cck-8 solution Search Results


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  • 99
    Millipore cck 8 solution
    Rapamycin protects astrocytes upon excretory/secretory product treatment via autophagy induction. Cells were pretreated with rapamycin, 3-methyladenine (3-MA), chloroquine (CQ), or bafilomycin A1 (BF) for 1 h and then incubated with 500 μg/ml A . cantonensis L5 excretory/secretory products (ESPs) for 12 h. The viability of astrocytes was analyzed by the <t>CCK-8</t> assay. The data are expressed as the means ± SD from three independent experiments ( n = 3). * P
    Cck 8 Solution, supplied by Millipore, used in various techniques. Bioz Stars score: 99/100, based on 345 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Beyotime cck 8 solution
    Effects of CA, TMZ, and CA + TMZ on cell proliferation. a The U251 cell viability was detected by <t>CCK-8</t> assay after the cells were treated with the indicated concentrations of CA. b The LN229 cell viability was detected by CCK-8 assay after the cells were treated with the indicated concentrations of CA. c The U251 cell viability was detected by CCK-8 assay after different treatments with TMZ or CA + TMZ. d The LN229 cell viability was detected by CCK-8 assay after different treatments with TMZ or CA + TMZ. The results shown are representative of three different experiments. *p
    Cck 8 Solution, supplied by Beyotime, used in various techniques. Bioz Stars score: 92/100, based on 492 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dojindo Labs cck 8 solution
    Overexpression of NDRG2 in U937 cells. (A) Cell lysates were fractionated into cytoplasmic and nuclear components. Western blotting using an anti-NDRG2 antibody was performed for each fraction. Lamin A/C and α-actinin were used as control for protein loading as well as marker proteins for nuclear and cytoplasmic fraction, respectively. (B, C) U937-mock and U937-NDRG2 cells were treated with 0.1 µg/ml PMA for 48 h. Cell viability was determined using either the trypan blue exclusion assay (B) or the <t>CCK-8</t> assay (C). The results represent the means±SD of duplicates. * p
    Cck 8 Solution, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 92/100, based on 2145 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Bimake cck 8 solution
    MI Exo promotes ADMSCs proliferation in vitro partly via ERK1/2 activation. ( A ) Inverted contrast phase microscopy showed that the number of ADMSCs was increased after treatment with MI Exo for 24 h compared with the results for control and Con Exo. Scale bar, 80 μm. ( B ) The proliferation rate of ADMSCs was measured using <t>CCK-8</t> assay after treatment with Con Exo and MI Exo for 24 h. Data are shown as mean ± SD. *, significantly different from control; *, p
    Cck 8 Solution, supplied by Bimake, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Sangon Biotech cck 8 solution
    SALL4 promotes ccRCC cells growth in vitro and in vivo. a Western blot analyses of SALL4 expression in ccRCC cells stably expressing indicated shRNA (shNC, negative control shRNA; sh#1 and sh#2, shRNAs targeting SALL4). b The <t>CCK-8</t> assays were performed in ACHN and 786-O cells treated with indicated shRNA. c Colony formation assays in ACHN and 786-O cells with indicated shRNA treatment. d Cell cycle distribution was examined by flow cytometry in ACHN and 786-O cells treated as indicated. e Cellular senescence was detected by SA-β-gal staining in ACHN and 786-O cells treated with shNC and shSALL4 (scale bar, 50 μm). f - i Scatter plot analyses were performed to determine the correlation between SALL4 and CCNE1 ( f ), CDK3 ( g ), E2F1 ( h ) and RB1 ( i ) mRNA expression levels in 533 ccRCC patients from TCGA database. Data were analyzed via LinkedOmics bioinformatics. j The image of dissected tumors from nude mice. k , l The growth curve ( k ) and their weights ( l ) of subcutaneous tumors formed by 786-O cells with indicated treatment. * P
    Cck 8 Solution, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 90/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Thermo Fisher cck 8 solution
    LncRNA-NEAT1 promoted the proliferation of HeLa and SiHa cells. ( A ) Cell viability of transfected HeLa and SiHa cells was detected by <t>CCK-8</t> assay. ( B ) The colony formation of transfected HeLa and SiHa cells was detected by anchorage-independent colony assay. Data were presented as mean ± standard deviation with three replicates. *P
    Cck 8 Solution, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 92/100, based on 865 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Toyobo cck 8 solution
    Effects of PADI3 on HCT116 and LoVo cells. RFP-expressing cells were used as controls. (A) Weak PADI3 expression was detected in HCT116 and LoVo cells. (B) Western blot analysis was used to measure PADI3 and RFP expression in both LoVo and HCT116 cells. (C, D) A <t>CCK-8</t> assay measured the proliferation of HCT116 and LoVo cells. (E) The colony formation ability of HCT116 cells was measured and statistically analyzed using a colony formation assay following 14 days of culture. (F) The colony formation ability of LoVo cells was measured and statistically analyzed using a colony formation assay following 14 days of culture. * indicates P
