u87 cells  (Boster Bio)


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    Boster Bio u87 cells
    Effect of GASC1 inhibition on key markers of GSC stemness-related signaling pathways. (A) Protein expression levels of key markers of GSC stemness-related signaling pathways, such as Gli1 (Shh), Hes1 (NOTCH) and β-catenin (Wnt) in GASC1-knockdown or vector CD133 + <t>U87</t> or U251 glioma cells. Decreased Gli1, Hes1 and β-catenin protein expression levels were observed in GASC1-knockdown CD133 + U87 glioma cells. (B) GASC1-knockdown decreased Gli1, Hes1 and β-catenin mRNA expression levels in CD133+ U87 or U251 glioma cells. One-way ANOVA followed by Tukey's post hoc test. (C) Effect of GASC1 inhibitor CA, NOTCH1 inhibitor DAPT and NOTCH1 overexpression on the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. The parental or NOTCH1-overexpressing CD133 + U87 or U251 cells were cultured with GASC1 inhibitor CA (10 µm) for 48 h for the tumorsphere assay. The CD133 + U87 or U251 cells were also treated with GASC1 inhibitor CA (10 µm) in the presence or absence of NOTCH1 inhibitor DAPT (10 µm) for 48 h, followed by the tumorsphere assay. NOTCH1-overexpression partly abrogated the CA-induced tumorsphere formation inhibition. NOTCH1 inhibitor DAPT enhanced the suppressive effect of the GASC1 inhibitor on the tumorsphere formation of CD133 + U87 or U251 cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P
    U87 Cells, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    u87 cells - by Bioz Stars, 2022-05
    93/100 stars

    Images

    1) Product Images from "GASC1 promotes glioma progression by enhancing NOTCH1 signaling"

    Article Title: GASC1 promotes glioma progression by enhancing NOTCH1 signaling

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2021.11949

    Effect of GASC1 inhibition on key markers of GSC stemness-related signaling pathways. (A) Protein expression levels of key markers of GSC stemness-related signaling pathways, such as Gli1 (Shh), Hes1 (NOTCH) and β-catenin (Wnt) in GASC1-knockdown or vector CD133 + U87 or U251 glioma cells. Decreased Gli1, Hes1 and β-catenin protein expression levels were observed in GASC1-knockdown CD133 + U87 glioma cells. (B) GASC1-knockdown decreased Gli1, Hes1 and β-catenin mRNA expression levels in CD133+ U87 or U251 glioma cells. One-way ANOVA followed by Tukey's post hoc test. (C) Effect of GASC1 inhibitor CA, NOTCH1 inhibitor DAPT and NOTCH1 overexpression on the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. The parental or NOTCH1-overexpressing CD133 + U87 or U251 cells were cultured with GASC1 inhibitor CA (10 µm) for 48 h for the tumorsphere assay. The CD133 + U87 or U251 cells were also treated with GASC1 inhibitor CA (10 µm) in the presence or absence of NOTCH1 inhibitor DAPT (10 µm) for 48 h, followed by the tumorsphere assay. NOTCH1-overexpression partly abrogated the CA-induced tumorsphere formation inhibition. NOTCH1 inhibitor DAPT enhanced the suppressive effect of the GASC1 inhibitor on the tumorsphere formation of CD133 + U87 or U251 cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P
    Figure Legend Snippet: Effect of GASC1 inhibition on key markers of GSC stemness-related signaling pathways. (A) Protein expression levels of key markers of GSC stemness-related signaling pathways, such as Gli1 (Shh), Hes1 (NOTCH) and β-catenin (Wnt) in GASC1-knockdown or vector CD133 + U87 or U251 glioma cells. Decreased Gli1, Hes1 and β-catenin protein expression levels were observed in GASC1-knockdown CD133 + U87 glioma cells. (B) GASC1-knockdown decreased Gli1, Hes1 and β-catenin mRNA expression levels in CD133+ U87 or U251 glioma cells. One-way ANOVA followed by Tukey's post hoc test. (C) Effect of GASC1 inhibitor CA, NOTCH1 inhibitor DAPT and NOTCH1 overexpression on the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. The parental or NOTCH1-overexpressing CD133 + U87 or U251 cells were cultured with GASC1 inhibitor CA (10 µm) for 48 h for the tumorsphere assay. The CD133 + U87 or U251 cells were also treated with GASC1 inhibitor CA (10 µm) in the presence or absence of NOTCH1 inhibitor DAPT (10 µm) for 48 h, followed by the tumorsphere assay. NOTCH1-overexpression partly abrogated the CA-induced tumorsphere formation inhibition. NOTCH1 inhibitor DAPT enhanced the suppressive effect of the GASC1 inhibitor on the tumorsphere formation of CD133 + U87 or U251 cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Techniques Used: Inhibition, Expressing, Plasmid Preparation, Over Expression, Cell Culture

