cells with etoposide Search Results


huh7  (FUJIFILM)
90
FUJIFILM huh7
A, FACS analyses showed that the sub-G1 phase <t>HuH7</t> cell population increased from approximately 0.7% to 7.7%, and cells in the G1 phase increased from approximately 69% to 87% 48 h after TGF-β1 treatment. Data represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05). B, Cdc2 kinase activity was determined based on the level of phosphorylated histone H1 using histone H1 as a substrate. Cdc2 was activated 48 h after TGF-β1 treatment in HuH7 cells. However, cdc2 was not activated in HuH7R cells, which were isolated as an apoptosis-resistant clone from TGF-β1-treated HuH7 cells. Roscovitine (Ros)-pretreated HuH7 cells did not show cdc2 activation. A representative image from three independent experiments is shown. C, After TGF-β1 treatment (48 h), we observed cdc2 Tyr15 dephosphorylation in association with Wee1 kinase down-regulation in apoptotic cells. Pretreatment with 20 µM roscovitine completely abolished apoptosis and restored Wee1 kinase expression. TGF-β1 treatment induced G1 cell cycle arrest in HuH7R cells; however, Wee1 kinase expression and non-phosphorylated cdc2 Tyr 15 were similar to those of roscovitine-pretreated HuH7 cells. A representative image of three experiments is shown. D, Wee1 down-regulation and cdc2 Tyr15 dephosphorylation commenced approximately 24 h after TGF-β1 treatment, which was similar to thea initiation of apoptosis. A representative Western blot image is shown in the upper panels. The results in the lower graphs represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05).
Huh7, supplied by FUJIFILM, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cells+with+etoposide/pmc04069002-13-6-14?v=FUJIFILM
Average 90 stars, based on 1 article reviews
huh7 - by Bioz Stars, 2026-08
90/100 stars
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etoposide resistant cell line cem vm-1  (CEM Corporation)
90
CEM Corporation etoposide resistant cell line cem vm-1
(A) Parental CEM and doxorubicin-resistant CEM (CEM DoxR ) were incubated with indicated dose of doxorubicin, CD95L, TRAIL or MPA for 48 hours. Cell death was measured using a MTT assay. (B) Flow cytometry analysis of the CD95 expression on the doxorubicin-resistant CEM. (C) Parental Jurkat and the selected doxorubicin resistant clones (Jurkat DoxR ) were incubated for 48 hours with doxorubicin and MPA at the indicated concentrations. MTT assay was performed to quantify cell death. (D) CEM and the <t>etoposide</t> resistant CEM-VM1 were incubated with the etoposide or MPA for 48 hours and cell death was assessed using MTT assay. Results shown represent the mean±SD of three independent experiments.
Etoposide Resistant Cell Line Cem Vm 1, supplied by CEM Corporation, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cells+with+etoposide/pmc02675064-109-2-6?v=CEM+Corporation
Average 90 stars, based on 1 article reviews
etoposide resistant cell line cem vm-1 - by Bioz Stars, 2026-08
90/100 stars
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etoposide-resistant h69 cells  (Marburg GmbH)
90
Marburg GmbH etoposide-resistant h69 cells
(A) Parental CEM and doxorubicin-resistant CEM (CEM DoxR ) were incubated with indicated dose of doxorubicin, CD95L, TRAIL or MPA for 48 hours. Cell death was measured using a MTT assay. (B) Flow cytometry analysis of the CD95 expression on the doxorubicin-resistant CEM. (C) Parental Jurkat and the selected doxorubicin resistant clones (Jurkat DoxR ) were incubated for 48 hours with doxorubicin and MPA at the indicated concentrations. MTT assay was performed to quantify cell death. (D) CEM and the <t>etoposide</t> resistant CEM-VM1 were incubated with the etoposide or MPA for 48 hours and cell death was assessed using MTT assay. Results shown represent the mean±SD of three independent experiments.
Etoposide Resistant H69 Cells, supplied by Marburg GmbH, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cells+with+etoposide/pm22237453-49-5-14?v=Marburg+GmbH
Average 90 stars, based on 1 article reviews
etoposide-resistant h69 cells - by Bioz Stars, 2026-08
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hela cell nuclear extract etoposide stimulated  (Rockland Immunochemicals)
N/A
HeLa Cell Nuclear Extract - Etoposide Stimulated - W09-001-A83
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hela whole cell lysate etoposide stimulated  (Rockland Immunochemicals)
N/A
HeLa Whole Cell Lysate - Etoposide Stimulated - W09-001-A80
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human etoposide-stimulated hela whole cell lysate  (Innovative Research Inc)
N/A
Human Etoposide-Stimulated HeLa Whole Cell Lysate from Innovative Research is provided as a Liquid (sterile filtered). Store at -70°C or below. If not using the entire volume immediately, store single-use aliquots to avoid repeated freeze/thaw
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hela cell nuclear extract - etoposide stimulated  (Aviva Systems)
N/A
Ready-to-use nuclear extracts produced by We are derived from cell lines or tissues using highly refined extraction protocols to ensure exceptionally high quality, protein integrity and lot-to-lot reproducibility. All extracts are tested by SDS-PAGE using
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hela whole cell lysate - etoposide stimulated  (Aviva Systems)
N/A
Ready-to-use whole cell lysates produced by We are derived from cell lines or tissues using highly refined extraction protocols to ensure exceptionally high quality, protein integrity and lot-to-lot reproducibility. All extracts are tested by SDS-PAGE
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Image Search Results