    Cck 8 Solution, supplied by Toyobo, used in various techniques. Bioz Stars score: 93/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Selleck Chemicals cck 8 solution
    XAV-939 treatment inhibited FAM46B silencing-induced PC cell proliferation and cell cycle process After P69 cells were transfected with siFAM46B-1 with or without XAV-939 treatment (20 μ m ), cell proliferation and cell cycle progression were measured by <t>CCK-8</t> assay a and flow cytometry b , c , and the expression of C-myc, Cyclin D1, and β-catenin was measured by western blotting d , e . PC-3 cells transfected with pLVX-Puro-FAM46B were treated with MG132 (50 μ m ) for 4 h, and the expression of FAM46B and β-catenin proteins was measured by western blotting f , g . β-catenin was immunoprecipitated and immunoblotted in P69 cells transfected with siFAM46B-1 with or without MG132 (50 μ m ) treatment for 4 h h . * P
    Cck 8 Solution, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Beijing CWBio cck 8 solution
    JTC-801 inhibits Hep G2 cell proliferation in the <t>CCK-8</t> assay. The results indicate that JTC-801 inhibited Hep G2 proliferation in a dose- and time-dependent manner. The relative cell proliferation is plotted following different doses of JTC-801 treatment for 24, 48 and 72 h. *P
    Cck 8 Solution, supplied by Beijing CWBio, 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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    Boster Bio cck 8 solution
    Both circ_0077837 and circ_0004826 exerted a tumor suppressive effect in BC cells. A, Transgene expression in EJ and 253J‐BV bladder cancer cell lines transduced with lentiviral vectors. Upper panels show phase contrast photomicrograph and lower panels show GFP fluorescence of the same field. B, Overexpression of circ_0077837 and circ_0004826 was confirmed via qRT‐PCR in BC cell lines EJ and 253J‐BV. C, Cell colony formation numbers were counted after transfection with OV‐NC, OV‐circ_7837, or OV‐circ_4826. D, <t>CCK‐8</t> assays were utilized to detect cell proliferation ability in EJ and 253J‐BV cells transfected with OV‐NC, OV‐circ_7837, or OV‐circ_4826. E and F, The migration potential of EJ and 253J‐BV cells transfected with the OV‐circ_7837 or OV‐circ_4826 than that treated with OV‐NC was damaged by the wound healing assay at 36 h after scratch and transwell migration assay (without Matrigel) at 36 h after incubation. G, Overexpression of OV‐circ_7837 or OV‐circ_4826 all impaired the invasive capacity of EJ and 253J‐BV cells as detected by transwell Matrigel invasion assay. Data are presented as means ± SD; n = 3. SD: standard deviation. OV‐: Overexpression; NC, empty vector; Circ‐7837, hsa_circ_0077837; Circ‐4826, hsa_circ_0004826; CCK‐8: cell counting kit‐8; OD: optical density. * P
    Cck 8 Solution, supplied by Boster Bio, used in various techniques. Bioz Stars score: 92/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    90
    Keygen Biotech cck 8 solution
    AGS and MKN28 human gastric cancer cell viability was significantly inhibited by the use of splicing factor 3b subunit 1 (SF3B1) small interfering RNA (siRNA) and pladienolide B. ( A ) The effect of siRNA and pladienolide B on SF3B1 expression was shown by quantitative analysis. ( B ) The chemical structure of pladienolide B, a selective mRNA splicing inhibitor of SF3B1. ( C ) The cell viability AGS and MKN28 human gastric cancer cells with SF3B1 siRNA and ( D ) pladienolide B evaluated by the Cell Counting Kit-8 <t>(CCK-8)</t> assay. The experiments were performed in triplicate. The mean±SD represents the data. * p
    Cck 8 Solution, supplied by Keygen Biotech, used in various techniques. Bioz Stars score: 90/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Peptide Institute cck 8 solution
    Effects of EGCG on HCC cell proliferation inhibition, S phage arrest, and apoptosis induction. ( A ) HCC cells were cultured with or without EGCG (25, 50, 100, 200 and 400 μM) for 24 h and cell viability was examined using the <t>CCK-8</t> method. ( B ) EGCG induced cell cycle arrest in HCC-LM3 and HepG2 cells. Cells were treated with the indicated concentrations of EGCG for 24 h, stained with propidium iodide, and analyzed by flow cytometry. ( C ) HCC-LM3 and HepG2 cells were treated with different concentrations of EGCG, and the cell apoptosis rate was examined by flow cytometry. ( D ) Western blot analysis of cleaved-caspase 3 and PARP in HCC cells treated with EGCG (0, 50, and 100 μM). β-actin was used as a loading control. Plotted values represent the mean ± standard error of three independent experiments (n = 3) (*P
    Cck 8 Solution, supplied by Peptide Institute, used in various techniques. Bioz Stars score: 92/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    Beijing Solarbio Science cck 8 solution
    Helicobacter pylori -specific lymphocyte responses and IFN-γ, interleukin-4 (IL-4), and interleukin-17 (IL-17) production in mice immunized with cholera toxin B subunit (CTB)-HUUC or CTB. (A) Assessment on proliferation of specific lymphocytes in mice after immunization with CTB-HUUC, CTB, or PBS. Splenic lymphocytes from mice immunized with CTB-HUUC, CTB, or PBS were stimulated with Concanavalin A (ConA), H. pylori lysates, H. pylori urease, or CTB. Cell proliferation was determined using <t>CCK-8</t> assay. The results were expressed as stimulation indices (SI) which represents the ratio between the proliferation rates of cells stimulated with antigens and those with the vehicle control. * p
