> cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) <t>Jurkat</t> and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P
    Human Acute T Lymphocytic Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human acute t lymphocytic leukemia cell line/product/ATCC
    Average 94 stars, based on 10 article reviews
    Price from $9.99 to $1999.99
    human acute t lymphocytic leukemia cell line - by Bioz Stars, 2022-12
    94/100 stars

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    1) Product Images from "Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy"

    Article Title: Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy

    Journal: Oncology Reports

    doi: 10.3892/or.2021.8241

    Niclosamide induces T-ALL cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P
    Figure Legend Snippet: Niclosamide induces T-ALL cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Techniques Used: Expressing, Western Blot

    Niclosamide induces T-ALL cell apoptosis in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of Bcl-2, cleaved caspase-3 and caspase-3 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P
    Figure Legend Snippet: Niclosamide induces T-ALL cell apoptosis in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of Bcl-2, cleaved caspase-3 and caspase-3 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Techniques Used: Expressing, Western Blot

    Niclosamide induces apoptosis in T-ALL cells. Jurkat and CCRF-CEM cells were treated with DMSO (vehicle control), and niclosamide for 24 h. (A) Flow cytometric analysis of apoptosis was evaluated by using Annexin V-FITC and PI double staining at 24 h posterior to the treatment. (B) Quantitative analysis of the apoptotic cells from A. The results are expressed as mean ± SEM. ****P
    Figure Legend Snippet: Niclosamide induces apoptosis in T-ALL cells. Jurkat and CCRF-CEM cells were treated with DMSO (vehicle control), and niclosamide for 24 h. (A) Flow cytometric analysis of apoptosis was evaluated by using Annexin V-FITC and PI double staining at 24 h posterior to the treatment. (B) Quantitative analysis of the apoptotic cells from A. The results are expressed as mean ± SEM. ****P

    Techniques Used: Double Staining

    Niclosamide effectively inhibits the viability of T-ALL cells in a dose- and time-dependent manner. Human T-ALL cells were treated with niclosamide for 24 h. Cell viability and proliferation was measured by MTT assays and flow cytometry of Ki-67 staining, respectively. MTT assays showed that niclosamide inhibited the proliferation of (A) Jurkat and (B) CCRF-CEM cells dose-dependently. (C) Jurkat and (D) CCRF-CEM cells were treated with niclosamide for 24, 48 and 72 h. MTT assays showed that niclosamide inhibited the proliferation of Jurkat and CCRF-CEM cells time-dependently. MFI of Ki-67 were examined by flow cytometry after incubation of (E) Jurkat and (F) CCRF-CEM cells treated with different doses of niclosamide for 24 h. Niclosamide treatment effectively inhibited the proliferation of T-ALL cells dose-dependently. The results are expressed as mean ± SEM. *P
    Figure Legend Snippet: Niclosamide effectively inhibits the viability of T-ALL cells in a dose- and time-dependent manner. Human T-ALL cells were treated with niclosamide for 24 h. Cell viability and proliferation was measured by MTT assays and flow cytometry of Ki-67 staining, respectively. MTT assays showed that niclosamide inhibited the proliferation of (A) Jurkat and (B) CCRF-CEM cells dose-dependently. (C) Jurkat and (D) CCRF-CEM cells were treated with niclosamide for 24, 48 and 72 h. MTT assays showed that niclosamide inhibited the proliferation of Jurkat and CCRF-CEM cells time-dependently. MFI of Ki-67 were examined by flow cytometry after incubation of (E) Jurkat and (F) CCRF-CEM cells treated with different doses of niclosamide for 24 h. Niclosamide treatment effectively inhibited the proliferation of T-ALL cells dose-dependently. The results are expressed as mean ± SEM. *P

    Techniques Used: MTT Assay, Flow Cytometry, Staining, Incubation

    2) Product Images from "Deciphering intratumoral heterogeneity using integrated clonal tracking and single-cell transcriptome analyses"

    Article Title: Deciphering intratumoral heterogeneity using integrated clonal tracking and single-cell transcriptome analyses

