kya1797k  (MedChemExpress)


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    MedChemExpress kya1797k
    BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by <t>KYA1797K.</t> All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Kya1797k, supplied by MedChemExpress, 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/kya1797k/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kya1797k - by Bioz Stars, 2022-05
    93/100 stars

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    1) Product Images from "BK polyomavirus infection promotes growth and aggressiveness in bladder cancer"

    Article Title: BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

    Journal: Virology Journal

    doi: 10.1186/s12985-020-01399-7

    BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Migration, Transwell Migration Assay, Wound Healing Assay, Transwell Invasion Assay

    BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Injection, Mouse Assay, In Vivo, Staining, TUNEL Assay, Immunohistochemistry

    BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Immunofluorescence, Staining, CCK-8 Assay

    2) Product Images from "BK polyomavirus infection promotes growth and aggressiveness in bladder cancer"

    Article Title: BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

    Journal: Virology Journal

    doi: 10.1186/s12985-020-01399-7

    BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Migration, Transwell Migration Assay, Wound Healing Assay, Transwell Invasion Assay

    BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Injection, Mouse Assay, In Vivo, Staining, TUNEL Assay, Immunohistochemistry

    BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Immunofluorescence, Staining, CCK-8 Assay

    3) Product Images from "BK polyomavirus infection promotes growth and aggressiveness in bladder cancer"

    Article Title: BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

    Journal: Virology Journal

    doi: 10.1186/s12985-020-01399-7

    BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Migration, Transwell Migration Assay, Wound Healing Assay, Transwell Invasion Assay

    BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Injection, Mouse Assay, In Vivo, Staining, TUNEL Assay, Immunohistochemistry

    BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P
    Figure Legend Snippet: BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Techniques Used: Infection, Immunofluorescence, Staining, CCK-8 Assay

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    MedChemExpress β catenin protein inhibitor
    Silencing microglial PKM2 reduces microglial activation and loss of neuronal synapses by <t>β-catenin</t> signaling pathway. A The percentage of microglia (CD45 lo CD11b + ) in the hippocampus, n = 6. B The expression level of CD86 in microglia detected by flow cytometry, n = 6. C The expression level of LAMP1 in microglia detected by flow cytometry, n = 6. D Western blot quantification of PSD95 and VGLUT1 in the hippocampus of vector and sh-PKM2 group, n = 4. E Western blot quantification of PSD95 and VGLUT1 in the cerebral cortex of vector and sh-PKM2 group, n = 4. F PSD95 (red) and IBA-1 (pink) immunofluorescence double staining in the hippocampus of the mice in each group were detected by IF; Bar = 200 μm, n = 4. G Western blot quantification of β-catenin, c-Myc, and CyclinD1 in the hippocampus of vector and sh-PKM2, n = 4. H Western blot quantification of β-catenin, c-Myc, and CyclinD1 in the cerebral cortex of vector and sh-PKM2, n = 4. Data are represented as mean score ± SEM, * P ≤ 0.05, ** P ≤ 0.01, **** P ≤ 0.0001
    β Catenin Protein Inhibitor, supplied by MedChemExpress, 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/β catenin protein inhibitor/product/MedChemExpress
    Average 93 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    β catenin protein inhibitor - by Bioz Stars, 2022-05
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    86
    MEDCHEMEXPRESS CO LTD kya1797k
    CRS-related NE promotes the motility of epithelial ovarian cancers via the β-catenin/SLUG axis in nude mouse models and in vitro. a Content of NE in mouse serum and tumor tissues from the control group and the CRS group was evaluated by ELISA ( n = 6). b Co-expression of β-catenin/NE in the tumor tissues obtained from animal models was examined by confocal laser scanning microscopy. CCK-8 assay was used to test the effects of different concentration of NE ( c ) and β-catenin inhibitor <t>KYA1797K</t> ( e ) on the viability of ovarian cancer cells at 24 h. d NE increased the expression of β-catenin and SLUG in ovarian cancer cells time-dependently. f Results from western blot showed that KYA inhibited NE-mediated upregulation of β-catenin and SLUG in ovarian cancer cells at 24 h. KYA reduced NE-induced pro-migration ( g ) and pro-invasion ( h ) effects on ovarian cancer cells at 24 h. * P
    Kya1797k, supplied by MEDCHEMEXPRESS CO LTD, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/kya1797k/product/MEDCHEMEXPRESS CO LTD
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    kya1797k - by Bioz Stars, 2022-05
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    Silencing microglial PKM2 reduces microglial activation and loss of neuronal synapses by β-catenin signaling pathway. A The percentage of microglia (CD45 lo CD11b + ) in the hippocampus, n = 6. B The expression level of CD86 in microglia detected by flow cytometry, n = 6. C The expression level of LAMP1 in microglia detected by flow cytometry, n = 6. D Western blot quantification of PSD95 and VGLUT1 in the hippocampus of vector and sh-PKM2 group, n = 4. E Western blot quantification of PSD95 and VGLUT1 in the cerebral cortex of vector and sh-PKM2 group, n = 4. F PSD95 (red) and IBA-1 (pink) immunofluorescence double staining in the hippocampus of the mice in each group were detected by IF; Bar = 200 μm, n = 4. G Western blot quantification of β-catenin, c-Myc, and CyclinD1 in the hippocampus of vector and sh-PKM2, n = 4. H Western blot quantification of β-catenin, c-Myc, and CyclinD1 in the cerebral cortex of vector and sh-PKM2, n = 4. Data are represented as mean score ± SEM, * P ≤ 0.05, ** P ≤ 0.01, **** P ≤ 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: Pyruvate kinase isoform M2 impairs cognition in systemic lupus erythematosus by promoting microglial synaptic pruning via the β-catenin signaling pathway