    Cck 8 Solution, supplied by Beijing Solarbio Science, used in various techniques. Bioz Stars score: 92/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    92
    TaKaRa cck 8 solution
    MYCN promotes tumor growth by repressing ELOVL2 in vitro and vivo. a and b BE(2)-C cells stably expressing the negative control or MYCN shRNA were further infected with a lentivirus expressing ELOVL2 shRNA. SK-N-AS cells stably expressing GFP or MYCN were further infected with a lentivirus expressing ELOVL2. The BE(2)-C ( a ) and SK-N-AS ( b ) cell proliferation rate was determined using <t>CCK-8</t> and a spectrophotometer at OD450. c and d BE(2)-C ( c ) and SK-N-AS ( d ) cells were treated as described in ( a ). Cells were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. e , f and g BE(2)-C were treated as described in ( a ) and injected subcutaneously into nude mice (n = 5 for each group). Tumors were compared ( e ) at the end of the experiment. Tumor growth curves ( f ) were measured starting at 7 days after inoculation. The DHA concentration of tumors ( g ) was measured by ELISA. h , i and j SK-N-AS were treated as described in ( a ) and injected subcutaneously into nude mice (n = 5 for each group). Tumors were compared ( h ) at the end of the experiment. Tumor growth curves ( i ) were measured starting at 7 days after inoculation. The DHA concentration of tumors ( j ) was measured by ELISA. k Representative IHC analysis of ELOVL2 and H2AK119ub protein expression in SK-N-AS cells stably expressing GFP or MYCN (up) and BE(2)-C cells stably expressing the negative control or MYCN shRNA (low). l , m , n and o The results of IHC analysis of ELOVL2 and H2AK119ub protein expression are presented as bar graphs of the mean number of the ELOVL2 and H2AK119ub positive rate. p and q ELOVL2 expression significantly correlated with MYCN expression in ALL (P) and MYCN (Q) amplification clinical tumor samples from the SEQC database. * P
    Cck 8 Solution, supplied by TaKaRa, 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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    92
    Promega cck 8 solution
    Effect of D206008 on cell viability and morphology. Notes: ( A ) The effect of different concentrations (0–100 µM) of D206008 on B16 melanoma cell viability was measured by <t>CCK-8</t> assay. The data are expressed as the mean ± SD (* P
    Cck 8 Solution, supplied by Promega, used in various techniques. Bioz Stars score: 92/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Enzo Biochem cck 8 solution
    CAP sensitizes MCF-7/TxR cells to Tx. ( A ) The effect of CAP on the sensitivity of MCF-7 and MCF-7/TxR to Tx was examined by colony formation. The area of colonies is represented by a bar graph. ( B ) Effect of Tx on the growth rate of MCF-7/TxR vs. MCF-7. Cell growth was examined by <t>CCK-8</t> assay. ( C ) Effect of CAP on growth rate of MCF-7/TxR in presence of Tx. All assays were performed in triplicate, and the results are expressed as mean ± SE. * p
    Cck 8 Solution, supplied by Enzo Biochem, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    93
    Abcam cck 8 solution
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    Cck 8 Solution, supplied by Abcam, used in various techniques. Bioz Stars score: 93/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alexis Inc cck 8 solution
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    Cck 8 Solution, supplied by Alexis Inc, used in various techniques. Bioz Stars score: 92/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Signalway Antibody cck 8 solution
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    Cck 8 Solution, supplied by Signalway Antibody, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    91
    KeyGene cck 8 solution
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    Cck 8 Solution, supplied by KeyGene, used in various techniques. Bioz Stars score: 91/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore 10ul cck 8 solution
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    10ul Cck 8 Solution, supplied by Millipore, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Dojindo Labs cck 8 solution reagent
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    Cck 8 Solution Reagent, supplied by Dojindo Labs, used in various techniques. Bioz Stars score: 90/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TransGen biotech co 10ul cck 8 solution
    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using <t>CCK-8</t> assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments
    10ul Cck 8 Solution, supplied by TransGen biotech co, used in various techniques. Bioz Stars score: 91/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Rapamycin protects astrocytes upon excretory/secretory product treatment via autophagy induction. Cells were pretreated with rapamycin, 3-methyladenine (3-MA), chloroquine (CQ), or bafilomycin A1 (BF) for 1 h and then incubated with 500 μg/ml A . cantonensis L5 excretory/secretory products (ESPs) for 12 h. The viability of astrocytes was analyzed by the CCK-8 assay. The data are expressed as the means ± SD from three independent experiments ( n = 3). * P