    Journal: Nature Communications

    doi: 10.1038/s41467-021-26771-1

    Relapsed leukemia cells generate greater clonal dominance in the PDX model than chemotherapy-naïve cells from the same patients. a Human B-ALL cells acquired from two patients at distinct disease stages (chemotherapy naïve and chemotherapy relapsed) were genetically labeled with DNA barcodes and transplanted into irradiated immunocompromised mice. Leukemia progression was monitored through peripheral blood analysis. b Human chimerism of the mouse peripheral blood following transplantation of diagnostic (naïve) and relapsed leukemia cells from the same patients. Each line depicts data from one mouse. c Number of unique DNA barcodes detected in the peripheral blood. Each line depicts data from one mouse. ** P
    Figure Legend Snippet: Relapsed leukemia cells generate greater clonal dominance in the PDX model than chemotherapy-naïve cells from the same patients. a Human B-ALL cells acquired from two patients at distinct disease stages (chemotherapy naïve and chemotherapy relapsed) were genetically labeled with DNA barcodes and transplanted into irradiated immunocompromised mice. Leukemia progression was monitored through peripheral blood analysis. b Human chimerism of the mouse peripheral blood following transplantation of diagnostic (naïve) and relapsed leukemia cells from the same patients. Each line depicts data from one mouse. c Number of unique DNA barcodes detected in the peripheral blood. Each line depicts data from one mouse. ** P

    Techniques Used: Labeling, Irradiation, Mouse Assay, Transplantation Assay, Diagnostic Assay

    3) Product Images from "MicroRNA-223 decreases cell proliferation, migration, invasion, and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O 1"

    Article Title: MicroRNA-223 decreases cell proliferation, migration, invasion, and enhances cell apoptosis in childhood acute lymphoblastic leukemia via targeting Forkhead box O 1

    Journal: Bioscience Reports

    doi: 10.1042/BSR20200485

    miR-223 inhibited the cell proliferation, colony formation ability and promoted cell apoptosis in ALL ( A ) The mRNA expression of miR-223 in CCRF-CEM and NALM-6 cells was detected by qRT-PCR. ( B ) The OD 450 value of CCRF-CEM and NALM-6 cells was determined by MTT assay. ( C ) The number of CCRF-CEM and NALM-6 cell colonies was confirmed by colony formation assay. ( D ) The apoptosis of CCRF-CEM and NALM-6 cells was detected by flow cytometry. **P
    Figure Legend Snippet: miR-223 inhibited the cell proliferation, colony formation ability and promoted cell apoptosis in ALL ( A ) The mRNA expression of miR-223 in CCRF-CEM and NALM-6 cells was detected by qRT-PCR. ( B ) The OD 450 value of CCRF-CEM and NALM-6 cells was determined by MTT assay. ( C ) The number of CCRF-CEM and NALM-6 cell colonies was confirmed by colony formation assay. ( D ) The apoptosis of CCRF-CEM and NALM-6 cells was detected by flow cytometry. **P

    Techniques Used: Expressing, Quantitative RT-PCR, MTT Assay, Colony Assay, Flow Cytometry

    FOXO1 reversed the effects of miR-223 in ALL cells ( A ) The protein expression of FOXO1in NALM-6 cells was detected by Western blot; ** P
    Figure Legend Snippet: FOXO1 reversed the effects of miR-223 in ALL cells ( A ) The protein expression of FOXO1in NALM-6 cells was detected by Western blot; ** P

    Techniques Used: Expressing, Western Blot

    miR-223 inhibited the cell invasion and migration in ALL ( A and B ) The number of invasion and migration cells in CCRF-CEM and NALM-6 cells was measured by transwell assay; magnification, ×200) **P
    Figure Legend Snippet: miR-223 inhibited the cell invasion and migration in ALL ( A and B ) The number of invasion and migration cells in CCRF-CEM and NALM-6 cells was measured by transwell assay; magnification, ×200) **P

    Techniques Used: Migration, Transwell Assay

    4) Product Images from "Extensive Remodeling of the Immune Microenvironment in B-cell Acute Lymphoblastic Leukemia"

    Article Title: Extensive Remodeling of the Immune Microenvironment in B-cell Acute Lymphoblastic Leukemia

