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  • 91
    Dojindo Labs cck 8 assay cck8
    Cck 8 Assay Cck8, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Beyotime cck 8 assay cck 8
    MVs promote the growth and migration of 786-0 cells in vitro. (A) <t>CCK-8</t> Assay. After 48-0 cells, MVs greatly promoted cell growth whereas pretreatment with RNase abrogated this effect. The cells incubated with M199 were regarded as control. * P
    Cck 8 Assay Cck 8, supplied by Beyotime, used in various techniques. Bioz Stars score: 86/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Beyotime cck 8 assay cck 8 reagent
    siRNA inhibited UBE2C expression in NPC cells and consequently resulted in attenuated cell proliferation. ( A ) C666-1 cells were transfected with si-UBE2C or si-Control or without siRNA (MOCK). Forty-eight hours later, UBE2C expression was assessed by PCR and immunofluorescence using TRITC-conjugated IgG (H+L). ( B ) Western blotting analysis the UBE2C protein expression in various cell lines post tranfection of siRNAs, the β-actin was used as loading controls. ( C ) Twenty-four and 48 h after transfection, <t>CCK-8</t> assays were used to analyze the proliferation of various types of NPC cells. Values of optical density (OD) were obtained by the absorbance at the dual wavelengths 450/630 nM, and the results indicating the cell viability were plotted as the percentage over controls (MOCK cells). * P
    Cck 8 Assay Cck 8 Reagent, supplied by Beyotime, used in various techniques. Bioz Stars score: 93/100, based on 135 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Beyotime cck 8 assay cck 8 detection kit
    Cell viability assay after infected with GCRV. After 0, 8, 24 and 72 h post infection, cells were evaluated using <t>CCK-8</t> assay, respectively. The mean of three replicates was shown with the ±standard deviation (S.D.). Significant difference between the control and treated group was indicated with asterisks (*: p
    Cck 8 Assay Cck 8 Detection Kit, supplied by Beyotime, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Boster Bio cck 8 kit
    The functional analysis of SNHG12 in HCC cells. a The SNHG12 expression level was determined by qPCR when SK-Hep1 and HCCLM9 cells were transfected with SNHG12-siRNA. b <t>CCK-8</t> assay was applied to detect the proliferation of SK-Hep1 cells. c CCK-8 assay was applied to detect the proliferation of HCCLM9 cells. d and e Flow cytometry assays were performed to analyze the apoptosis of SK-Hep1 and HCCLM9 cells after treatment with SNHG12-siRNA and stained with apoptosis markers (FITC-Annexin V and PI). f and g The ability of cancer cell invasion was measured by using transwell assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×250 and × 100]. h and i The ability of cancer cell migration was measured by using wound-healing assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×100]. Data represented the mean ± SD from three independent experiments. * P
    Cck 8 Kit, supplied by Boster Bio, used in various techniques. Bioz Stars score: 99/100, based on 135 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Boster Bio cck 8 assay
    The functional analysis of SNHG12 in HCC cells. a The SNHG12 expression level was determined by qPCR when SK-Hep1 and HCCLM9 cells were transfected with SNHG12-siRNA. b <t>CCK-8</t> assay was applied to detect the proliferation of SK-Hep1 cells. c CCK-8 assay was applied to detect the proliferation of HCCLM9 cells. d and e Flow cytometry assays were performed to analyze the apoptosis of SK-Hep1 and HCCLM9 cells after treatment with SNHG12-siRNA and stained with apoptosis markers (FITC-Annexin V and PI). f and g The ability of cancer cell invasion was measured by using transwell assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×250 and × 100]. h and i The ability of cancer cell migration was measured by using wound-healing assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×100]. Data represented the mean ± SD from three independent experiments. * P
    Cck 8 Assay, supplied by Boster Bio, used in various techniques. Bioz Stars score: 91/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dojindo Labs cck 8
    ( a ) The vitality of hFOB1.19 cell treated with different concentrations of oleandrin for 24 h that detected by <t>CCK-8</t> assays; n = 5, Mean ± SEM; ND: no difference, vs. control (0 nM) group; ( b ) The apoptosis of hFOB1.19 cells treated with different concentrations of oleandrin that detected by FCM; and ( c ) Statistical analysis of the total apoptosis rate of hFOB1.19 cells followed by FCM detection; n = 3, Mean ± SEM; ND: no difference, vs. control (0 nM) group.
    Cck 8, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 94/100, based on 5096 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dojindo Labs cck8 assay cholecystokinin 8 cck 8 assay
    ( a ) The vitality of hFOB1.19 cell treated with different concentrations of oleandrin for 24 h that detected by <t>CCK-8</t> assays; n = 5, Mean ± SEM; ND: no difference, vs. control (0 nM) group; ( b ) The apoptosis of hFOB1.19 cells treated with different concentrations of oleandrin that detected by FCM; and ( c ) Statistical analysis of the total apoptosis rate of hFOB1.19 cells followed by FCM detection; n = 3, Mean ± SEM; ND: no difference, vs. control (0 nM) group.
    Cck8 Assay Cholecystokinin 8 Cck 8 Assay, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 92/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dojindo Labs cell counting kit 8 cck 8 assay cck 8
    The cancer oncogene effect of CCND2 was mediated by HOXA11-AS in nephroblastoma cells. A. The viability of HFWT cells in each group detected by <t>CCK-8;</t> B. The apoptosis of HFWT cells in each group detected by flow cytometry; C. The cell cycle distribution of HFWT cells in each group detected by flow cytometry; D. The expressions of Ki67, CCND2 and cleaved-caspase-3 in HFWT cells detected by RT-qPCR and Western blot analysis. The values in the figures were quantitative data, and expressed as mean ± standard deviation. Unpaired t test was used for the comparison between groups. * P