    doi: 10.1186/s12974-021-02279-9

    Figure Lengend Snippet: Silencing microglial PKM2 reduces microglial activation and loss of neuronal synapses by β-catenin signaling pathway. A The percentage of microglia (CD45 lo CD11b + ) in the hippocampus, n = 6. B The expression level of CD86 in microglia detected by flow cytometry, n = 6. C The expression level of LAMP1 in microglia detected by flow cytometry, n = 6. D Western blot quantification of PSD95 and VGLUT1 in the hippocampus of vector and sh-PKM2 group, n = 4. E Western blot quantification of PSD95 and VGLUT1 in the cerebral cortex of vector and sh-PKM2 group, n = 4. F PSD95 (red) and IBA-1 (pink) immunofluorescence double staining in the hippocampus of the mice in each group were detected by IF; Bar = 200 μm, n = 4. G Western blot quantification of β-catenin, c-Myc, and CyclinD1 in the hippocampus of vector and sh-PKM2, n = 4. H Western blot quantification of β-catenin, c-Myc, and CyclinD1 in the cerebral cortex of vector and sh-PKM2, n = 4. Data are represented as mean score ± SEM, * P ≤ 0.05, ** P ≤ 0.01, **** P ≤ 0.0001

    Article Snippet: PKM2 overexpression plasmid was purchased from Nanjing Jereh Company (China), and RFectPM Eukaryotic DNA Transfection Kit was purchased from Changzhou EMI Company (China). β-catenin protein inhibitor (KYA1797K) was purchased from MCE Company (USA).

    Techniques: Activation Assay, Expressing, Flow Cytometry, Western Blot, Plasmid Preparation, Immunofluorescence, Double Staining, Mouse Assay

    PKM2 facilitates phagocytosis via the β-catenin signaling pathway. A The mRNA expression levels of β-catenin , c-Myc , and Cyclin-D1 detected by RT-PCR analysis at 24 h after plasmid transfection. B The protein expression of β-Catenin, c-Myc, and Cyclin-D1 detected by Western blot analysis 24 h after plasmid transfection. C Western blot quantification of β-catenin, c-Myc, and Cyclin-D1 in the hippocampus of control and MLP/lpr mice, n = 4. D BV2 cells were treated with different concentrations of β-catenin inhibitor (KYA1797K) for 24 h. CCK8 detected the cytotoxicity of KYA1797K to BV2 cells. E Transient transfection of BV2 cells with the negative control plasmid (NC) or PKM2 over-expressed plasmid (PKM2). After transfection, BV2 cells were treated with or without 200 ng/mL β-catenin inhibitor (KYA1797K) for 24 h. Then, a phagocytic function test was performed, and the phagocytosis of BV2 cells was detected by flow cytometry. F Transient transfection of BV2 cells with NC or PKM2 over-expressed plasmid, 24 h later, BV2 cells were treated with or without 200 ng/mL β-catenin inhibitor (KYA1797K) for 24 h. The expression level of LAMP1 was detected by flow cytometry. G BV2 cells were transiently transfected with NC or PKM2 over-expressed plasmid (PKM2); 24 h later, BV2 cells were treated with or without 200 ng/mL KYA1797K for 24 h, and then co-cultured with HT22 cells. Finally, a Western blot was used to analyze the protein level of PSD95. Data are presented as mean scores ± SEM, * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001. n = 3 per group