    GASC1 inhibition suppresses invasion and metastasis ability in CD133 + U87 or U251 glioma stem-like cells. (A) Invasion chamber assay and wound healing migration assay for PCGCs with or without GASC1-knockdown. For the invasion chamber assay, a hollow plastic chamber sealed at one end with a porous membrane was suspended over a larger well containing cell culture medium. Cells were placed inside the chamber and allowed to migrate through the pores to the other side of the membrane for 48 h. Migratory cells were then stained and counted. For the wound healing migration assay, cells were plated in 24-well plates after they grew to 70–90% confluence. A scratch wound was made using a same pipette tip. The medium was replaced, and the wounds were imaged at 48 h. (B) The relative fractions for invasion and (C) migration detection in GASC1-specific shRNA, vector and control cells were plotted. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P
    Figure Legend Snippet: GASC1 inhibition suppresses invasion and metastasis ability in CD133 + U87 or U251 glioma stem-like cells. (A) Invasion chamber assay and wound healing migration assay for PCGCs with or without GASC1-knockdown. For the invasion chamber assay, a hollow plastic chamber sealed at one end with a porous membrane was suspended over a larger well containing cell culture medium. Cells were placed inside the chamber and allowed to migrate through the pores to the other side of the membrane for 48 h. Migratory cells were then stained and counted. For the wound healing migration assay, cells were plated in 24-well plates after they grew to 70–90% confluence. A scratch wound was made using a same pipette tip. The medium was replaced, and the wounds were imaged at 48 h. (B) The relative fractions for invasion and (C) migration detection in GASC1-specific shRNA, vector and control cells were plotted. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Techniques Used: Inhibition, Invasion Chamber Assay, Migration, Cell Culture, Staining, Transferring, shRNA, Plasmid Preparation

    Characterization of PCGCs and CD133 + PCGC spheres. (A) Representative microscopic images of PCGCs and tumorspheres of CD133 + PCGCs (scale bar, 50 µm). Fresh primary glioma samples were dissociated and propagated as non-adherent neurospheres in serum-free defined medium. (B) Western blotting of GASC1 expression in CD133 + or parental PCGC. A higher GASC1 protein expression was observed in the CD133 + PCGC. (C) Reverse transcription-quantitative polymerase chain reaction of GASC1 mRNA expression levels in CD133 + or parental U87, U251 and PCGC. Data are expressed as the mean±SEM (n=3). Unpaired Student t-test, *P
    Figure Legend Snippet: Characterization of PCGCs and CD133 + PCGC spheres. (A) Representative microscopic images of PCGCs and tumorspheres of CD133 + PCGCs (scale bar, 50 µm). Fresh primary glioma samples were dissociated and propagated as non-adherent neurospheres in serum-free defined medium. (B) Western blotting of GASC1 expression in CD133 + or parental PCGC. A higher GASC1 protein expression was observed in the CD133 + PCGC. (C) Reverse transcription-quantitative polymerase chain reaction of GASC1 mRNA expression levels in CD133 + or parental U87, U251 and PCGC. Data are expressed as the mean±SEM (n=3). Unpaired Student t-test, *P

    Techniques Used: Western Blot, Expressing, Real-time Polymerase Chain Reaction

    GASC1 inhibition suppresses the clone forming ability and tumorsphere formation in CD133 + U87 or U251 glioma stem-like cells. (A) Clonogenic assays examining the effects of GASC1-knockout on cell proliferation in U87 or U251 glioma cells with or without GASC1-knockdown. Cells were seeded into 6-well plates at a density of 500 cells/well and then cultured for 5 days, followed by crystal violet staining. (B) Tumorsphere assay of GASC1-knockout on CD133 + U87 or U251 glioma cells with or without GASC1-knockdown (scale bar, 100 µm). Single cells from tumorspheres were seeded at a density of 20,000 cells/ml in a 10 ml GSC growth medium in a 10-cm culture dish. The cells were incubated at 37°C, 5% CO 2 for 5 days to generate bulk cultured tumorspheres. (C) Representative flow cytometry images of cell cycle distribution and apoptosis in CD133 + U87 or U251 glioma cells with or without GASC1-knockdown. (D) Quantitative analysis for stained colonies and tumorspheres in different group panels. shRNA-mediated GASC1 silencing significantly decreased the cloning ability of U87 or U251 glioma cells and the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P
    Figure Legend Snippet: GASC1 inhibition suppresses the clone forming ability and tumorsphere formation in CD133 + U87 or U251 glioma stem-like cells. (A) Clonogenic assays examining the effects of GASC1-knockout on cell proliferation in U87 or U251 glioma cells with or without GASC1-knockdown. Cells were seeded into 6-well plates at a density of 500 cells/well and then cultured for 5 days, followed by crystal violet staining. (B) Tumorsphere assay of GASC1-knockout on CD133 + U87 or U251 glioma cells with or without GASC1-knockdown (scale bar, 100 µm). Single cells from tumorspheres were seeded at a density of 20,000 cells/ml in a 10 ml GSC growth medium in a 10-cm culture dish. The cells were incubated at 37°C, 5% CO 2 for 5 days to generate bulk cultured tumorspheres. (C) Representative flow cytometry images of cell cycle distribution and apoptosis in CD133 + U87 or U251 glioma cells with or without GASC1-knockdown. (D) Quantitative analysis for stained colonies and tumorspheres in different group panels. shRNA-mediated GASC1 silencing significantly decreased the cloning ability of U87 or U251 glioma cells and the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Techniques Used: Inhibition, Knock-Out, Cell Culture, Staining, Incubation, Flow Cytometry, shRNA, Clone Assay

    2) Product Images from "Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro"

    Article Title: Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro

    Journal: International Journal of Clinical and Experimental Pathology

    doi:

    Effects of RKIP on cells migration in human U87 glioma cell by means of wound healing assay. The relative distance was ratio of experimental group distance vs. the distance of the cell-blank scratch at 12 h, 14 h and 48 h after transfection. * P
    Figure Legend Snippet: Effects of RKIP on cells migration in human U87 glioma cell by means of wound healing assay. The relative distance was ratio of experimental group distance vs. the distance of the cell-blank scratch at 12 h, 14 h and 48 h after transfection. * P