    Journal: Cancer cell

    doi: 10.1016/j.ccell.2020.04.015

    Non-classical Monocyte Abundance Predicts Inferior Overall Survival in Pediatric B-ALL Cases. A-B , Kaplan-Meier analysis of newly-diagnosed pediatric B-ALL patient (A) overall survival (OS) and (B) relapse-free survival (RFS). Patients were separated on the basis of absolute monocytosis at disease presentation, with two cohorts absolute monocyte counts (AMC) > 1000 cells/μL and AMC ≤ 1000 cells/μL. Number of patients indicated (n). Log-rank tests of equality were used to compare the differences in survival rates. C-D, Kaplan-Meier analysis of adolescent/young adult (AYA) human B-ALL patient (C) overall survival and (D) ). Monocyte High patients represent the upper-quartile of monocyte scores, and Monocyte Low represents the lower-quartile. Number of patients indicated (n).
    Figure Legend Snippet: Non-classical Monocyte Abundance Predicts Inferior Overall Survival in Pediatric B-ALL Cases. A-B , Kaplan-Meier analysis of newly-diagnosed pediatric B-ALL patient (A) overall survival (OS) and (B) relapse-free survival (RFS). Patients were separated on the basis of absolute monocytosis at disease presentation, with two cohorts absolute monocyte counts (AMC) > 1000 cells/μL and AMC ≤ 1000 cells/μL. Number of patients indicated (n). Log-rank tests of equality were used to compare the differences in survival rates. C-D, Kaplan-Meier analysis of adolescent/young adult (AYA) human B-ALL patient (C) overall survival and (D) ). Monocyte High patients represent the upper-quartile of monocyte scores, and Monocyte Low represents the lower-quartile. Number of patients indicated (n).

    Techniques Used:

    5) Product Images from "Glucocorticoid Resistant Pediatric Acute Lymphoblastic Leukemia Samples Display Altered Splicing Profile and Vulnerability to Spliceosome Modulation"

    Article Title: Glucocorticoid Resistant Pediatric Acute Lymphoblastic Leukemia Samples Display Altered Splicing Profile and Vulnerability to Spliceosome Modulation

    Journal: Cancers

    doi: 10.3390/cancers12030723

    Response of (GC-resistant) T-cell ALL cells to splicing modulation. The figure illustrates the effects of splicing modulation on T-ALL cell lines and primary childhood samples as well as non-malignant specimens. ( A ) Response to Plad-B of GC-sensitive CCRF-CEM-WT cells as well as its GC-resistant sublines: CEM-R30dm, CEM-R5 and CEM-R5C3 in a 72 h MTT assay. The plot depicts the mean ± SD of at least 3 independent experiments. ( B , C ) Time-dependent inhibition of proliferation ( B ) and cell cycle arrest ( C ) induced by treatment with 4 nM Plad-B in CEM-WT and CEM-R30dm. The panel depicts the mean ± SD of 2 independent experiments. T-test was used for ( B ); asterisks in ( B , C ) indicate statistical significance ( p
    Figure Legend Snippet: Response of (GC-resistant) T-cell ALL cells to splicing modulation. The figure illustrates the effects of splicing modulation on T-ALL cell lines and primary childhood samples as well as non-malignant specimens. ( A ) Response to Plad-B of GC-sensitive CCRF-CEM-WT cells as well as its GC-resistant sublines: CEM-R30dm, CEM-R5 and CEM-R5C3 in a 72 h MTT assay. The plot depicts the mean ± SD of at least 3 independent experiments. ( B , C ) Time-dependent inhibition of proliferation ( B ) and cell cycle arrest ( C ) induced by treatment with 4 nM Plad-B in CEM-WT and CEM-R30dm. The panel depicts the mean ± SD of 2 independent experiments. T-test was used for ( B ); asterisks in ( B , C ) indicate statistical significance ( p

    Techniques Used: MTT Assay, Inhibition

    6) Product Images from "ARRB1-promoted NOTCH1 degradation is suppressed by oncomiR miR-223 in T cell acute lymphoblastic leukemia"