    Journal: PLoS Neglected Tropical Diseases

    Article Title: The excretory/secretory products of fifth-stage larval Angiostrongylus cantonensis induces autophagy via the Sonic hedgehog pathway in mouse brain astrocytes

    doi: 10.1371/journal.pntd.0008290

    Figure Lengend Snippet: Rapamycin protects astrocytes upon excretory/secretory product treatment via autophagy induction. Cells were pretreated with rapamycin, 3-methyladenine (3-MA), chloroquine (CQ), or bafilomycin A1 (BF) for 1 h and then incubated with 500 μg/ml A . cantonensis L5 excretory/secretory products (ESPs) for 12 h. The viability of astrocytes was analyzed by the CCK-8 assay. The data are expressed as the means ± SD from three independent experiments ( n = 3). * P

    Article Snippet: Cell viability assay To detect cell viability in astrocytes after treatment with ESPs or drugs, the cells (1x107 cells/ml) were incubated with 50 ml of CCK-8 solution (Cell Counting Kit-8) (Sigma-Aldrich, USA) at 37°C in the dark with mild shaking for 1 h. In the presence of cells, highly water-soluble tetrazolium salt WST-8 [2-(2-methoxy-4-nitrophenyl)-3-(4-nitrophenyl)-5-(2, 4-disulfophenyl)- 2H-tetrazolium, monosodium salt] produces formazan dye.

    Techniques: Incubation, CCK-8 Assay

    Effects of CA, TMZ, and CA + TMZ on cell proliferation. a The U251 cell viability was detected by CCK-8 assay after the cells were treated with the indicated concentrations of CA. b The LN229 cell viability was detected by CCK-8 assay after the cells were treated with the indicated concentrations of CA. c The U251 cell viability was detected by CCK-8 assay after different treatments with TMZ or CA + TMZ. d The LN229 cell viability was detected by CCK-8 assay after different treatments with TMZ or CA + TMZ. The results shown are representative of three different experiments. *p

    Journal: Journal of Neuro-Oncology

    Article Title: Carnosic acid potentiates the anticancer effect of temozolomide by inducing apoptosis and autophagy in glioma

    doi: 10.1007/s11060-018-03043-5

    Figure Lengend Snippet: Effects of CA, TMZ, and CA + TMZ on cell proliferation. a The U251 cell viability was detected by CCK-8 assay after the cells were treated with the indicated concentrations of CA. b The LN229 cell viability was detected by CCK-8 assay after the cells were treated with the indicated concentrations of CA. c The U251 cell viability was detected by CCK-8 assay after different treatments with TMZ or CA + TMZ. d The LN229 cell viability was detected by CCK-8 assay after different treatments with TMZ or CA + TMZ. The results shown are representative of three different experiments. *p

    Article Snippet: The cells were then incubated with CA, TMZ, or CA + TMZ at the indicated concentrations for 24 h, 48 h, and 72 h. Subsequently, each well was filled with 10 µL CCK-8 solution (Beyotime, Shanghai, China), and the plate was incubated for 4 h at 37 °C.