    Techniques Used: Migration, Wound Healing Assay, Transfection

    The effects of RKIP on the proliferation of U87 glioma cells. To determine the effects of RKIP on the ability of proliferation in U87 cells, the MTT assays were carried out to detected the proliferations of cells that over-expressing or down regulating of RKIP. The results showed that RKIP had little effects on the proliferation of U87 glioma cells.
    Figure Legend Snippet: The effects of RKIP on the proliferation of U87 glioma cells. To determine the effects of RKIP on the ability of proliferation in U87 cells, the MTT assays were carried out to detected the proliferations of cells that over-expressing or down regulating of RKIP. The results showed that RKIP had little effects on the proliferation of U87 glioma cells.

    Techniques Used: MTT Assay, Expressing

    Effects of RKIP on cells invasion in human U87 glioma cell by means of Transwell assay. The number of glioma cells cross through the membrane was recorded. * P
    Figure Legend Snippet: Effects of RKIP on cells invasion in human U87 glioma cell by means of Transwell assay. The number of glioma cells cross through the membrane was recorded. * P

    Techniques Used: Transwell Assay

    Effects of over-expressing and knockdown RKIP on protein expression in human U87 glioma cells. A. The RKIP protein relative expressions (vs. GAPDH), B. The protein relative expression of MMP-2, MMP-9 and HMGA2, * P
    Figure Legend Snippet: Effects of over-expressing and knockdown RKIP on protein expression in human U87 glioma cells. A. The RKIP protein relative expressions (vs. GAPDH), B. The protein relative expression of MMP-2, MMP-9 and HMGA2, * P

    Techniques Used: Expressing

    Effects of over-expressing and knockdown RKIP on mRNA expressions in human U87 glioma cells. A. The RKIP mRNA relative expressions (vs. GAPDH), B. The MMP-2 mRNA relative expression (vs. GAPDH), C. The MMP-9 mRNA relative expressions (vs. GAPDH), D. The HMGA2 mRNA relative expression (vs. GAPDH), * P
    Figure Legend Snippet: Effects of over-expressing and knockdown RKIP on mRNA expressions in human U87 glioma cells. A. The RKIP mRNA relative expressions (vs. GAPDH), B. The MMP-2 mRNA relative expression (vs. GAPDH), C. The MMP-9 mRNA relative expressions (vs. GAPDH), D. The HMGA2 mRNA relative expression (vs. GAPDH), * P

    Techniques Used: Expressing

    3) Product Images from "Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway"

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    Journal: Oncotarget

    doi: 10.18632/oncotarget.23317

    Metformin inhibits AKT/mTOR pathway activated by TGF-β1 ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1-induced AKT/mTOR pathway. ( B ) Western blot results of the inhibitory effect of NVP-BEZ235 on N-cadherin, Vimentin and MMP-9 expression in LN18 and U87 cells.
    Figure Legend Snippet: Metformin inhibits AKT/mTOR pathway activated by TGF-β1 ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1-induced AKT/mTOR pathway. ( B ) Western blot results of the inhibitory effect of NVP-BEZ235 on N-cadherin, Vimentin and MMP-9 expression in LN18 and U87 cells.

    Techniques Used: Western Blot, Expressing

    Metformin inhibits TGF-β1-induced EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to metformin for 48 hours. ( B ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) with or without metformin for 48 hours under light microscope (×100 magnification). ( C ) Western blot results of dose-dependent inhibition effect of metformin on N-cadherin, Vimentin expression in LN18 and U87 cells. ( D ) Western blot results of dose-dependent inhibition effect of metformin on Snail, Slug expression in LN18 and U87 cells.
    Figure Legend Snippet: Metformin inhibits TGF-β1-induced EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to metformin for 48 hours. ( B ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) with or without metformin for 48 hours under light microscope (×100 magnification). ( C ) Western blot results of dose-dependent inhibition effect of metformin on N-cadherin, Vimentin expression in LN18 and U87 cells. ( D ) Western blot results of dose-dependent inhibition effect of metformin on Snail, Slug expression in LN18 and U87 cells.

    Techniques Used: MTT Assay, Light Microscopy, Western Blot, Inhibition, Expressing

    Metformin (Met) suppresses TGF-β1-induced cell migration and invasion ( A ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without metformin. Quantification histograms show the mean levels of migration distance observed in three random fields for each condition. ( B ) Representative Transwell photographs show invasion capacity in LN18 and U87 (×100 magnification) cells following exposure to TGF-β1 with or without metformin. Quantification histograms show the mean levels of the numbers of cells counted in five random fields on each filter for each condition. * P
    Figure Legend Snippet: Metformin (Met) suppresses TGF-β1-induced cell migration and invasion ( A ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without metformin. Quantification histograms show the mean levels of migration distance observed in three random fields for each condition. ( B ) Representative Transwell photographs show invasion capacity in LN18 and U87 (×100 magnification) cells following exposure to TGF-β1 with or without metformin. Quantification histograms show the mean levels of the numbers of cells counted in five random fields on each filter for each condition. * P