    Cell Counting Kit 8 Cck 8 Assay Cck 8, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 91/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore sincalide
    Hypothesized roles of endogenous dopaminergic and cholecystokinin responses to enterocolitic agents in zebrafish larvae (A) Exposure to DSS increases neutrophilic inflammation. Treatment with cabergoline or <t>sincalide</t> alleviates neutrophilic inflammation. Haloperidol and devazepide or lorglumide may inhibit endogenous dopamine and CCK-8, respectively, exacerbating the DSS-induced inflammatory response. This suggests endogenous dopamine and CCK-8 may limit the extent of the DSS-induced inflammatory response. (B) Exposure to TNBS increases neutrophilic inflammation. Treatment with cabergoline or sincalide alleviates neutrophilic inflammation. Haloperidol has no effect on TNBS-induced inflammatory response suggesting there may be no endogenous CCK-8 response to TNBS. Devazepide or lorglumide exacerbates the TNBS-induced inflammatory response suggesting endogenous dopamine may limit the extent of the TNBS-induced inflammatory response.
    Sincalide, supplied by Millipore, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Millipore cck 8 reagent
    Function of cvTBLR1 ( A ) Overexpression of cvTBLR1 using nuclear export sequence (NES) fused cvTBLR1 (AA89-514) construct to create LNCaP –NEScvTBLR1 cells. ( B ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in hormone free media. ( C ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( D ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in hormone free media. ( E ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( F ) Cellular proliferation comparison of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells over 6 days by <t>CCK-8</t> assay. ( G ) Migration assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control. ( H ) Invasion assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control and representative pictures of membrane.
    Cck 8 Reagent, supplied by Millipore, used in various techniques. Bioz Stars score: 92/100, based on 168 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Santa Cruz Biotechnology cck 8 kit
    Function of cvTBLR1 ( A ) Overexpression of cvTBLR1 using nuclear export sequence (NES) fused cvTBLR1 (AA89-514) construct to create LNCaP –NEScvTBLR1 cells. ( B ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in hormone free media. ( C ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( D ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in hormone free media. ( E ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( F ) Cellular proliferation comparison of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells over 6 days by <t>CCK-8</t> assay. ( G ) Migration assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control. ( H ) Invasion assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control and representative pictures of membrane.
    Cck 8 Kit, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dojindo Labs cck 8 reagent
    Functional consequences of ectopic ROR2 expression in RKO and SW620 cell lines. a ROR2 qRT-PCR of RKO and SW620 cell lines with ectopic ROR2 expression (pROR2 transfection) and control (pFLAG-CMV-4™ transfection) relative to expression in HCT116 cell lines. All expression results normalised against 3 housekeeping genes ( n = 1). b <t>CCK-8</t> proliferation assay of RKO and SW620 cells with and without ectopic ROR2 expression ( n = 3). c Wound healing assay comparing percentage area of wound covered by RKO cells with and without ectopic ROR2 expression over a 4 day period ( n = 1). d Images of RKO cells in wound healing assay on day 0 and day 3 comparing cells with and without ectopic ROR2 expression. e Wound healing assay comparing percentage area of wound covered by SW620 cells with and without ectopic ROR2 expression over a 12 day period ( n = 1). f Images of SW620 cells in wound healing assay on day 0 and day 9 comparing cells with and without ectopic ROR2 expression
    Cck 8 Reagent, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 94/100, based on 1336 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Keygen Biotech cck 8 kit
    Over-regulated miR-490-3p significantly inhibited the proliferation, migratory, invasion activities and promoted apoptotic rate of CRC cells (HCT116 and SW480). A, miR-490-3p highly expressed in HCT116 and SW480 cells after transfection with miR-mimic. B, <t>CCK-8</t> assay was used to assess the proliferation ability of CRC cells transfected with miR-mimic or NC respectively. C, wound healing assay was used to elucidate the migratory ability of CRC cells transfected with miR-mimic or NC respectively. D, transwell invasion assay was used to assess the invasion ability of CRC cells transfected with miR-mimic or NC respectively. E, flow cytometry analysis was used to assess the apoptotic rate of CRC cells transfected with miR-mimic or NC respectively. * P
    Cck 8 Kit, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 90/100, based on 37 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Sangon Biotech cck 8 reagent
    Over-regulated miR-490-3p significantly inhibited the proliferation, migratory, invasion activities and promoted apoptotic rate of CRC cells (HCT116 and SW480). A, miR-490-3p highly expressed in HCT116 and SW480 cells after transfection with miR-mimic. B, <t>CCK-8</t> assay was used to assess the proliferation ability of CRC cells transfected with miR-mimic or NC respectively. C, wound healing assay was used to elucidate the migratory ability of CRC cells transfected with miR-mimic or NC respectively. D, transwell invasion assay was used to assess the invasion ability of CRC cells transfected with miR-mimic or NC respectively. E, flow cytometry analysis was used to assess the apoptotic rate of CRC cells transfected with miR-mimic or NC respectively. * P
    Cck 8 Reagent, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 92/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    MVs promote the growth and migration of 786-0 cells in vitro. (A) CCK-8 Assay. After 48-0 cells, MVs greatly promoted cell growth whereas pretreatment with RNase abrogated this effect. The cells incubated with M199 were regarded as control. * P