    Article Title: ARRB1-promoted NOTCH1 degradation is suppressed by oncomiR miR-223 in T cell acute lymphoblastic leukemia

    Journal: Cancer research

    doi: 10.1158/0008-5472.CAN-19-1471

    ARRB1 inhibits the tumor progression of human T-ALL cells. (A) GFP- and firefly luciferase-tagged Jurkat cells with ARRB1 overexpression (β1) or knockdown (sh-1 and sh-2) were tail-vein injected into irradiated NOD/SCID mice (n=5 per group). Twenty-one days after injection, bioluminescence images were obtained after administrating the mice D-Luciferin sodium salt. Subsequently, the mice were sacrificed, the spleens were spliced and stained with an anti-CD45RA antibody, and the bone marrow of the femurs was flushed out and subjected to anti-GFP immunostaining to assess the leukemia burden. Black scale bar, 500 μm; white scale bar, 100 μm. (B) The histogram shows the scores for the CD45RA + cells in the spleens. Image Pro Plus was used to calculate the scores, and three samples were counted for each group. (C) The histogram shows the rate of the GFP + cells in bone marrow. Three samples were counted for each group. (D) The survival curve of the mice (n=9 per group) tail-vein injected with Jurkat cells that were transduced with retroviruses expressing shRNAs targeting ARRB1, full-length ARRB1 or scrambled sequence expressing vector (scr). (E) CCK8 assay. The effect of ARRB1 overexpression or silencing on the proliferation of the T-ALL cell lines Jurkat, Molt4, and CCRF-CEM. “**” p
    Figure Legend Snippet: ARRB1 inhibits the tumor progression of human T-ALL cells. (A) GFP- and firefly luciferase-tagged Jurkat cells with ARRB1 overexpression (β1) or knockdown (sh-1 and sh-2) were tail-vein injected into irradiated NOD/SCID mice (n=5 per group). Twenty-one days after injection, bioluminescence images were obtained after administrating the mice D-Luciferin sodium salt. Subsequently, the mice were sacrificed, the spleens were spliced and stained with an anti-CD45RA antibody, and the bone marrow of the femurs was flushed out and subjected to anti-GFP immunostaining to assess the leukemia burden. Black scale bar, 500 μm; white scale bar, 100 μm. (B) The histogram shows the scores for the CD45RA + cells in the spleens. Image Pro Plus was used to calculate the scores, and three samples were counted for each group. (C) The histogram shows the rate of the GFP + cells in bone marrow. Three samples were counted for each group. (D) The survival curve of the mice (n=9 per group) tail-vein injected with Jurkat cells that were transduced with retroviruses expressing shRNAs targeting ARRB1, full-length ARRB1 or scrambled sequence expressing vector (scr). (E) CCK8 assay. The effect of ARRB1 overexpression or silencing on the proliferation of the T-ALL cell lines Jurkat, Molt4, and CCRF-CEM. “**” p

    Techniques Used: Luciferase, Over Expression, Injection, Irradiation, Mouse Assay, Staining, Immunostaining, Transduction, Expressing, Sequencing, Plasmid Preparation, CCK-8 Assay

    7) Product Images from "A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions"

    Article Title: A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2018.09.025

    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p
    Figure Legend Snippet: The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p

    Techniques Used: Infection, Immunostaining

    8) Product Images from "A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions"

    Article Title: A Simplified System to Express Circularized Inhibitors of miRNA for Stable and Potent Suppression of miRNA Functions

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2018.09.025

    The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p
    Figure Legend Snippet: The Circular Bulged Anti-miR223 Effectively Antagonizes OncomiR miR223 and Induces Apoptosis in T-ALL Cells (A) Human T-ALL cell lines Jurkat (JK) (a) and CCRF-CEM (CEM) (b) were infected with linBulg223 or cirBulg223 retrovirus, which also expresses RFP. At 48 hr after infection, the cells were fixed and subjected to immunostaining with the cleaved caspase-3 antibody. Cell nuclei were counterstained with DAPI. The cleaved caspase-3-positive cells and their RFP+ and DAPI+ counterparts are indicated by arrows. Assays were done in triplicate. Representative images are shown. Scale bar, 25 μm. (B) Quantitative analysis of apoptosis in the infected (RFP+) cells. *p