    Techniques Used: Migration

    Metformin (Met) reduces cancer stem-like properties generated by induction of TGF-β1 ( A ) Metformin inhibited gliosphere formation in LN18 and U87 cells stimulated by exposure to TGF-β1 (10 ng/ml). Representative images of gliosphere were photographed under Olympus microscope (×100 magnification). Histograms show the numbers of gliosphere in different treatment groups. ( B ) Western blot results of inhibitory effect of metformin on stemness-related proteins stimulated by exposure to TGF-β1 in LN18 and U87 cells. ** P
    Figure Legend Snippet: Metformin (Met) reduces cancer stem-like properties generated by induction of TGF-β1 ( A ) Metformin inhibited gliosphere formation in LN18 and U87 cells stimulated by exposure to TGF-β1 (10 ng/ml). Representative images of gliosphere were photographed under Olympus microscope (×100 magnification). Histograms show the numbers of gliosphere in different treatment groups. ( B ) Western blot results of inhibitory effect of metformin on stemness-related proteins stimulated by exposure to TGF-β1 in LN18 and U87 cells. ** P

    Techniques Used: Generated, Microscopy, Western Blot

    ZEB1 is associated with the inhibitory effect of metformin on TGF-β1 induced EMT-like process in GBM cells ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1- induced ZEB1 expression in LN18 and U87 cells. ( B ) Western blot results of the effect of ZEB1 knockdown with two different shRNAs (shZEB1-1 and shZEB1-2) and control shRNA (shCtrl) on expression of ZEB1 in LN18 and U87 cells. ( C ) Western blot results of the effect of ZEB1 knockdown on expression of N-cadherin, Vimentin and MMP-9 induced by TGF-β1. ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without ZEB1 knockdown. Quantification histograms show the mean level of migration distance observed in three random fields for each condition. * P
    Figure Legend Snippet: ZEB1 is associated with the inhibitory effect of metformin on TGF-β1 induced EMT-like process in GBM cells ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1- induced ZEB1 expression in LN18 and U87 cells. ( B ) Western blot results of the effect of ZEB1 knockdown with two different shRNAs (shZEB1-1 and shZEB1-2) and control shRNA (shCtrl) on expression of ZEB1 in LN18 and U87 cells. ( C ) Western blot results of the effect of ZEB1 knockdown on expression of N-cadherin, Vimentin and MMP-9 induced by TGF-β1. ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without ZEB1 knockdown. Quantification histograms show the mean level of migration distance observed in three random fields for each condition. * P

    Techniques Used: Western Blot, Expressing, shRNA, Migration

    TGF-β1 induces an EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to TGF-β1 for 48 hours. ( B ) Western blot results of expressions of EMT-related proteins and transcription factors derived from LN18 and U87 cells treated with increasing concentration of TGF-β1 (0, 5, 10 and 20 ng/ml) for 48 hours. ( C ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) for 48 hours under light microscope (×100 magnification). ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) compared with control group. Histograms show the mean level of migration distance observed in three random fields for each condition. * P
    Figure Legend Snippet: TGF-β1 induces an EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to TGF-β1 for 48 hours. ( B ) Western blot results of expressions of EMT-related proteins and transcription factors derived from LN18 and U87 cells treated with increasing concentration of TGF-β1 (0, 5, 10 and 20 ng/ml) for 48 hours. ( C ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) for 48 hours under light microscope (×100 magnification). ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) compared with control group. Histograms show the mean level of migration distance observed in three random fields for each condition. * P

    Techniques Used: MTT Assay, Western Blot, Derivative Assay, Concentration Assay, Light Microscopy, Migration

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    Boster Bio u87 cells
    Effect of GASC1 inhibition on key markers of GSC stemness-related signaling pathways. (A) Protein expression levels of key markers of GSC stemness-related signaling pathways, such as Gli1 (Shh), Hes1 (NOTCH) and β-catenin (Wnt) in GASC1-knockdown or vector CD133 + <t>U87</t> or U251 glioma cells. Decreased Gli1, Hes1 and β-catenin protein expression levels were observed in GASC1-knockdown CD133 + U87 glioma cells. (B) GASC1-knockdown decreased Gli1, Hes1 and β-catenin mRNA expression levels in CD133+ U87 or U251 glioma cells. One-way ANOVA followed by Tukey's post hoc test. (C) Effect of GASC1 inhibitor CA, NOTCH1 inhibitor DAPT and NOTCH1 overexpression on the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. The parental or NOTCH1-overexpressing CD133 + U87 or U251 cells were cultured with GASC1 inhibitor CA (10 µm) for 48 h for the tumorsphere assay. The CD133 + U87 or U251 cells were also treated with GASC1 inhibitor CA (10 µm) in the presence or absence of NOTCH1 inhibitor DAPT (10 µm) for 48 h, followed by the tumorsphere assay. NOTCH1-overexpression partly abrogated the CA-induced tumorsphere formation inhibition. NOTCH1 inhibitor DAPT enhanced the suppressive effect of the GASC1 inhibitor on the tumorsphere formation of CD133 + U87 or U251 cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P
    U87 Cells, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/u87 cells/product/Boster Bio
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    u87 cells - by Bioz Stars, 2022-05
    93/100 stars
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    Effect of GASC1 inhibition on key markers of GSC stemness-related signaling pathways. (A) Protein expression levels of key markers of GSC stemness-related signaling pathways, such as Gli1 (Shh), Hes1 (NOTCH) and β-catenin (Wnt) in GASC1-knockdown or vector CD133 + U87 or U251 glioma cells. Decreased Gli1, Hes1 and β-catenin protein expression levels were observed in GASC1-knockdown CD133 + U87 glioma cells. (B) GASC1-knockdown decreased Gli1, Hes1 and β-catenin mRNA expression levels in CD133+ U87 or U251 glioma cells. One-way ANOVA followed by Tukey's post hoc test. (C) Effect of GASC1 inhibitor CA, NOTCH1 inhibitor DAPT and NOTCH1 overexpression on the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. The parental or NOTCH1-overexpressing CD133 + U87 or U251 cells were cultured with GASC1 inhibitor CA (10 µm) for 48 h for the tumorsphere assay. The CD133 + U87 or U251 cells were also treated with GASC1 inhibitor CA (10 µm) in the presence or absence of NOTCH1 inhibitor DAPT (10 µm) for 48 h, followed by the tumorsphere assay. NOTCH1-overexpression partly abrogated the CA-induced tumorsphere formation inhibition. NOTCH1 inhibitor DAPT enhanced the suppressive effect of the GASC1 inhibitor on the tumorsphere formation of CD133 + U87 or U251 cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Journal: Molecular Medicine Reports