    Journal: PLoS ONE

    Article Title: Microvesicles Derived from Human Wharton's Jelly Mesenchymal Stem Cells Promote Human Renal Cancer Cell Growth and Aggressiveness through Induction of Hepatocyte Growth Factor

    doi: 10.1371/journal.pone.0096836

    Figure Lengend Snippet: MVs promote the growth and migration of 786-0 cells in vitro. (A) CCK-8 Assay. After 48-0 cells, MVs greatly promoted cell growth whereas pretreatment with RNase abrogated this effect. The cells incubated with M199 were regarded as control. * P

    Article Snippet: CCK-8 assay CCK-8 (Beyotime institute of biotechnology, Jiangsu, CHINA) was used to determine in vitro growth of tumor cells.

    Techniques: Migration, In Vitro, CCK-8 Assay, Incubation

    siRNA inhibited UBE2C expression in NPC cells and consequently resulted in attenuated cell proliferation. ( A ) C666-1 cells were transfected with si-UBE2C or si-Control or without siRNA (MOCK). Forty-eight hours later, UBE2C expression was assessed by PCR and immunofluorescence using TRITC-conjugated IgG (H+L). ( B ) Western blotting analysis the UBE2C protein expression in various cell lines post tranfection of siRNAs, the β-actin was used as loading controls. ( C ) Twenty-four and 48 h after transfection, CCK-8 assays were used to analyze the proliferation of various types of NPC cells. Values of optical density (OD) were obtained by the absorbance at the dual wavelengths 450/630 nM, and the results indicating the cell viability were plotted as the percentage over controls (MOCK cells). * P

    Journal: BMC Cancer

    Article Title: High expression of ubiquitin-conjugating enzyme 2C (UBE2C) correlates with nasopharyngeal carcinoma progression

    doi: 10.1186/1471-2407-13-192

    Figure Lengend Snippet: siRNA inhibited UBE2C expression in NPC cells and consequently resulted in attenuated cell proliferation. ( A ) C666-1 cells were transfected with si-UBE2C or si-Control or without siRNA (MOCK). Forty-eight hours later, UBE2C expression was assessed by PCR and immunofluorescence using TRITC-conjugated IgG (H+L). ( B ) Western blotting analysis the UBE2C protein expression in various cell lines post tranfection of siRNAs, the β-actin was used as loading controls. ( C ) Twenty-four and 48 h after transfection, CCK-8 assays were used to analyze the proliferation of various types of NPC cells. Values of optical density (OD) were obtained by the absorbance at the dual wavelengths 450/630 nM, and the results indicating the cell viability were plotted as the percentage over controls (MOCK cells). * P

    Article Snippet: Briefly, 4×103 cells were seeded in 96-well plates at either 24 and 48 h after transfection with or without siRNAs, then 10 μl CCK-8 reagent (Beyotime Institute of Biotechnology, Jiangsu, China) plus 100 μl basal DMEM medium was added per well, and the absorbance of the samples was measured.

    Techniques: Expressing, Transfection, Polymerase Chain Reaction, Immunofluorescence, Western Blot, CCK-8 Assay

    Cell viability assay after infected with GCRV. After 0, 8, 24 and 72 h post infection, cells were evaluated using CCK-8 assay, respectively. The mean of three replicates was shown with the ±standard deviation (S.D.). Significant difference between the control and treated group was indicated with asterisks (*: p

    Journal: International Journal of Molecular Sciences

    Article Title: Transcriptomics Sequencing Provides Insights into Understanding the Mechanism of Grass Carp Reovirus Infection

    doi: 10.3390/ijms19020488

    Figure Lengend Snippet: Cell viability assay after infected with GCRV. After 0, 8, 24 and 72 h post infection, cells were evaluated using CCK-8 assay, respectively. The mean of three replicates was shown with the ±standard deviation (S.D.). Significant difference between the control and treated group was indicated with asterisks (*: p

    Article Snippet: CCK-8 Assay CCK-8 detection kit (Beyotime, Shanghai, China) was used to measure cell viability according to the manufacturer’s instructions.

    Techniques: Viability Assay, Infection, CCK-8 Assay, Standard Deviation

    PSAT1 is a target of ATF4 in ER-negative breast cancer. a Expression profile of ATF4 in ER-negative breast cancer tissues ( n = 179) and ER-positive breast cancer tissues ( n = 601) (TCGA). b Relative expression of ATF4 in ER-negative breast cancer tissues ( n = 179) in comparison with non-tumor normal tissues ( n = 114) (TCGA). c Correlation between PSAT1 and ATF4 mRNA expression in samples from 179 patients with ER-negative breast cancer from the TCGA database. d Real-time PCR analysis show ATF4 siRNA inhibited the mRNA expression of PSAT1 in MDA-MB-468 and BT-549 cells compared to negative control cells. . These results were normalized to the expression of β-actin. The values of the NC group were normalized to 1. e Western blot shows PSAT1 expression was decreased in ATF4 silenced MDA-MB-468 and BT-549 cells compared to negative control cells. f The growth rate of the indicated cells was evaluated using a CCK-8 assay. g Schematic representation of the predicated ATF4 binding site within the PSAT1 promoter. h RT-PCR of the ChIP products validated the binding capacity of ATF4 to the PSAT1 promtor. The results of IgG were normalized to 1. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: PSAT1 is regulated by ATF4 and enhances cell proliferation via the GSK3β/β-catenin/cyclin D1 signaling pathway in ER-negative breast cancer

    doi: 10.1186/s13046-017-0648-4

    Figure Lengend Snippet: PSAT1 is a target of ATF4 in ER-negative breast cancer. a Expression profile of ATF4 in ER-negative breast cancer tissues ( n = 179) and ER-positive breast cancer tissues ( n = 601) (TCGA). b Relative expression of ATF4 in ER-negative breast cancer tissues ( n = 179) in comparison with non-tumor normal tissues ( n = 114) (TCGA). c Correlation between PSAT1 and ATF4 mRNA expression in samples from 179 patients with ER-negative breast cancer from the TCGA database. d Real-time PCR analysis show ATF4 siRNA inhibited the mRNA expression of PSAT1 in MDA-MB-468 and BT-549 cells compared to negative control cells. . These results were normalized to the expression of β-actin. The values of the NC group were normalized to 1. e Western blot shows PSAT1 expression was decreased in ATF4 silenced MDA-MB-468 and BT-549 cells compared to negative control cells. f The growth rate of the indicated cells was evaluated using a CCK-8 assay. g Schematic representation of the predicated ATF4 binding site within the PSAT1 promoter. h RT-PCR of the ChIP products validated the binding capacity of ATF4 to the PSAT1 promtor. The results of IgG were normalized to 1. * P

    Article Snippet: Cell proliferation assays A cell proliferation assay was performed with a CCK-8 kit (Beyotime Institute of Biotechnology, Shanghai, China) according to the manufacturer’s instructions.