    Techniques Used: Infection, Immunostaining

    9) Product Images from "Matrine induced G0/G1 arrest and apoptosis in human acute T-cell lymphoblastic leukemia (T-ALL) cells"

    Article Title: Matrine induced G0/G1 arrest and apoptosis in human acute T-cell lymphoblastic leukemia (T-ALL) cells

    Journal: Bosnian Journal of Basic Medical Sciences

    doi: 10.17305/bjbms.2017.2457

    Hierarchical clustering of the RNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 49 RNAs, 24 were upregulated and 3 were downregulated and exhibited ≥2-fold change in expression relative to the untreated CCRF-CEM control cells. All experiments were performed in triplicate and Hs18s, GAPDH , and HPRT1 were used as housekeeping controls. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. CDKN1A ( p = 0.000159), IL6 ( p = 0.000011), KDR ( p = 0.001288), and VEGFC ( p = 0.000004) gene expressions were prominently upregulated, whereas BCL 2 ( p = 0.002893), CDKN 3 ( p = 0.000024), and E2F 1 ( p = 0.000128) gene expressions were downregulated in matrine-treated CCRF-CEM cells compared with untreated control CCRF-CEM cells.
    Figure Legend Snippet: Hierarchical clustering of the RNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 49 RNAs, 24 were upregulated and 3 were downregulated and exhibited ≥2-fold change in expression relative to the untreated CCRF-CEM control cells. All experiments were performed in triplicate and Hs18s, GAPDH , and HPRT1 were used as housekeeping controls. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. CDKN1A ( p = 0.000159), IL6 ( p = 0.000011), KDR ( p = 0.001288), and VEGFC ( p = 0.000004) gene expressions were prominently upregulated, whereas BCL 2 ( p = 0.002893), CDKN 3 ( p = 0.000024), and E2F 1 ( p = 0.000128) gene expressions were downregulated in matrine-treated CCRF-CEM cells compared with untreated control CCRF-CEM cells.

    Techniques Used: RNA Expression, Expressing

    Hierarchical clustering of the miRNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 44 miRNAs, 42 were downregulated and exhibited ≥2-fold change in expression relative to untreated control CCRF-CEM cells. All experiments were performed in triplicate and RNU6-2 was used as an endogenous control. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. Hsa-miR-376b-3p ( p = 0.008), hsa-miR-106b-3p ( p = 0.028), hsa-miR-20a-3p ( p = 0.014), hsa-miR-519a-3p ( p = 0.00534), and hsa-miR-204-5p ( p = 0.001) expression levels were significantly decreased in the matrine-treated compared to untreated control cells.
    Figure Legend Snippet: Hierarchical clustering of the miRNA expression profiles of CCRF-CEM cells after matrine treatment. From the total of 44 miRNAs, 42 were downregulated and exhibited ≥2-fold change in expression relative to untreated control CCRF-CEM cells. All experiments were performed in triplicate and RNU6-2 was used as an endogenous control. For each treatment group, the cells were treated with 2.5 mg/ml matrine for 48 hours. Hsa-miR-376b-3p ( p = 0.008), hsa-miR-106b-3p ( p = 0.028), hsa-miR-20a-3p ( p = 0.014), hsa-miR-519a-3p ( p = 0.00534), and hsa-miR-204-5p ( p = 0.001) expression levels were significantly decreased in the matrine-treated compared to untreated control cells.