    Article Title: GASC1 promotes glioma progression by enhancing NOTCH1 signaling

    doi: 10.3892/mmr.2021.11949

    Figure Lengend Snippet: Effect of GASC1 inhibition on key markers of GSC stemness-related signaling pathways. (A) Protein expression levels of key markers of GSC stemness-related signaling pathways, such as Gli1 (Shh), Hes1 (NOTCH) and β-catenin (Wnt) in GASC1-knockdown or vector CD133 + U87 or U251 glioma cells. Decreased Gli1, Hes1 and β-catenin protein expression levels were observed in GASC1-knockdown CD133 + U87 glioma cells. (B) GASC1-knockdown decreased Gli1, Hes1 and β-catenin mRNA expression levels in CD133+ U87 or U251 glioma cells. One-way ANOVA followed by Tukey's post hoc test. (C) Effect of GASC1 inhibitor CA, NOTCH1 inhibitor DAPT and NOTCH1 overexpression on the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. The parental or NOTCH1-overexpressing CD133 + U87 or U251 cells were cultured with GASC1 inhibitor CA (10 µm) for 48 h for the tumorsphere assay. The CD133 + U87 or U251 cells were also treated with GASC1 inhibitor CA (10 µm) in the presence or absence of NOTCH1 inhibitor DAPT (10 µm) for 48 h, followed by the tumorsphere assay. NOTCH1-overexpression partly abrogated the CA-induced tumorsphere formation inhibition. NOTCH1 inhibitor DAPT enhanced the suppressive effect of the GASC1 inhibitor on the tumorsphere formation of CD133 + U87 or U251 cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Article Snippet: CD133+ cell isolation As described in our previous study , U87 cells, U251 cells or human glioma primary culture cells were isolated using CD133 magnetic microbeads.

    Techniques: Inhibition, Expressing, Plasmid Preparation, Over Expression, Cell Culture

    GASC1 inhibition suppresses invasion and metastasis ability in CD133 + U87 or U251 glioma stem-like cells. (A) Invasion chamber assay and wound healing migration assay for PCGCs with or without GASC1-knockdown. For the invasion chamber assay, a hollow plastic chamber sealed at one end with a porous membrane was suspended over a larger well containing cell culture medium. Cells were placed inside the chamber and allowed to migrate through the pores to the other side of the membrane for 48 h. Migratory cells were then stained and counted. For the wound healing migration assay, cells were plated in 24-well plates after they grew to 70–90% confluence. A scratch wound was made using a same pipette tip. The medium was replaced, and the wounds were imaged at 48 h. (B) The relative fractions for invasion and (C) migration detection in GASC1-specific shRNA, vector and control cells were plotted. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Journal: Molecular Medicine Reports

    Article Title: GASC1 promotes glioma progression by enhancing NOTCH1 signaling

    doi: 10.3892/mmr.2021.11949

    Figure Lengend Snippet: GASC1 inhibition suppresses invasion and metastasis ability in CD133 + U87 or U251 glioma stem-like cells. (A) Invasion chamber assay and wound healing migration assay for PCGCs with or without GASC1-knockdown. For the invasion chamber assay, a hollow plastic chamber sealed at one end with a porous membrane was suspended over a larger well containing cell culture medium. Cells were placed inside the chamber and allowed to migrate through the pores to the other side of the membrane for 48 h. Migratory cells were then stained and counted. For the wound healing migration assay, cells were plated in 24-well plates after they grew to 70–90% confluence. A scratch wound was made using a same pipette tip. The medium was replaced, and the wounds were imaged at 48 h. (B) The relative fractions for invasion and (C) migration detection in GASC1-specific shRNA, vector and control cells were plotted. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Article Snippet: CD133+ cell isolation As described in our previous study , U87 cells, U251 cells or human glioma primary culture cells were isolated using CD133 magnetic microbeads.