    Journal: Journal of Neuroinflammation

    Article Title: Pyruvate kinase isoform M2 impairs cognition in systemic lupus erythematosus by promoting microglial synaptic pruning via the β-catenin signaling pathway

    doi: 10.1186/s12974-021-02279-9

    Figure Lengend Snippet: PKM2 facilitates phagocytosis via the β-catenin signaling pathway. A The mRNA expression levels of β-catenin , c-Myc , and Cyclin-D1 detected by RT-PCR analysis at 24 h after plasmid transfection. B The protein expression of β-Catenin, c-Myc, and Cyclin-D1 detected by Western blot analysis 24 h after plasmid transfection. C Western blot quantification of β-catenin, c-Myc, and Cyclin-D1 in the hippocampus of control and MLP/lpr mice, n = 4. D BV2 cells were treated with different concentrations of β-catenin inhibitor (KYA1797K) for 24 h. CCK8 detected the cytotoxicity of KYA1797K to BV2 cells. E Transient transfection of BV2 cells with the negative control plasmid (NC) or PKM2 over-expressed plasmid (PKM2). After transfection, BV2 cells were treated with or without 200 ng/mL β-catenin inhibitor (KYA1797K) for 24 h. Then, a phagocytic function test was performed, and the phagocytosis of BV2 cells was detected by flow cytometry. F Transient transfection of BV2 cells with NC or PKM2 over-expressed plasmid, 24 h later, BV2 cells were treated with or without 200 ng/mL β-catenin inhibitor (KYA1797K) for 24 h. The expression level of LAMP1 was detected by flow cytometry. G BV2 cells were transiently transfected with NC or PKM2 over-expressed plasmid (PKM2); 24 h later, BV2 cells were treated with or without 200 ng/mL KYA1797K for 24 h, and then co-cultured with HT22 cells. Finally, a Western blot was used to analyze the protein level of PSD95. Data are presented as mean scores ± SEM, * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001. n = 3 per group

    Article Snippet: PKM2 overexpression plasmid was purchased from Nanjing Jereh Company (China), and RFectPM Eukaryotic DNA Transfection Kit was purchased from Changzhou EMI Company (China). β-catenin protein inhibitor (KYA1797K) was purchased from MCE Company (USA).

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Plasmid Preparation, Transfection, Western Blot, Mouse Assay, Negative Control, Flow Cytometry, Cell Culture

    BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Journal: Virology Journal

    Article Title: BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

    doi: 10.1186/s12985-020-01399-7

    Figure Lengend Snippet: BKPyV infection promotes proliferation, invasion and migration of bladder cancer cells. a , b BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by colony formation. c – h BKPyV infection significantly promoted migration of T24 and HTB-9 cells, as measured by the Transwell migration assay ( c , d ) and wound healing assay ( e – h ) after infected with BKPyV 48 h. i , j Transwell invasion assay showed that BKPyV infection significantly promoted invasiveness of T24 and HTB-9 cells. These effect was significantly reversed by KYA1797K. All images were taken at 100× magnification. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Article Snippet: After infection for 2 hours, cells were washed three times with phosphate-buffered saline (Kaiji Co. Ltd., Shanghai, China), then were cultured using medium containing 2% serum with and without 15 μM KYA1797K (Med Chem Express, Princeton, NJ, USA), a potent and selective β-catenin inhibitor.

    Techniques: Infection, Migration, Transwell Migration Assay, Wound Healing Assay, Transwell Invasion Assay

    BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Journal: Virology Journal

    Article Title: BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

    doi: 10.1186/s12985-020-01399-7

    Figure Lengend Snippet: BKPyV infection enhances bladder tumor growth and metastasis. a T24, HTB-9 and their respective BKPyV-infected cells were injected subcutaneously into nude mice with subsequent intraperitoneal injection of KYA1797K (20 mg/kg) ( n = 5). Tumor volumes ( b , c ) of mice were measured every 5 days. BKPyV infection significantly promoted tumor growth in vivo. The effect was significantly reversed by KYA1797K. Tumors were subjected to H E staining ( d ) (200×) and TUNEL immunohistochemistry ( e , f ) (200×). TUNEL staining showed that BKPyV infection significantly induced tumor apoptosis. The effect was significantly reversed by KYA1797K. g Representative images of liver, metastatic nodules (indicated by arrows) are shown. h Livers were subjected to H E staining (original magnification,40×; smaller image at lower left, 200×). Liver metastasis was found only in the BKPyV-infected group. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Article Snippet: After infection for 2 hours, cells were washed three times with phosphate-buffered saline (Kaiji Co. Ltd., Shanghai, China), then were cultured using medium containing 2% serum with and without 15 μM KYA1797K (Med Chem Express, Princeton, NJ, USA), a potent and selective β-catenin inhibitor.

    Techniques: Infection, Injection, Mouse Assay, In Vivo, Staining, TUNEL Assay, Immunohistochemistry

    BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Journal: Virology Journal

    Article Title: BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

    doi: 10.1186/s12985-020-01399-7

    Figure Lengend Snippet: BKPyV infection in bladder cancer cells is a non-lytic infection (MOI 2; 48 h post infection). a Immunofluorescence staining was performed (red: LTag, blue, DNA, and images were taken at 400× magnification). b , c BKPyV infection significantly increased growth in T24 and HTB-9 cells, as measured by CCK-8. The effect was significantly reversed by KYA1797K. All graphs represent the mean ± SD obtained from three independent experiments. * P

    Article Snippet: After infection for 2 hours, cells were washed three times with phosphate-buffered saline (Kaiji Co. Ltd., Shanghai, China), then were cultured using medium containing 2% serum with and without 15 μM KYA1797K (Med Chem Express, Princeton, NJ, USA), a potent and selective β-catenin inhibitor.

    Techniques: Infection, Immunofluorescence, Staining, CCK-8 Assay

    CRS-related NE promotes the motility of epithelial ovarian cancers via the β-catenin/SLUG axis in nude mouse models and in vitro. a Content of NE in mouse serum and tumor tissues from the control group and the CRS group was evaluated by ELISA ( n = 6). b Co-expression of β-catenin/NE in the tumor tissues obtained from animal models was examined by confocal laser scanning microscopy. CCK-8 assay was used to test the effects of different concentration of NE ( c ) and β-catenin inhibitor KYA1797K ( e ) on the viability of ovarian cancer cells at 24 h. d NE increased the expression of β-catenin and SLUG in ovarian cancer cells time-dependently. f Results from western blot showed that KYA inhibited NE-mediated upregulation of β-catenin and SLUG in ovarian cancer cells at 24 h. KYA reduced NE-induced pro-migration ( g ) and pro-invasion ( h ) effects on ovarian cancer cells at 24 h. * P

    Journal: Cell Death & Disease

    Article Title: Melatonin suppresses chronic restraint stress-mediated metastasis of epithelial ovarian cancer via NE/AKT/β-catenin/SLUG axis

    doi: 10.1038/s41419-020-02906-y

    Figure Lengend Snippet: CRS-related NE promotes the motility of epithelial ovarian cancers via the β-catenin/SLUG axis in nude mouse models and in vitro. a Content of NE in mouse serum and tumor tissues from the control group and the CRS group was evaluated by ELISA ( n = 6). b Co-expression of β-catenin/NE in the tumor tissues obtained from animal models was examined by confocal laser scanning microscopy. CCK-8 assay was used to test the effects of different concentration of NE ( c ) and β-catenin inhibitor KYA1797K ( e ) on the viability of ovarian cancer cells at 24 h. d NE increased the expression of β-catenin and SLUG in ovarian cancer cells time-dependently. f Results from western blot showed that KYA inhibited NE-mediated upregulation of β-catenin and SLUG in ovarian cancer cells at 24 h. KYA reduced NE-induced pro-migration ( g ) and pro-invasion ( h ) effects on ovarian cancer cells at 24 h. * P

    Article Snippet: Cell Counting Kit-8 (CCK-8) assay The work concentration of SKL2001 (MCE, HY-101085), NE (MCE, HY-13715), KYA1797K (MCE, HY-101090), AKTi VIII (MCE, HY-10355), and MLT (MCE) was determined by CCK-8 assay.

    Techniques: In Vitro, Enzyme-linked Immunosorbent Assay, Expressing, Confocal Laser Scanning Microscopy, CCK-8 Assay, Concentration Assay, Western Blot, Migration