    Techniques: CCK-8 Assay

    Dose-dependent effects of BSSG on cell proliferation. Dose-dependent effects of BSSG on cell proliferation were determined by CCK-8 assay and the data are plotted as percentages of control cell proliferation. Data are presented as Mean ± SD ( n = 6); * P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Microarray Analysis of mRNA and MicroRNA Expression Profile Reveals the Role of β-Sitosterol-D-glucoside in the Proliferation of Neural Stem Cell

    doi: 10.1155/2013/360302

    Figure Lengend Snippet: Dose-dependent effects of BSSG on cell proliferation. Dose-dependent effects of BSSG on cell proliferation were determined by CCK-8 assay and the data are plotted as percentages of control cell proliferation. Data are presented as Mean ± SD ( n = 6); * P

    Article Snippet: The cells were treated for 72 h as described, whereafter CCK-8 solution (Beyotime Biotech, Haimen, China) was added to the cell culture medium to a final concentration of 10 μ L/100 μ L and incubated for another 4 h at 37°C.

    Techniques: CCK-8 Assay

    Comparison of NSC Proliferation Promoted by BSSG, BFGF, and EGF. Comparison of NSC proliferation promoted by BSSG, bFGF and EGF was determined by CCK-8 assay and the data are plotted as percentages of control cell proliferation. Data are presented as Mean ± SD ( n = 6); ** P

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Microarray Analysis of mRNA and MicroRNA Expression Profile Reveals the Role of β-Sitosterol-D-glucoside in the Proliferation of Neural Stem Cell

    doi: 10.1155/2013/360302

    Figure Lengend Snippet: Comparison of NSC Proliferation Promoted by BSSG, BFGF, and EGF. Comparison of NSC proliferation promoted by BSSG, bFGF and EGF was determined by CCK-8 assay and the data are plotted as percentages of control cell proliferation. Data are presented as Mean ± SD ( n = 6); ** P

    Article Snippet: The cells were treated for 72 h as described, whereafter CCK-8 solution (Beyotime Biotech, Haimen, China) was added to the cell culture medium to a final concentration of 10 μ L/100 μ L and incubated for another 4 h at 37°C.

    Techniques: CCK-8 Assay

    Overexpression of NDRG2 in U937 cells. (A) Cell lysates were fractionated into cytoplasmic and nuclear components. Western blotting using an anti-NDRG2 antibody was performed for each fraction. Lamin A/C and α-actinin were used as control for protein loading as well as marker proteins for nuclear and cytoplasmic fraction, respectively. (B, C) U937-mock and U937-NDRG2 cells were treated with 0.1 µg/ml PMA for 48 h. Cell viability was determined using either the trypan blue exclusion assay (B) or the CCK-8 assay (C). The results represent the means±SD of duplicates. * p

    Journal: Immune Network

    Article Title: NDRG2 Promotes GATA-1 Expression through Regulation of the JAK2/STAT Pathway in PMA-stimulated U937 Cells

    doi: 10.4110/in.2011.11.6.348

    Figure Lengend Snippet: Overexpression of NDRG2 in U937 cells. (A) Cell lysates were fractionated into cytoplasmic and nuclear components. Western blotting using an anti-NDRG2 antibody was performed for each fraction. Lamin A/C and α-actinin were used as control for protein loading as well as marker proteins for nuclear and cytoplasmic fraction, respectively. (B, C) U937-mock and U937-NDRG2 cells were treated with 0.1 µg/ml PMA for 48 h. Cell viability was determined using either the trypan blue exclusion assay (B) or the CCK-8 assay (C). The results represent the means±SD of duplicates. * p

    Article Snippet: Then, 10µl of CCK-8 solution (Dojindo, Gaithersburg, MD) was added to each well.

    Techniques: Over Expression, Western Blot, Marker, Trypan Blue Exclusion Assay, CCK-8 Assay

    Isorhamnetin inhibits proliferation and induces apoptosis of breast cancer cells. (A) The cells were treated with various concentrations of isorhamnetin for 72 h, cell proliferation was determined using a Cell Counting kit-8 (CCK-8) assay and the IC 50 was calculated. * P

    Journal: Molecular Medicine Reports

    Article Title: Isorhamnetin inhibits cell proliferation and induces apoptosis in breast cancer via Akt and mitogen-activated protein kinase kinase signaling pathways

    doi: 10.3892/mmr.2015.4269

    Figure Lengend Snippet: Isorhamnetin inhibits proliferation and induces apoptosis of breast cancer cells. (A) The cells were treated with various concentrations of isorhamnetin for 72 h, cell proliferation was determined using a Cell Counting kit-8 (CCK-8) assay and the IC 50 was calculated. * P