    Techniques: Inhibition, Invasion Chamber Assay, Migration, Cell Culture, Staining, Transferring, shRNA, Plasmid Preparation

    Characterization of PCGCs and CD133 + PCGC spheres. (A) Representative microscopic images of PCGCs and tumorspheres of CD133 + PCGCs (scale bar, 50 µm). Fresh primary glioma samples were dissociated and propagated as non-adherent neurospheres in serum-free defined medium. (B) Western blotting of GASC1 expression in CD133 + or parental PCGC. A higher GASC1 protein expression was observed in the CD133 + PCGC. (C) Reverse transcription-quantitative polymerase chain reaction of GASC1 mRNA expression levels in CD133 + or parental U87, U251 and PCGC. Data are expressed as the mean±SEM (n=3). Unpaired Student t-test, *P

    Journal: Molecular Medicine Reports

    Article Title: GASC1 promotes glioma progression by enhancing NOTCH1 signaling

    doi: 10.3892/mmr.2021.11949

    Figure Lengend Snippet: Characterization of PCGCs and CD133 + PCGC spheres. (A) Representative microscopic images of PCGCs and tumorspheres of CD133 + PCGCs (scale bar, 50 µm). Fresh primary glioma samples were dissociated and propagated as non-adherent neurospheres in serum-free defined medium. (B) Western blotting of GASC1 expression in CD133 + or parental PCGC. A higher GASC1 protein expression was observed in the CD133 + PCGC. (C) Reverse transcription-quantitative polymerase chain reaction of GASC1 mRNA expression levels in CD133 + or parental U87, U251 and PCGC. Data are expressed as the mean±SEM (n=3). Unpaired Student t-test, *P

    Article Snippet: CD133+ cell isolation As described in our previous study , U87 cells, U251 cells or human glioma primary culture cells were isolated using CD133 magnetic microbeads.

    Techniques: Western Blot, Expressing, Real-time Polymerase Chain Reaction

    GASC1 inhibition suppresses the clone forming ability and tumorsphere formation in CD133 + U87 or U251 glioma stem-like cells. (A) Clonogenic assays examining the effects of GASC1-knockout on cell proliferation in U87 or U251 glioma cells with or without GASC1-knockdown. Cells were seeded into 6-well plates at a density of 500 cells/well and then cultured for 5 days, followed by crystal violet staining. (B) Tumorsphere assay of GASC1-knockout on CD133 + U87 or U251 glioma cells with or without GASC1-knockdown (scale bar, 100 µm). Single cells from tumorspheres were seeded at a density of 20,000 cells/ml in a 10 ml GSC growth medium in a 10-cm culture dish. The cells were incubated at 37°C, 5% CO 2 for 5 days to generate bulk cultured tumorspheres. (C) Representative flow cytometry images of cell cycle distribution and apoptosis in CD133 + U87 or U251 glioma cells with or without GASC1-knockdown. (D) Quantitative analysis for stained colonies and tumorspheres in different group panels. shRNA-mediated GASC1 silencing significantly decreased the cloning ability of U87 or U251 glioma cells and the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Journal: Molecular Medicine Reports

    Article Title: GASC1 promotes glioma progression by enhancing NOTCH1 signaling

    doi: 10.3892/mmr.2021.11949

    Figure Lengend Snippet: GASC1 inhibition suppresses the clone forming ability and tumorsphere formation in CD133 + U87 or U251 glioma stem-like cells. (A) Clonogenic assays examining the effects of GASC1-knockout on cell proliferation in U87 or U251 glioma cells with or without GASC1-knockdown. Cells were seeded into 6-well plates at a density of 500 cells/well and then cultured for 5 days, followed by crystal violet staining. (B) Tumorsphere assay of GASC1-knockout on CD133 + U87 or U251 glioma cells with or without GASC1-knockdown (scale bar, 100 µm). Single cells from tumorspheres were seeded at a density of 20,000 cells/ml in a 10 ml GSC growth medium in a 10-cm culture dish. The cells were incubated at 37°C, 5% CO 2 for 5 days to generate bulk cultured tumorspheres. (C) Representative flow cytometry images of cell cycle distribution and apoptosis in CD133 + U87 or U251 glioma cells with or without GASC1-knockdown. (D) Quantitative analysis for stained colonies and tumorspheres in different group panels. shRNA-mediated GASC1 silencing significantly decreased the cloning ability of U87 or U251 glioma cells and the tumorsphere formation ability of CD133 + U87 or U251 glioma cells. Data are expressed as the mean±SD (n=3). Unpaired Student t-test, *P

    Article Snippet: CD133+ cell isolation As described in our previous study , U87 cells, U251 cells or human glioma primary culture cells were isolated using CD133 magnetic microbeads.

    Techniques: Inhibition, Knock-Out, Cell Culture, Staining, Incubation, Flow Cytometry, shRNA, Clone Assay

    Effects of RKIP on cells migration in human U87 glioma cell by means of wound healing assay. The relative distance was ratio of experimental group distance vs. the distance of the cell-blank scratch at 12 h, 14 h and 48 h after transfection. * P

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro

    doi:

    Figure Lengend Snippet: Effects of RKIP on cells migration in human U87 glioma cell by means of wound healing assay. The relative distance was ratio of experimental group distance vs. the distance of the cell-blank scratch at 12 h, 14 h and 48 h after transfection. * P

    Article Snippet: The human glioma cell line U87 were pursued from The Second Affiliated Hospital of Harbin Medical University and were cultured in DEME (Boster Biology Co., Wuhan, China) supplemented with 10% FBS.

    Techniques: Migration, Wound Healing Assay, Transfection

    The effects of RKIP on the proliferation of U87 glioma cells. To determine the effects of RKIP on the ability of proliferation in U87 cells, the MTT assays were carried out to detected the proliferations of cells that over-expressing or down regulating of RKIP. The results showed that RKIP had little effects on the proliferation of U87 glioma cells.