    Techniques: Expressing, Real-time Polymerase Chain Reaction, Multiple Displacement Amplification, Negative Control, Western Blot, CCK-8 Assay, Binding Assay, Reverse Transcription Polymerase Chain Reaction, Chromatin Immunoprecipitation

    Overexpression of PSAT1 promoted the proliferation of ER-negative breast cancer cells. a Overexpression of PSAT1 in BT-549 cells was analyzed by WB. β-tubulin was used as a loading control. b The proliferation of BT-549 cells with stably up-regulated PSAT1 were tested by CCK-8 assay. c Overexpression of PSAT1 enhanced the colony formation ability of BT-549 cells. The values of the vector-control cells were normalized to 1. In (B) and (C), the results are expressed as the mean ± SD; n = 3. d The cell cycle was analyzed in BT-549 cells with stable overexpression of PSAT1 by flow cytometry. ** p

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: PSAT1 is regulated by ATF4 and enhances cell proliferation via the GSK3β/β-catenin/cyclin D1 signaling pathway in ER-negative breast cancer

    doi: 10.1186/s13046-017-0648-4

    Figure Lengend Snippet: Overexpression of PSAT1 promoted the proliferation of ER-negative breast cancer cells. a Overexpression of PSAT1 in BT-549 cells was analyzed by WB. β-tubulin was used as a loading control. b The proliferation of BT-549 cells with stably up-regulated PSAT1 were tested by CCK-8 assay. c Overexpression of PSAT1 enhanced the colony formation ability of BT-549 cells. The values of the vector-control cells were normalized to 1. In (B) and (C), the results are expressed as the mean ± SD; n = 3. d The cell cycle was analyzed in BT-549 cells with stable overexpression of PSAT1 by flow cytometry. ** p

    Article Snippet: Cell proliferation assays A cell proliferation assay was performed with a CCK-8 kit (Beyotime Institute of Biotechnology, Shanghai, China) according to the manufacturer’s instructions.

    Techniques: Over Expression, Western Blot, Stable Transfection, CCK-8 Assay, Plasmid Preparation, Flow Cytometry, Cytometry

    Knockdown of PSAT1 inhibited tumorigenicity of ER-negative breast cancer cells. a Western blot shows PSAT1 expression in HCC70 and MDA-MB-468 cells infected with Lenti-shPSAT1 or control. β-tubulin was used as a loading control. b CCK-8 assay was performed to determine the effect of PSAT1 silencing on the proliferation of the indicated cells at the indicated time points. c Knockdown of PSAT1 suppressed the colony formation ability of HCC70 and MDA-MB-468 cells compared with that of control cells. The values of the control cells were normalized to 1. For ( b ) and ( c ), the results are expressed as the mean ± SD; n = 3. d Cell cycle analysis of the indicated cells according to flow cytometry. * p

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: PSAT1 is regulated by ATF4 and enhances cell proliferation via the GSK3β/β-catenin/cyclin D1 signaling pathway in ER-negative breast cancer

    doi: 10.1186/s13046-017-0648-4

    Figure Lengend Snippet: Knockdown of PSAT1 inhibited tumorigenicity of ER-negative breast cancer cells. a Western blot shows PSAT1 expression in HCC70 and MDA-MB-468 cells infected with Lenti-shPSAT1 or control. β-tubulin was used as a loading control. b CCK-8 assay was performed to determine the effect of PSAT1 silencing on the proliferation of the indicated cells at the indicated time points. c Knockdown of PSAT1 suppressed the colony formation ability of HCC70 and MDA-MB-468 cells compared with that of control cells. The values of the control cells were normalized to 1. For ( b ) and ( c ), the results are expressed as the mean ± SD; n = 3. d Cell cycle analysis of the indicated cells according to flow cytometry. * p

    Article Snippet: Cell proliferation assays A cell proliferation assay was performed with a CCK-8 kit (Beyotime Institute of Biotechnology, Shanghai, China) according to the manufacturer’s instructions.

    Techniques: Western Blot, Expressing, Multiple Displacement Amplification, Infection, CCK-8 Assay, Cell Cycle Assay, Flow Cytometry, Cytometry

    The functional analysis of SNHG12 in HCC cells. a The SNHG12 expression level was determined by qPCR when SK-Hep1 and HCCLM9 cells were transfected with SNHG12-siRNA. b CCK-8 assay was applied to detect the proliferation of SK-Hep1 cells. c CCK-8 assay was applied to detect the proliferation of HCCLM9 cells. d and e Flow cytometry assays were performed to analyze the apoptosis of SK-Hep1 and HCCLM9 cells after treatment with SNHG12-siRNA and stained with apoptosis markers (FITC-Annexin V and PI). f and g The ability of cancer cell invasion was measured by using transwell assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×250 and × 100]. h and i The ability of cancer cell migration was measured by using wound-healing assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×100]. Data represented the mean ± SD from three independent experiments. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: Long non-coding RNA small nucleolar RNA host gene 12 (SNHG12) promotes tumorigenesis and metastasis by targeting miR-199a/b-5p in hepatocellular carcinoma

    doi: 10.1186/s13046-016-0486-9

    Figure Lengend Snippet: The functional analysis of SNHG12 in HCC cells. a The SNHG12 expression level was determined by qPCR when SK-Hep1 and HCCLM9 cells were transfected with SNHG12-siRNA. b CCK-8 assay was applied to detect the proliferation of SK-Hep1 cells. c CCK-8 assay was applied to detect the proliferation of HCCLM9 cells. d and e Flow cytometry assays were performed to analyze the apoptosis of SK-Hep1 and HCCLM9 cells after treatment with SNHG12-siRNA and stained with apoptosis markers (FITC-Annexin V and PI). f and g The ability of cancer cell invasion was measured by using transwell assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×250 and × 100]. h and i The ability of cancer cell migration was measured by using wound-healing assay when SNHG12 was downregulated in SK-Hep1 and HCCLM9 cells [original magnification, ×100]. Data represented the mean ± SD from three independent experiments. * P