    Techniques Used: Expressing

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    ATCC human acute t lymphocytic leukemia cell line
    Niclosamide induces <t>T-ALL</t> cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) <t>Jurkat</t> and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P
    Human Acute T Lymphocytic Leukemia Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human acute t lymphocytic leukemia cell line/product/ATCC
    Average 94 stars, based on 5 article reviews
    Price from $9.99 to $1999.99
    human acute t lymphocytic leukemia cell line - by Bioz Stars, 2022-12
    94/100 stars
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    Niclosamide induces T-ALL cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Journal: Oncology Reports

    Article Title: Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy

    doi: 10.3892/or.2021.8241

    Figure Lengend Snippet: Niclosamide induces T-ALL cell autophagy in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of LC3B, p62 and ATG5 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Article Snippet: Human T-ALL cell lines Jurkat and CCRF-CEM (obtained from the American Type Culture Collection; ATCC), were kept at 37°C in RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.) supplemented with 10% heat-inactivated fetal bovine serum (FBS; HyClone; GE Healthcare Life Sciences), 1 mM sodium pyruvate (HyClone; GE Healthcare Life Sciences), 100 U/ml penicillin, and 100 µg/ml streptomycin (Invitrogen; Thermo Fisher Scientific, Inc.), and maintained in a humidified atmosphere containing 95% air and 5% CO2.

    Techniques: Expressing, Western Blot

    Niclosamide induces T-ALL cell apoptosis in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of Bcl-2, cleaved caspase-3 and caspase-3 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Journal: Oncology Reports

    Article Title: Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy

    doi: 10.3892/or.2021.8241

    Figure Lengend Snippet: Niclosamide induces T-ALL cell apoptosis in a dose-dependent manner. The cells were treated with different doses of niclosamide for 24 h, and the expression of Bcl-2, cleaved caspase-3 and caspase-3 were measured by western blot analysis in (A) Jurkat and (B) CCRF-CEM cells. β-actin protein was used in these experiments as the loading control. The results are expressed as mean ± SEM. *P

    Article Snippet: Human T-ALL cell lines Jurkat and CCRF-CEM (obtained from the American Type Culture Collection; ATCC), were kept at 37°C in RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.) supplemented with 10% heat-inactivated fetal bovine serum (FBS; HyClone; GE Healthcare Life Sciences), 1 mM sodium pyruvate (HyClone; GE Healthcare Life Sciences), 100 U/ml penicillin, and 100 µg/ml streptomycin (Invitrogen; Thermo Fisher Scientific, Inc.), and maintained in a humidified atmosphere containing 95% air and 5% CO2.

    Techniques: Expressing, Western Blot

    Niclosamide induces apoptosis in T-ALL cells. Jurkat and CCRF-CEM cells were treated with DMSO (vehicle control), and niclosamide for 24 h. (A) Flow cytometric analysis of apoptosis was evaluated by using Annexin V-FITC and PI double staining at 24 h posterior to the treatment. (B) Quantitative analysis of the apoptotic cells from A. The results are expressed as mean ± SEM. ****P

    Journal: Oncology Reports

    Article Title: Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy

    doi: 10.3892/or.2021.8241

    Figure Lengend Snippet: Niclosamide induces apoptosis in T-ALL cells. Jurkat and CCRF-CEM cells were treated with DMSO (vehicle control), and niclosamide for 24 h. (A) Flow cytometric analysis of apoptosis was evaluated by using Annexin V-FITC and PI double staining at 24 h posterior to the treatment. (B) Quantitative analysis of the apoptotic cells from A. The results are expressed as mean ± SEM. ****P

    Article Snippet: Human T-ALL cell lines Jurkat and CCRF-CEM (obtained from the American Type Culture Collection; ATCC), were kept at 37°C in RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.) supplemented with 10% heat-inactivated fetal bovine serum (FBS; HyClone; GE Healthcare Life Sciences), 1 mM sodium pyruvate (HyClone; GE Healthcare Life Sciences), 100 U/ml penicillin, and 100 µg/ml streptomycin (Invitrogen; Thermo Fisher Scientific, Inc.), and maintained in a humidified atmosphere containing 95% air and 5% CO2.