A, FACS analyses showed that the sub-G1 phase HuH7 cell population increased from approximately 0.7% to 7.7%, and cells in the G1 phase increased from approximately 69% to 87% 48 h after TGF-β1 treatment. Data represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05). B, Cdc2 kinase activity was determined based on the level of phosphorylated histone H1 using histone H1 as a substrate. Cdc2 was activated 48 h after TGF-β1 treatment in HuH7 cells. However, cdc2 was not activated in HuH7R cells, which were isolated as an apoptosis-resistant clone from TGF-β1-treated HuH7 cells. Roscovitine (Ros)-pretreated HuH7 cells did not show cdc2 activation. A representative image from three independent experiments is shown. C, After TGF-β1 treatment (48 h), we observed cdc2 Tyr15 dephosphorylation in association with Wee1 kinase down-regulation in apoptotic cells. Pretreatment with 20 µM roscovitine completely abolished apoptosis and restored Wee1 kinase expression. TGF-β1 treatment induced G1 cell cycle arrest in HuH7R cells; however, Wee1 kinase expression and non-phosphorylated cdc2 Tyr 15 were similar to those of roscovitine-pretreated HuH7 cells. A representative image of three experiments is shown. D, Wee1 down-regulation and cdc2 Tyr15 dephosphorylation commenced approximately 24 h after TGF-β1 treatment, which was similar to thea initiation of apoptosis. A representative Western blot image is shown in the upper panels. The results in the lower graphs represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05).

Journal: PLoS ONE

Article Title: Efficient Induction of Apoptosis by Wee1 Kinase Inhibition in Hepatocellular Carcinoma Cells

doi: 10.1371/journal.pone.0100495

Figure Lengend Snippet: A, FACS analyses showed that the sub-G1 phase HuH7 cell population increased from approximately 0.7% to 7.7%, and cells in the G1 phase increased from approximately 69% to 87% 48 h after TGF-β1 treatment. Data represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05). B, Cdc2 kinase activity was determined based on the level of phosphorylated histone H1 using histone H1 as a substrate. Cdc2 was activated 48 h after TGF-β1 treatment in HuH7 cells. However, cdc2 was not activated in HuH7R cells, which were isolated as an apoptosis-resistant clone from TGF-β1-treated HuH7 cells. Roscovitine (Ros)-pretreated HuH7 cells did not show cdc2 activation. A representative image from three independent experiments is shown. C, After TGF-β1 treatment (48 h), we observed cdc2 Tyr15 dephosphorylation in association with Wee1 kinase down-regulation in apoptotic cells. Pretreatment with 20 µM roscovitine completely abolished apoptosis and restored Wee1 kinase expression. TGF-β1 treatment induced G1 cell cycle arrest in HuH7R cells; however, Wee1 kinase expression and non-phosphorylated cdc2 Tyr 15 were similar to those of roscovitine-pretreated HuH7 cells. A representative image of three experiments is shown. D, Wee1 down-regulation and cdc2 Tyr15 dephosphorylation commenced approximately 24 h after TGF-β1 treatment, which was similar to thea initiation of apoptosis. A representative Western blot image is shown in the upper panels. The results in the lower graphs represent the means ± S.D. of three experiments. * indicates significant differences between each group (P<0.05).