    Article Snippet: Cell proliferation assay A total of 3 × 104 cells were seeded in each well of a 96-well plate, and incubated for 24 h. Ten Microliter WST-8 from the CCK-8 Kit (Boster, Wuhan, China) was then added to each well.

    Techniques: Functional Assay, Expressing, Real-time Polymerase Chain Reaction, Transfection, CCK-8 Assay, Flow Cytometry, Cytometry, Staining, Transwell Assay, Migration, Wound Healing Assay

    Overexpression of decorin ameliorated the angiogenesis impaired by high glucose (HG). ( A – C ) The expression of decorin and VEGF. ( D , E ) The tube formation test; the photographs were taken at a magnification of 100×. ( F , G ) The cell wound healing test; the photographs were taken in a magnification of 100×. ( H , I ) The apoptosis rate analyzed by an Annexin V–FITC kit through flow cytometry. ( J ) The proliferative ability assessed with a CCK8 assay. All data are presented as the mean ± SEM. *p

    Journal: Scientific Reports

    Article Title: Overexpression of decorin promoted angiogenesis in diabetic cardiomyopathy via IGF1R-AKT-VEGF signaling

    doi: 10.1038/srep44473

    Figure Lengend Snippet: Overexpression of decorin ameliorated the angiogenesis impaired by high glucose (HG). ( A – C ) The expression of decorin and VEGF. ( D , E ) The tube formation test; the photographs were taken at a magnification of 100×. ( F , G ) The cell wound healing test; the photographs were taken in a magnification of 100×. ( H , I ) The apoptosis rate analyzed by an Annexin V–FITC kit through flow cytometry. ( J ) The proliferative ability assessed with a CCK8 assay. All data are presented as the mean ± SEM. *p

    Article Snippet: CCK8 assay A cell counting kit 8 (CCK8) assay was carried out using a CCK8 assay kit (Boster, China) to evaluate the proliferative activity following the manufacturer’s instructions.

    Techniques: Over Expression, Expressing, Flow Cytometry, Cytometry, CCK-8 Assay

    The AKT inhibitor MK2206 abolished the effects induced by overexpression of decorin. ( A ) The tube formation test; the photographs were taken at a magnification of 100×. ( B ) The cell wound healing test; the photographs were taken at a magnification of 100×. ( C ) The apoptosis assay. ( D ) CCK8 assessment. ( E , F ) The expression of VEGF, Bcl2, and Bax and the phosphorylation of AKT and AP 1. All data are presented as the mean ± SEM. *p

    Journal: Scientific Reports

    Article Title: Overexpression of decorin promoted angiogenesis in diabetic cardiomyopathy via IGF1R-AKT-VEGF signaling

    doi: 10.1038/srep44473

    Figure Lengend Snippet: The AKT inhibitor MK2206 abolished the effects induced by overexpression of decorin. ( A ) The tube formation test; the photographs were taken at a magnification of 100×. ( B ) The cell wound healing test; the photographs were taken at a magnification of 100×. ( C ) The apoptosis assay. ( D ) CCK8 assessment. ( E , F ) The expression of VEGF, Bcl2, and Bax and the phosphorylation of AKT and AP 1. All data are presented as the mean ± SEM. *p

    Article Snippet: CCK8 assay A cell counting kit 8 (CCK8) assay was carried out using a CCK8 assay kit (Boster, China) to evaluate the proliferative activity following the manufacturer’s instructions.

    Techniques: Over Expression, Apoptosis Assay, Expressing

    The IGF1R antibody (αIGF1R) blocked the effects induced by overexpression of decorin. ( A , B ) The tube formation test; the photographs were taken at a magnification of 100×. ( C , D ) The cell wound healing test; the photographs were taken at a magnification of 100×. ( E , F ) The apoptosis assay. ( G ) CCK8 assessment. ( H , I ) The expression of VEGF, Bcl2, and Bax and the phosphorylation of AKT and AP 1. All data are presented as the mean ± SEM. *p

    Journal: Scientific Reports

    Article Title: Overexpression of decorin promoted angiogenesis in diabetic cardiomyopathy via IGF1R-AKT-VEGF signaling

    doi: 10.1038/srep44473

    Figure Lengend Snippet: The IGF1R antibody (αIGF1R) blocked the effects induced by overexpression of decorin. ( A , B ) The tube formation test; the photographs were taken at a magnification of 100×. ( C , D ) The cell wound healing test; the photographs were taken at a magnification of 100×. ( E , F ) The apoptosis assay. ( G ) CCK8 assessment. ( H , I ) The expression of VEGF, Bcl2, and Bax and the phosphorylation of AKT and AP 1. All data are presented as the mean ± SEM. *p

    Article Snippet: CCK8 assay A cell counting kit 8 (CCK8) assay was carried out using a CCK8 assay kit (Boster, China) to evaluate the proliferative activity following the manufacturer’s instructions.