    Techniques: Double Staining

    Niclosamide effectively inhibits the viability of T-ALL cells in a dose- and time-dependent manner. Human T-ALL cells were treated with niclosamide for 24 h. Cell viability and proliferation was measured by MTT assays and flow cytometry of Ki-67 staining, respectively. MTT assays showed that niclosamide inhibited the proliferation of (A) Jurkat and (B) CCRF-CEM cells dose-dependently. (C) Jurkat and (D) CCRF-CEM cells were treated with niclosamide for 24, 48 and 72 h. MTT assays showed that niclosamide inhibited the proliferation of Jurkat and CCRF-CEM cells time-dependently. MFI of Ki-67 were examined by flow cytometry after incubation of (E) Jurkat and (F) CCRF-CEM cells treated with different doses of niclosamide for 24 h. Niclosamide treatment effectively inhibited the proliferation of T-ALL cells dose-dependently. The results are expressed as mean ± SEM. *P

    Journal: Oncology Reports

    Article Title: Niclosamide suppresses T-cell acute lymphoblastic leukemia growth through activation of apoptosis and autophagy

    doi: 10.3892/or.2021.8241

    Figure Lengend Snippet: Niclosamide effectively inhibits the viability of T-ALL cells in a dose- and time-dependent manner. Human T-ALL cells were treated with niclosamide for 24 h. Cell viability and proliferation was measured by MTT assays and flow cytometry of Ki-67 staining, respectively. MTT assays showed that niclosamide inhibited the proliferation of (A) Jurkat and (B) CCRF-CEM cells dose-dependently. (C) Jurkat and (D) CCRF-CEM cells were treated with niclosamide for 24, 48 and 72 h. MTT assays showed that niclosamide inhibited the proliferation of Jurkat and CCRF-CEM cells time-dependently. MFI of Ki-67 were examined by flow cytometry after incubation of (E) Jurkat and (F) CCRF-CEM cells treated with different doses of niclosamide for 24 h. Niclosamide treatment effectively inhibited the proliferation of T-ALL cells dose-dependently. The results are expressed as mean ± SEM. *P

    Article Snippet: Human T-ALL cell lines Jurkat and CCRF-CEM (obtained from the American Type Culture Collection; ATCC), were kept at 37°C in RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.) supplemented with 10% heat-inactivated fetal bovine serum (FBS; HyClone; GE Healthcare Life Sciences), 1 mM sodium pyruvate (HyClone; GE Healthcare Life Sciences), 100 U/ml penicillin, and 100 µg/ml streptomycin (Invitrogen; Thermo Fisher Scientific, Inc.), and maintained in a humidified atmosphere containing 95% air and 5% CO2.

    Techniques: MTT Assay, Flow Cytometry, Staining, Incubation

    Relapsed leukemia cells generate greater clonal dominance in the PDX model than chemotherapy-naïve cells from the same patients. a Human B-ALL cells acquired from two patients at distinct disease stages (chemotherapy naïve and chemotherapy relapsed) were genetically labeled with DNA barcodes and transplanted into irradiated immunocompromised mice. Leukemia progression was monitored through peripheral blood analysis. b Human chimerism of the mouse peripheral blood following transplantation of diagnostic (naïve) and relapsed leukemia cells from the same patients. Each line depicts data from one mouse. c Number of unique DNA barcodes detected in the peripheral blood. Each line depicts data from one mouse. ** P

    Journal: Nature Communications

    Article Title: Deciphering intratumoral heterogeneity using integrated clonal tracking and single-cell transcriptome analyses

    doi: 10.1038/s41467-021-26771-1

    Figure Lengend Snippet: Relapsed leukemia cells generate greater clonal dominance in the PDX model than chemotherapy-naïve cells from the same patients. a Human B-ALL cells acquired from two patients at distinct disease stages (chemotherapy naïve and chemotherapy relapsed) were genetically labeled with DNA barcodes and transplanted into irradiated immunocompromised mice. Leukemia progression was monitored through peripheral blood analysis. b Human chimerism of the mouse peripheral blood following transplantation of diagnostic (naïve) and relapsed leukemia cells from the same patients. Each line depicts data from one mouse. c Number of unique DNA barcodes detected in the peripheral blood. Each line depicts data from one mouse. ** P

    Article Snippet: Cas9 and sgRNA double transduced human B-ALL cells were cocultured with irradiated (5,000 cGy) OP9 mouse bone marrow stroma cells (ATCC) for 48 h at 37 °C under humidified 5% CO2 condition.

    Techniques: Labeling, Irradiation, Mouse Assay, Transplantation Assay, Diagnostic Assay