    Article Snippet: The cells were then treated with various concentrations of isorhamnetin (100, 33.3, 11.1, 3.7, 1.2, 0.4 and 0 µ M) for 48 h, and cell proliferation rates were determined by adding 10 µ l CCK-8 solution (Dojindo Molecular Technologies, Inc., Kumamoto, Japan) prior to incubation at 37°C for 2 h. The absorbance was measured at a wavelength of 450 nm using a SpectraMax 190 Microplate Reader (Molecular Devices, LLC, Sunnyvale, CA, USA).

    Techniques: Cell Counting, CCK-8 Assay

    MI Exo promotes ADMSCs proliferation in vitro partly via ERK1/2 activation. ( A ) Inverted contrast phase microscopy showed that the number of ADMSCs was increased after treatment with MI Exo for 24 h compared with the results for control and Con Exo. Scale bar, 80 μm. ( B ) The proliferation rate of ADMSCs was measured using CCK-8 assay after treatment with Con Exo and MI Exo for 24 h. Data are shown as mean ± SD. *, significantly different from control; *, p

    Journal: Theranostics

    Article Title: Cardio-renal Exosomes in Myocardial Infarction Serum Regulate Proangiogenic Paracrine Signaling in Adipose Mesenchymal Stem Cells

    doi: 10.7150/thno.37678

    Figure Lengend Snippet: MI Exo promotes ADMSCs proliferation in vitro partly via ERK1/2 activation. ( A ) Inverted contrast phase microscopy showed that the number of ADMSCs was increased after treatment with MI Exo for 24 h compared with the results for control and Con Exo. Scale bar, 80 μm. ( B ) The proliferation rate of ADMSCs was measured using CCK-8 assay after treatment with Con Exo and MI Exo for 24 h. Data are shown as mean ± SD. *, significantly different from control; *, p

    Article Snippet: After the indicated treatments, 10 µL CCK-8 solution (Bimake, China) was added into each well.

    Techniques: In Vitro, Activation Assay, Microscopy, CCK-8 Assay

    SALL4 promotes ccRCC cells growth in vitro and in vivo. a Western blot analyses of SALL4 expression in ccRCC cells stably expressing indicated shRNA (shNC, negative control shRNA; sh#1 and sh#2, shRNAs targeting SALL4). b The CCK-8 assays were performed in ACHN and 786-O cells treated with indicated shRNA. c Colony formation assays in ACHN and 786-O cells with indicated shRNA treatment. d Cell cycle distribution was examined by flow cytometry in ACHN and 786-O cells treated as indicated. e Cellular senescence was detected by SA-β-gal staining in ACHN and 786-O cells treated with shNC and shSALL4 (scale bar, 50 μm). f - i Scatter plot analyses were performed to determine the correlation between SALL4 and CCNE1 ( f ), CDK3 ( g ), E2F1 ( h ) and RB1 ( i ) mRNA expression levels in 533 ccRCC patients from TCGA database. Data were analyzed via LinkedOmics bioinformatics. j The image of dissected tumors from nude mice. k , l The growth curve ( k ) and their weights ( l ) of subcutaneous tumors formed by 786-O cells with indicated treatment. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: VHL mutation-mediated SALL4 overexpression promotes tumorigenesis and vascularization of clear cell renal cell carcinoma via Akt/GSK-3β signaling

    doi: 10.1186/s13046-020-01609-8

    Figure Lengend Snippet: SALL4 promotes ccRCC cells growth in vitro and in vivo. a Western blot analyses of SALL4 expression in ccRCC cells stably expressing indicated shRNA (shNC, negative control shRNA; sh#1 and sh#2, shRNAs targeting SALL4). b The CCK-8 assays were performed in ACHN and 786-O cells treated with indicated shRNA. c Colony formation assays in ACHN and 786-O cells with indicated shRNA treatment. d Cell cycle distribution was examined by flow cytometry in ACHN and 786-O cells treated as indicated. e Cellular senescence was detected by SA-β-gal staining in ACHN and 786-O cells treated with shNC and shSALL4 (scale bar, 50 μm). f - i Scatter plot analyses were performed to determine the correlation between SALL4 and CCNE1 ( f ), CDK3 ( g ), E2F1 ( h ) and RB1 ( i ) mRNA expression levels in 533 ccRCC patients from TCGA database. Data were analyzed via LinkedOmics bioinformatics. j The image of dissected tumors from nude mice. k , l The growth curve ( k ) and their weights ( l ) of subcutaneous tumors formed by 786-O cells with indicated treatment. * P

    Article Snippet: Cell growth was monitored by incubation with CCK-8 solution (Sangon Biotech) following the manufacturer’s protocols.