    Techniques: Over Expression, Apoptosis Assay, Expressing

    VO-OHpic significantly attenuates the cytotoxicity of MPS on EPCs. a The flow cytometry analysis shows that EPCs positively express CD34, VEGFR2, and CD133. b The cytotoxicity of MPS on EPCs viability was evaluated with CCK-8 at the concentrations of 0, 10, 20, and 50 μM after 48 h. c VO-OHpic effectively attenuates the detrimental effects of MPS (50 μM) on EPCs viability at concentrations of 0.1, 1, and 10 μM. d P-AKT and t-AKT protein levels were determined by western blot analysis at 48 h. e Band density ratios of p-AKT to t-AKT in the western blots were quantified by densitometry. All experiments were repeated for three times; * P

    Journal: Stem Cell Research & Therapy

    Article Title: PTEN inhibitor VO-OHpic attenuates GC-associated endothelial progenitor cell dysfunction and osteonecrosis of the femoral head via activating Nrf2 signaling and inhibiting mitochondrial apoptosis pathway

    doi: 10.1186/s13287-020-01658-y

    Figure Lengend Snippet: VO-OHpic significantly attenuates the cytotoxicity of MPS on EPCs. a The flow cytometry analysis shows that EPCs positively express CD34, VEGFR2, and CD133. b The cytotoxicity of MPS on EPCs viability was evaluated with CCK-8 at the concentrations of 0, 10, 20, and 50 μM after 48 h. c VO-OHpic effectively attenuates the detrimental effects of MPS (50 μM) on EPCs viability at concentrations of 0.1, 1, and 10 μM. d P-AKT and t-AKT protein levels were determined by western blot analysis at 48 h. e Band density ratios of p-AKT to t-AKT in the western blots were quantified by densitometry. All experiments were repeated for three times; * P

    Article Snippet: Cell viability assay The viability of EPCs was determined with a cell counting kit-8 (Boster, China, AR1160).

    Techniques: Flow Cytometry, CCK-8 Assay, Western Blot

    ( a ) The vitality of hFOB1.19 cell treated with different concentrations of oleandrin for 24 h that detected by CCK-8 assays; n = 5, Mean ± SEM; ND: no difference, vs. control (0 nM) group; ( b ) The apoptosis of hFOB1.19 cells treated with different concentrations of oleandrin that detected by FCM; and ( c ) Statistical analysis of the total apoptosis rate of hFOB1.19 cells followed by FCM detection; n = 3, Mean ± SEM; ND: no difference, vs. control (0 nM) group.

    Journal: International Journal of Molecular Sciences

    Article Title: Regulation of Intrinsic and Extrinsic Apoptotic Pathways in Osteosarcoma Cells Following Oleandrin Treatment

    doi: 10.3390/ijms17111950

    Figure Lengend Snippet: ( a ) The vitality of hFOB1.19 cell treated with different concentrations of oleandrin for 24 h that detected by CCK-8 assays; n = 5, Mean ± SEM; ND: no difference, vs. control (0 nM) group; ( b ) The apoptosis of hFOB1.19 cells treated with different concentrations of oleandrin that detected by FCM; and ( c ) Statistical analysis of the total apoptosis rate of hFOB1.19 cells followed by FCM detection; n = 3, Mean ± SEM; ND: no difference, vs. control (0 nM) group.

    Article Snippet: Then, cells were treated with various concentration of oleandrin (0, 25, 50, 75 and 100 nM) for 24 h. Then, CCK-8 agent (Dojindo Laboratories, Kumamoto, Japan) was added to each well and incubated for another 3 h. The absorption at 450 nm was determined using an automatic ELIASA microplate reader as reported above.

    Techniques: CCK-8 Assay

    Proliferation of cells cultured in different media. Cells were cultured in GM, IM, and CM for 14 days. At each time point, cell number was determined using CCK-8 cell proliferation/cell viability kit. The amount of cells would be proportional to the absorbance at 450 nm. The results were presented as the means ± standard deviation ( n = 6). *Significant difference ( P

    Journal: BioMed Research International

    Article Title: Evaluation of Insulin Medium or Chondrogenic Medium on Proliferation and Chondrogenesis of ATDC5 Cells

    doi: 10.1155/2014/569241

    Figure Lengend Snippet: Proliferation of cells cultured in different media. Cells were cultured in GM, IM, and CM for 14 days. At each time point, cell number was determined using CCK-8 cell proliferation/cell viability kit. The amount of cells would be proportional to the absorbance at 450 nm. The results were presented as the means ± standard deviation ( n = 6). *Significant difference ( P

    Article Snippet: Briefly, at each time point, cells were seeded at 96-well plate with 1000 cells per well followed by aspiration of the old medium and replacement with 110 μ L of fresh medium containing CCK-8 regent (Dojindo, premix 10 μ L of CCK-8 every 100 μ L of medium).

    Techniques: Cell Culture, CCK-8 Assay, Standard Deviation

    The cancer oncogene effect of CCND2 was mediated by HOXA11-AS in nephroblastoma cells. A. The viability of HFWT cells in each group detected by CCK-8; B. The apoptosis of HFWT cells in each group detected by flow cytometry; C. The cell cycle distribution of HFWT cells in each group detected by flow cytometry; D. The expressions of Ki67, CCND2 and cleaved-caspase-3 in HFWT cells detected by RT-qPCR and Western blot analysis. The values in the figures were quantitative data, and expressed as mean ± standard deviation. Unpaired t test was used for the comparison between groups. * P

    Journal: American Journal of Cancer Research

    Article Title: Long non-coding RNA HOXA11-AS upregulates Cyclin D2 to inhibit apoptosis and promote cell cycle progression in nephroblastoma by recruiting forkhead box P2

    doi:

    Figure Lengend Snippet: The cancer oncogene effect of CCND2 was mediated by HOXA11-AS in nephroblastoma cells. A. The viability of HFWT cells in each group detected by CCK-8; B. The apoptosis of HFWT cells in each group detected by flow cytometry; C. The cell cycle distribution of HFWT cells in each group detected by flow cytometry; D. The expressions of Ki67, CCND2 and cleaved-caspase-3 in HFWT cells detected by RT-qPCR and Western blot analysis. The values in the figures were quantitative data, and expressed as mean ± standard deviation. Unpaired t test was used for the comparison between groups. * P

    Article Snippet: Cell proliferation was measured using a CCK-8 kit (Dojindo Laboratories, Kumamoto, Japan).