Article Snippet: The human hepatocellular carcinoma cell line, HuH7, was purchased from the Riken Cell Bank (Wako, Saitama, Japan).

Techniques: Activity Assay, Isolation, Activation Assay, De-Phosphorylation Assay, Expressing, Western Blot

A, The number of sub-G1 HuH7 cells significantly increased after PD166285 treatment (200 nM). PD166285-mediated apoptosis of HuH7 cells was completely inhibited by pretreatment with 20 µM roscovitine (Ros). * indicates significant differences between each group (P<0.05). The results are presented as means ± S.D. of three experiments. B, PD166285 decreased the number of HuH7 cells in a concentration-dependent manner after 72 h. * indicates significant differences between each group (P<0.05). The representative results of three independent experiments are shown. C and D, Wee1 kinase-specific siRNAs (18-2 or 18-3) significantly reduced the total number of cells and increased the sub-G1 cell population 48 h after transfection in a concentration-dependent manner compared with control-vector transfectants. * indicates significant differences between each group (P<0.05).

Journal: PLoS ONE

Article Title: Efficient Induction of Apoptosis by Wee1 Kinase Inhibition in Hepatocellular Carcinoma Cells

doi: 10.1371/journal.pone.0100495

Figure Lengend Snippet: A, The number of sub-G1 HuH7 cells significantly increased after PD166285 treatment (200 nM). PD166285-mediated apoptosis of HuH7 cells was completely inhibited by pretreatment with 20 µM roscovitine (Ros). * indicates significant differences between each group (P<0.05). The results are presented as means ± S.D. of three experiments. B, PD166285 decreased the number of HuH7 cells in a concentration-dependent manner after 72 h. * indicates significant differences between each group (P<0.05). The representative results of three independent experiments are shown. C and D, Wee1 kinase-specific siRNAs (18-2 or 18-3) significantly reduced the total number of cells and increased the sub-G1 cell population 48 h after transfection in a concentration-dependent manner compared with control-vector transfectants. * indicates significant differences between each group (P<0.05).

Article Snippet: The human hepatocellular carcinoma cell line, HuH7, was purchased from the Riken Cell Bank (Wako, Saitama, Japan).

Techniques: Concentration Assay, Transfection, Plasmid Preparation

(A) Parental CEM and doxorubicin-resistant CEM (CEM DoxR ) were incubated with indicated dose of doxorubicin, CD95L, TRAIL or MPA for 48 hours. Cell death was measured using a MTT assay. (B) Flow cytometry analysis of the CD95 expression on the doxorubicin-resistant CEM. (C) Parental Jurkat and the selected doxorubicin resistant clones (Jurkat DoxR ) were incubated for 48 hours with doxorubicin and MPA at the indicated concentrations. MTT assay was performed to quantify cell death. (D) CEM and the etoposide resistant CEM-VM1 were incubated with the etoposide or MPA for 48 hours and cell death was assessed using MTT assay. Results shown represent the mean±SD of three independent experiments.

Journal: PLoS ONE

Article Title: The Necrotic Signal Induced by Mycophenolic Acid Overcomes Apoptosis-Resistance in Tumor Cells

doi: 10.1371/journal.pone.0005493

Figure Lengend Snippet: (A) Parental CEM and doxorubicin-resistant CEM (CEM DoxR ) were incubated with indicated dose of doxorubicin, CD95L, TRAIL or MPA for 48 hours. Cell death was measured using a MTT assay. (B) Flow cytometry analysis of the CD95 expression on the doxorubicin-resistant CEM. (C) Parental Jurkat and the selected doxorubicin resistant clones (Jurkat DoxR ) were incubated for 48 hours with doxorubicin and MPA at the indicated concentrations. MTT assay was performed to quantify cell death. (D) CEM and the etoposide resistant CEM-VM1 were incubated with the etoposide or MPA for 48 hours and cell death was assessed using MTT assay. Results shown represent the mean±SD of three independent experiments.

Article Snippet: Using the etoposide resistant cell line CEM VM-1 , we observed that it displayed a similar sensitivity to MPA compared to the parental cell line ( ).

Techniques: Incubation, MTT Assay, Flow Cytometry, Expressing, Clone Assay