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro

    doi:

    Figure Lengend Snippet: The effects of RKIP on the proliferation of U87 glioma cells. To determine the effects of RKIP on the ability of proliferation in U87 cells, the MTT assays were carried out to detected the proliferations of cells that over-expressing or down regulating of RKIP. The results showed that RKIP had little effects on the proliferation of U87 glioma cells.

    Article Snippet: The human glioma cell line U87 were pursued from The Second Affiliated Hospital of Harbin Medical University and were cultured in DEME (Boster Biology Co., Wuhan, China) supplemented with 10% FBS.

    Techniques: MTT Assay, Expressing

    Effects of RKIP on cells invasion in human U87 glioma cell by means of Transwell assay. The number of glioma cells cross through the membrane was recorded. * P

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro

    doi:

    Figure Lengend Snippet: Effects of RKIP on cells invasion in human U87 glioma cell by means of Transwell assay. The number of glioma cells cross through the membrane was recorded. * P

    Article Snippet: The human glioma cell line U87 were pursued from The Second Affiliated Hospital of Harbin Medical University and were cultured in DEME (Boster Biology Co., Wuhan, China) supplemented with 10% FBS.

    Techniques: Transwell Assay

    Effects of over-expressing and knockdown RKIP on protein expression in human U87 glioma cells. A. The RKIP protein relative expressions (vs. GAPDH), B. The protein relative expression of MMP-2, MMP-9 and HMGA2, * P

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro

    doi:

    Figure Lengend Snippet: Effects of over-expressing and knockdown RKIP on protein expression in human U87 glioma cells. A. The RKIP protein relative expressions (vs. GAPDH), B. The protein relative expression of MMP-2, MMP-9 and HMGA2, * P

    Article Snippet: The human glioma cell line U87 were pursued from The Second Affiliated Hospital of Harbin Medical University and were cultured in DEME (Boster Biology Co., Wuhan, China) supplemented with 10% FBS.

    Techniques: Expressing

    Effects of over-expressing and knockdown RKIP on mRNA expressions in human U87 glioma cells. A. The RKIP mRNA relative expressions (vs. GAPDH), B. The MMP-2 mRNA relative expression (vs. GAPDH), C. The MMP-9 mRNA relative expressions (vs. GAPDH), D. The HMGA2 mRNA relative expression (vs. GAPDH), * P

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: Raf kinase inhibitor protein (RKIP) inhibits the cell migration and invasion in human glioma cell lines in vitro

    doi:

    Figure Lengend Snippet: Effects of over-expressing and knockdown RKIP on mRNA expressions in human U87 glioma cells. A. The RKIP mRNA relative expressions (vs. GAPDH), B. The MMP-2 mRNA relative expression (vs. GAPDH), C. The MMP-9 mRNA relative expressions (vs. GAPDH), D. The HMGA2 mRNA relative expression (vs. GAPDH), * P

    Article Snippet: The human glioma cell line U87 were pursued from The Second Affiliated Hospital of Harbin Medical University and were cultured in DEME (Boster Biology Co., Wuhan, China) supplemented with 10% FBS.

    Techniques: Expressing

    Metformin inhibits AKT/mTOR pathway activated by TGF-β1 ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1-induced AKT/mTOR pathway. ( B ) Western blot results of the inhibitory effect of NVP-BEZ235 on N-cadherin, Vimentin and MMP-9 expression in LN18 and U87 cells.

    Journal: Oncotarget

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    doi: 10.18632/oncotarget.23317

    Figure Lengend Snippet: Metformin inhibits AKT/mTOR pathway activated by TGF-β1 ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1-induced AKT/mTOR pathway. ( B ) Western blot results of the inhibitory effect of NVP-BEZ235 on N-cadherin, Vimentin and MMP-9 expression in LN18 and U87 cells.

    Article Snippet: Western blottingThe LN18 and U87 cells were cultured in 6-well plates and treated by drugs.

    Techniques: Western Blot, Expressing

    Metformin inhibits TGF-β1-induced EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to metformin for 48 hours. ( B ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) with or without metformin for 48 hours under light microscope (×100 magnification). ( C ) Western blot results of dose-dependent inhibition effect of metformin on N-cadherin, Vimentin expression in LN18 and U87 cells. ( D ) Western blot results of dose-dependent inhibition effect of metformin on Snail, Slug expression in LN18 and U87 cells.

    Journal: Oncotarget

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    doi: 10.18632/oncotarget.23317

    Figure Lengend Snippet: Metformin inhibits TGF-β1-induced EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to metformin for 48 hours. ( B ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) with or without metformin for 48 hours under light microscope (×100 magnification). ( C ) Western blot results of dose-dependent inhibition effect of metformin on N-cadherin, Vimentin expression in LN18 and U87 cells. ( D ) Western blot results of dose-dependent inhibition effect of metformin on Snail, Slug expression in LN18 and U87 cells.

    Article Snippet: Western blottingThe LN18 and U87 cells were cultured in 6-well plates and treated by drugs.