    Techniques: CCK-8 Assay, Flow Cytometry, Quantitative RT-PCR, Western Blot, Standard Deviation

    HOXA11-AS inhibits apoptosis and promotes cell cycle progression of nephroblastoma in vitro . A. RT-qPCR was used to detect the HOXA11-AS expression in HEK-293A, HFWT and SK-NEP-1 cells; B. RT-qPCR was used to detect the interference efficiency of three sh-HOXA11-AS plasmids; C. CCK-8 was used to detect the viability of HFWT cells; D. Flow cytometry was used to detect the apoptosis of HFWT cells in each group; E. Flow cytometry was used to detect the cell cycle distribution of HFWT cells in each group; F. RT-qPCR and Western blot analysis were used to detect the expression of Ki67 and cleaved-caspase-3 in HFWT cells. The values in the figures were quantitative data, and expressed as mean ± standard deviation. One-way ANOVA was used for the data comparison among multiple groups, with Tukey’s post hoc test. Repeated measures ANOVA was used to the data comparison between groups at different time points and Bonferroni was used for post hoc test. * P

    Journal: American Journal of Cancer Research

    Article Title: Long non-coding RNA HOXA11-AS upregulates Cyclin D2 to inhibit apoptosis and promote cell cycle progression in nephroblastoma by recruiting forkhead box P2

    doi:

    Figure Lengend Snippet: HOXA11-AS inhibits apoptosis and promotes cell cycle progression of nephroblastoma in vitro . A. RT-qPCR was used to detect the HOXA11-AS expression in HEK-293A, HFWT and SK-NEP-1 cells; B. RT-qPCR was used to detect the interference efficiency of three sh-HOXA11-AS plasmids; C. CCK-8 was used to detect the viability of HFWT cells; D. Flow cytometry was used to detect the apoptosis of HFWT cells in each group; E. Flow cytometry was used to detect the cell cycle distribution of HFWT cells in each group; F. RT-qPCR and Western blot analysis were used to detect the expression of Ki67 and cleaved-caspase-3 in HFWT cells. The values in the figures were quantitative data, and expressed as mean ± standard deviation. One-way ANOVA was used for the data comparison among multiple groups, with Tukey’s post hoc test. Repeated measures ANOVA was used to the data comparison between groups at different time points and Bonferroni was used for post hoc test. * P

    Article Snippet: Cell proliferation was measured using a CCK-8 kit (Dojindo Laboratories, Kumamoto, Japan).

    Techniques: In Vitro, Quantitative RT-PCR, Expressing, CCK-8 Assay, Flow Cytometry, Western Blot, Standard Deviation

    Hypothesized roles of endogenous dopaminergic and cholecystokinin responses to enterocolitic agents in zebrafish larvae (A) Exposure to DSS increases neutrophilic inflammation. Treatment with cabergoline or sincalide alleviates neutrophilic inflammation. Haloperidol and devazepide or lorglumide may inhibit endogenous dopamine and CCK-8, respectively, exacerbating the DSS-induced inflammatory response. This suggests endogenous dopamine and CCK-8 may limit the extent of the DSS-induced inflammatory response. (B) Exposure to TNBS increases neutrophilic inflammation. Treatment with cabergoline or sincalide alleviates neutrophilic inflammation. Haloperidol has no effect on TNBS-induced inflammatory response suggesting there may be no endogenous CCK-8 response to TNBS. Devazepide or lorglumide exacerbates the TNBS-induced inflammatory response suggesting endogenous dopamine may limit the extent of the TNBS-induced inflammatory response.

    Journal: The FEBS journal

    Article Title: A whole animal chemical screen approach to identify modifiers of intestinal neutrophilic inflammation

    doi: 10.1111/febs.13976

    Figure Lengend Snippet: Hypothesized roles of endogenous dopaminergic and cholecystokinin responses to enterocolitic agents in zebrafish larvae (A) Exposure to DSS increases neutrophilic inflammation. Treatment with cabergoline or sincalide alleviates neutrophilic inflammation. Haloperidol and devazepide or lorglumide may inhibit endogenous dopamine and CCK-8, respectively, exacerbating the DSS-induced inflammatory response. This suggests endogenous dopamine and CCK-8 may limit the extent of the DSS-induced inflammatory response. (B) Exposure to TNBS increases neutrophilic inflammation. Treatment with cabergoline or sincalide alleviates neutrophilic inflammation. Haloperidol has no effect on TNBS-induced inflammatory response suggesting there may be no endogenous CCK-8 response to TNBS. Devazepide or lorglumide exacerbates the TNBS-induced inflammatory response suggesting endogenous dopamine may limit the extent of the TNBS-induced inflammatory response.

    Article Snippet: Lorglumide and sincalide (Sigma-Aldrich) were dissolved in water.

    Techniques: CCK-8 Assay

    Function of cvTBLR1 ( A ) Overexpression of cvTBLR1 using nuclear export sequence (NES) fused cvTBLR1 (AA89-514) construct to create LNCaP –NEScvTBLR1 cells. ( B ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in hormone free media. ( C ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( D ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in hormone free media. ( E ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( F ) Cellular proliferation comparison of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells over 6 days by CCK-8 assay. ( G ) Migration assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control. ( H ) Invasion assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control and representative pictures of membrane.