    Techniques: In Vitro, In Vivo, Western Blot, Expressing, Stable Transfection, shRNA, Negative Control, CCK-8 Assay, Flow Cytometry, Staining, Mouse Assay

    SALL4 induces ccRCC angiogenesis in vitro. a Enriched gene ontology (GO) term and KEGG pathway analysis of genes significantly correlated with SALL4 in ccRCC. b , c Gene set enrichment analysis (GSEA) profiles for the genes significantly correlated with SALL4 in ccRCC. Data ( a - c ) from TCGA database were analyzed via LinkedOmics bioinformatics. d HUVECs were treated with serum-free medium (SFM) or conditioned medium (CMs) from ACHN-shNC/shSALL4 cells. After treatment for 72 h, CCK-8 assays were performed to evaluate cell proliferation. e Flow cytometry analyses of cell cycle distribution in HUVECs treated with SFM or CMs from ACHN-shNC/shSALL4 cells. f Wound-healing assay was performed to determine the migration of HUVECs with CMs treatment (scale bar, 200 μm). g Representative images and quantification analyses of the recruitment of HUVECs co-cultured with indicated CMs ( upper ) or ACHN-shNC/shSALL4 cells ( lower ) in lower chambers (scale bar, 100 μm). h, i Representative images ( h ) and quantification analyses ( i ) of tube formation in HUVECs treated with SFM or indicated CMs (scale bar, 100 μm). j The expression level of VEGFA in CMs from ACHN-shNC/shSALL4 cells was detected by ELISA assay. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: VHL mutation-mediated SALL4 overexpression promotes tumorigenesis and vascularization of clear cell renal cell carcinoma via Akt/GSK-3β signaling

    doi: 10.1186/s13046-020-01609-8

    Figure Lengend Snippet: SALL4 induces ccRCC angiogenesis in vitro. a Enriched gene ontology (GO) term and KEGG pathway analysis of genes significantly correlated with SALL4 in ccRCC. b , c Gene set enrichment analysis (GSEA) profiles for the genes significantly correlated with SALL4 in ccRCC. Data ( a - c ) from TCGA database were analyzed via LinkedOmics bioinformatics. d HUVECs were treated with serum-free medium (SFM) or conditioned medium (CMs) from ACHN-shNC/shSALL4 cells. After treatment for 72 h, CCK-8 assays were performed to evaluate cell proliferation. e Flow cytometry analyses of cell cycle distribution in HUVECs treated with SFM or CMs from ACHN-shNC/shSALL4 cells. f Wound-healing assay was performed to determine the migration of HUVECs with CMs treatment (scale bar, 200 μm). g Representative images and quantification analyses of the recruitment of HUVECs co-cultured with indicated CMs ( upper ) or ACHN-shNC/shSALL4 cells ( lower ) in lower chambers (scale bar, 100 μm). h, i Representative images ( h ) and quantification analyses ( i ) of tube formation in HUVECs treated with SFM or indicated CMs (scale bar, 100 μm). j The expression level of VEGFA in CMs from ACHN-shNC/shSALL4 cells was detected by ELISA assay. * P

    Article Snippet: Cell growth was monitored by incubation with CCK-8 solution (Sangon Biotech) following the manufacturer’s protocols.

    Techniques: In Vitro, CCK-8 Assay, Flow Cytometry, Wound Healing Assay, Migration, Cell Culture, Expressing, Enzyme-linked Immunosorbent Assay

    LncRNA-NEAT1 promoted the proliferation of HeLa and SiHa cells. ( A ) Cell viability of transfected HeLa and SiHa cells was detected by CCK-8 assay. ( B ) The colony formation of transfected HeLa and SiHa cells was detected by anchorage-independent colony assay. Data were presented as mean ± standard deviation with three replicates. *P

    Journal: OncoTargets and therapy

    Article Title: Long Non-Coding RNA-NEAT1 Promotes Cell Migration and Invasion via Regulating miR-124/NF-κB Pathway in Cervical Cancer

    doi: 10.2147/OTT.S220306

    Figure Lengend Snippet: LncRNA-NEAT1 promoted the proliferation of HeLa and SiHa cells. ( A ) Cell viability of transfected HeLa and SiHa cells was detected by CCK-8 assay. ( B ) The colony formation of transfected HeLa and SiHa cells was detected by anchorage-independent colony assay. Data were presented as mean ± standard deviation with three replicates. *P

    Article Snippet: At 24, 48, 72, and 96 h post-culturing, cells were incubated with CCK-8 solution (Invitrogen) for 4 h. The optical density (OD) at 450 nm was detected by a spectrophotometer (Bio-Rad, USA).