    Techniques: MTT Assay, Light Microscopy, Western Blot, Inhibition, Expressing

    Metformin (Met) suppresses TGF-β1-induced cell migration and invasion ( A ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without metformin. Quantification histograms show the mean levels of migration distance observed in three random fields for each condition. ( B ) Representative Transwell photographs show invasion capacity in LN18 and U87 (×100 magnification) cells following exposure to TGF-β1 with or without metformin. Quantification histograms show the mean levels of the numbers of cells counted in five random fields on each filter for each condition. * P

    Journal: Oncotarget

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    doi: 10.18632/oncotarget.23317

    Figure Lengend Snippet: Metformin (Met) suppresses TGF-β1-induced cell migration and invasion ( A ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without metformin. Quantification histograms show the mean levels of migration distance observed in three random fields for each condition. ( B ) Representative Transwell photographs show invasion capacity in LN18 and U87 (×100 magnification) cells following exposure to TGF-β1 with or without metformin. Quantification histograms show the mean levels of the numbers of cells counted in five random fields on each filter for each condition. * P

    Article Snippet: Western blottingThe LN18 and U87 cells were cultured in 6-well plates and treated by drugs.

    Techniques: Migration

    Metformin (Met) reduces cancer stem-like properties generated by induction of TGF-β1 ( A ) Metformin inhibited gliosphere formation in LN18 and U87 cells stimulated by exposure to TGF-β1 (10 ng/ml). Representative images of gliosphere were photographed under Olympus microscope (×100 magnification). Histograms show the numbers of gliosphere in different treatment groups. ( B ) Western blot results of inhibitory effect of metformin on stemness-related proteins stimulated by exposure to TGF-β1 in LN18 and U87 cells. ** P

    Journal: Oncotarget

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    doi: 10.18632/oncotarget.23317

    Figure Lengend Snippet: Metformin (Met) reduces cancer stem-like properties generated by induction of TGF-β1 ( A ) Metformin inhibited gliosphere formation in LN18 and U87 cells stimulated by exposure to TGF-β1 (10 ng/ml). Representative images of gliosphere were photographed under Olympus microscope (×100 magnification). Histograms show the numbers of gliosphere in different treatment groups. ( B ) Western blot results of inhibitory effect of metformin on stemness-related proteins stimulated by exposure to TGF-β1 in LN18 and U87 cells. ** P

    Article Snippet: Western blottingThe LN18 and U87 cells were cultured in 6-well plates and treated by drugs.

    Techniques: Generated, Microscopy, Western Blot

    ZEB1 is associated with the inhibitory effect of metformin on TGF-β1 induced EMT-like process in GBM cells ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1- induced ZEB1 expression in LN18 and U87 cells. ( B ) Western blot results of the effect of ZEB1 knockdown with two different shRNAs (shZEB1-1 and shZEB1-2) and control shRNA (shCtrl) on expression of ZEB1 in LN18 and U87 cells. ( C ) Western blot results of the effect of ZEB1 knockdown on expression of N-cadherin, Vimentin and MMP-9 induced by TGF-β1. ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without ZEB1 knockdown. Quantification histograms show the mean level of migration distance observed in three random fields for each condition. * P

    Journal: Oncotarget

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    doi: 10.18632/oncotarget.23317

    Figure Lengend Snippet: ZEB1 is associated with the inhibitory effect of metformin on TGF-β1 induced EMT-like process in GBM cells ( A ) Western blot results of the inhibitory effect of metformin on TGF-β1- induced ZEB1 expression in LN18 and U87 cells. ( B ) Western blot results of the effect of ZEB1 knockdown with two different shRNAs (shZEB1-1 and shZEB1-2) and control shRNA (shCtrl) on expression of ZEB1 in LN18 and U87 cells. ( C ) Western blot results of the effect of ZEB1 knockdown on expression of N-cadherin, Vimentin and MMP-9 induced by TGF-β1. ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) with or without ZEB1 knockdown. Quantification histograms show the mean level of migration distance observed in three random fields for each condition. * P

    Article Snippet: Western blottingThe LN18 and U87 cells were cultured in 6-well plates and treated by drugs.

    Techniques: Western Blot, Expressing, shRNA, Migration

    TGF-β1 induces an EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to TGF-β1 for 48 hours. ( B ) Western blot results of expressions of EMT-related proteins and transcription factors derived from LN18 and U87 cells treated with increasing concentration of TGF-β1 (0, 5, 10 and 20 ng/ml) for 48 hours. ( C ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) for 48 hours under light microscope (×100 magnification). ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) compared with control group. Histograms show the mean level of migration distance observed in three random fields for each condition. * P

    Journal: Oncotarget

    Article Title: Metformin inhibits TGF-β1-induced epithelial-to-mesenchymal transition-like process and stem-like properties in GBM via AKT/mTOR/ZEB1 pathway

    doi: 10.18632/oncotarget.23317

    Figure Lengend Snippet: TGF-β1 induces an EMT-like process in GBM cells ( A ) MTT assay of cell viability in LN18 and U87 cells following exposure to TGF-β1 for 48 hours. ( B ) Western blot results of expressions of EMT-related proteins and transcription factors derived from LN18 and U87 cells treated with increasing concentration of TGF-β1 (0, 5, 10 and 20 ng/ml) for 48 hours. ( C ) The morphological changes of LN18 and U87 cells after exposure to TGF-β1 (10 ng/ml) for 48 hours under light microscope (×100 magnification). ( D ) Representative wound-healing images show migratory capacity in LN18 (×100 magnification) and U87 (×40 magnification) cells following exposure to TGF-β1 (10 ng/ml) compared with control group. Histograms show the mean level of migration distance observed in three random fields for each condition. * P

    Article Snippet: Western blottingThe LN18 and U87 cells were cultured in 6-well plates and treated by drugs.

    Techniques: MTT Assay, Western Blot, Derivative Assay, Concentration Assay, Light Microscopy, Migration