    Journal: Oncotarget

    Article Title: Cytoplasmic, full length and novel cleaved variant, TBLR1 reduces apoptosis in prostate cancer under androgen deprivation

    doi: 10.18632/oncotarget.9005

    Figure Lengend Snippet: Function of cvTBLR1 ( A ) Overexpression of cvTBLR1 using nuclear export sequence (NES) fused cvTBLR1 (AA89-514) construct to create LNCaP –NEScvTBLR1 cells. ( B ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in hormone free media. ( C ) Caspase 3/7 luciferase assay measuring apoptosis in LNCaP pBabe and LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( D ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in hormone free media. ( E ) Quantification of the percentage of TUNEL-positive cells of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells in 150 μM bicalutamide media. ( F ) Cellular proliferation comparison of LNCaP pBabe vs. LNCaP NEScvTBLR1 cells over 6 days by CCK-8 assay. ( G ) Migration assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control. ( H ) Invasion assay of LNCaP-NEScvTBLR1 compared to LNCaP pBabe control and representative pictures of membrane.

    Article Snippet: Cell growth was monitored every 2 days by addition of 50 μl of CCK-8 reagent (Sigma Life Sciences) to the well, incubated at 37°C for 1 hour and absorbance was measured at 450 nm.

    Techniques: Over Expression, Sequencing, Construct, Luciferase, TUNEL Assay, CCK-8 Assay, Migration, Invasion Assay

    Functional consequences of ectopic ROR2 expression in RKO and SW620 cell lines. a ROR2 qRT-PCR of RKO and SW620 cell lines with ectopic ROR2 expression (pROR2 transfection) and control (pFLAG-CMV-4™ transfection) relative to expression in HCT116 cell lines. All expression results normalised against 3 housekeeping genes ( n = 1). b CCK-8 proliferation assay of RKO and SW620 cells with and without ectopic ROR2 expression ( n = 3). c Wound healing assay comparing percentage area of wound covered by RKO cells with and without ectopic ROR2 expression over a 4 day period ( n = 1). d Images of RKO cells in wound healing assay on day 0 and day 3 comparing cells with and without ectopic ROR2 expression. e Wound healing assay comparing percentage area of wound covered by SW620 cells with and without ectopic ROR2 expression over a 12 day period ( n = 1). f Images of SW620 cells in wound healing assay on day 0 and day 9 comparing cells with and without ectopic ROR2 expression

    Journal: BMC Cancer

    Article Title: ROR2 is epigenetically inactivated in the early stages of colorectal neoplasia and is associated with proliferation and migration

    doi: 10.1186/s12885-016-2576-7

    Figure Lengend Snippet: Functional consequences of ectopic ROR2 expression in RKO and SW620 cell lines. a ROR2 qRT-PCR of RKO and SW620 cell lines with ectopic ROR2 expression (pROR2 transfection) and control (pFLAG-CMV-4™ transfection) relative to expression in HCT116 cell lines. All expression results normalised against 3 housekeeping genes ( n = 1). b CCK-8 proliferation assay of RKO and SW620 cells with and without ectopic ROR2 expression ( n = 3). c Wound healing assay comparing percentage area of wound covered by RKO cells with and without ectopic ROR2 expression over a 4 day period ( n = 1). d Images of RKO cells in wound healing assay on day 0 and day 3 comparing cells with and without ectopic ROR2 expression. e Wound healing assay comparing percentage area of wound covered by SW620 cells with and without ectopic ROR2 expression over a 12 day period ( n = 1). f Images of SW620 cells in wound healing assay on day 0 and day 9 comparing cells with and without ectopic ROR2 expression

    Article Snippet: Cells were allowed to adhere for 2 h before 3 wells of ROR2 knockdown cells and 3 wells of control cells were treated with 10 μl of CCK-8 reagent (Dojindo Molecular Technologies, Inc. Rockville, MD) before the plate was wrapped in foil.

    Techniques: Functional Assay, Expressing, Quantitative RT-PCR, Transfection, CCK-8 Assay, Proliferation Assay, Wound Healing Assay

    Over-regulated miR-490-3p significantly inhibited the proliferation, migratory, invasion activities and promoted apoptotic rate of CRC cells (HCT116 and SW480). A, miR-490-3p highly expressed in HCT116 and SW480 cells after transfection with miR-mimic. B, CCK-8 assay was used to assess the proliferation ability of CRC cells transfected with miR-mimic or NC respectively. C, wound healing assay was used to elucidate the migratory ability of CRC cells transfected with miR-mimic or NC respectively. D, transwell invasion assay was used to assess the invasion ability of CRC cells transfected with miR-mimic or NC respectively. E, flow cytometry analysis was used to assess the apoptotic rate of CRC cells transfected with miR-mimic or NC respectively. * P

    Journal: Journal of Cancer

    Article Title: MiR-490-3p Functions As a Tumor Suppressor by Inhibiting Oncogene VDAC1 Expression in Colorectal Cancer

    doi: 10.7150/jca.23662

    Figure Lengend Snippet: Over-regulated miR-490-3p significantly inhibited the proliferation, migratory, invasion activities and promoted apoptotic rate of CRC cells (HCT116 and SW480). A, miR-490-3p highly expressed in HCT116 and SW480 cells after transfection with miR-mimic. B, CCK-8 assay was used to assess the proliferation ability of CRC cells transfected with miR-mimic or NC respectively. C, wound healing assay was used to elucidate the migratory ability of CRC cells transfected with miR-mimic or NC respectively. D, transwell invasion assay was used to assess the invasion ability of CRC cells transfected with miR-mimic or NC respectively. E, flow cytometry analysis was used to assess the apoptotic rate of CRC cells transfected with miR-mimic or NC respectively. * P

    Article Snippet: Cell proliferation assay Cell proliferation was measured by CCK-8 kit (KeyGEN BioTECH, China) according to the manufacturer's instructions.

    Techniques: Transfection, CCK-8 Assay, Wound Healing Assay, Transwell Invasion Assay, Flow Cytometry, Cytometry