    Techniques: Transfection, CCK-8 Assay, Colony Assay, Standard Deviation

    Effects of PADI3 on HCT116 and LoVo cells. RFP-expressing cells were used as controls. (A) Weak PADI3 expression was detected in HCT116 and LoVo cells. (B) Western blot analysis was used to measure PADI3 and RFP expression in both LoVo and HCT116 cells. (C, D) A CCK-8 assay measured the proliferation of HCT116 and LoVo cells. (E) The colony formation ability of HCT116 cells was measured and statistically analyzed using a colony formation assay following 14 days of culture. (F) The colony formation ability of LoVo cells was measured and statistically analyzed using a colony formation assay following 14 days of culture. * indicates P

    Journal: Cancer Biology & Medicine

    Article Title: PADI3 induces cell cycle arrest via the Sirt2/AKT/p21 pathway and acts as a tumor suppressor gene in colon cancer

    doi: 10.20892/j.issn.2095-3941.2019.0065

    Figure Lengend Snippet: Effects of PADI3 on HCT116 and LoVo cells. RFP-expressing cells were used as controls. (A) Weak PADI3 expression was detected in HCT116 and LoVo cells. (B) Western blot analysis was used to measure PADI3 and RFP expression in both LoVo and HCT116 cells. (C, D) A CCK-8 assay measured the proliferation of HCT116 and LoVo cells. (E) The colony formation ability of HCT116 cells was measured and statistically analyzed using a colony formation assay following 14 days of culture. (F) The colony formation ability of LoVo cells was measured and statistically analyzed using a colony formation assay following 14 days of culture. * indicates P

    Article Snippet: After culturing for 48 h at 37°C with 5% CO2 , CCK-8 solution (Toyobo, Japan) at a concentration of 10 μL/well was added to the cell culture medium, and culturing was continued for another 2 h. The absorbance was measured at 450 nm with a spectrophotometer (SpectraMax 190, Molecular Devices, USA).

    Techniques: Expressing, Western Blot, CCK-8 Assay, Colony Assay

    Functional analysis of different PADI3 domains. (A) Predicting the PADI3-domain structure using SMART. (B) Western blot analysis was used to detect the expression of different PADI3 domains in HCT116 cells. (C) CCK-8 assay was used to measure the cell proliferation activity of different PADI3 domains. * indicates P

    Journal: Cancer Biology & Medicine

    Article Title: PADI3 induces cell cycle arrest via the Sirt2/AKT/p21 pathway and acts as a tumor suppressor gene in colon cancer

    doi: 10.20892/j.issn.2095-3941.2019.0065

    Figure Lengend Snippet: Functional analysis of different PADI3 domains. (A) Predicting the PADI3-domain structure using SMART. (B) Western blot analysis was used to detect the expression of different PADI3 domains in HCT116 cells. (C) CCK-8 assay was used to measure the cell proliferation activity of different PADI3 domains. * indicates P

    Article Snippet: After culturing for 48 h at 37°C with 5% CO2 , CCK-8 solution (Toyobo, Japan) at a concentration of 10 μL/well was added to the cell culture medium, and culturing was continued for another 2 h. The absorbance was measured at 450 nm with a spectrophotometer (SpectraMax 190, Molecular Devices, USA).

    Techniques: Functional Assay, Western Blot, Expressing, CCK-8 Assay, Activity Assay

    Effects of Sirt2 on PADI3-expressing HCT116 cells. PADI3-expressing HCT116 cells were transfected with pCDNA3.1-Sirt2-iso1 plasmids (OE-PADI3-Sirt2-iso1) or pCDNA3.1-Sirt2-iso2 plasmids (OE-PADI3-Sirt2-iso2) separately. PADI3-expressing HCT116 cells were used as the positive control, and RFP-expressing HCT116 cells were used as the negative control. (A) Western blot analysis was used to measure the expression of AKT, p-AKT, Snail and p21. (B) A CCK-8 assay was used to measure cell proliferation. (C) The cell cycle was analyzed using FCM. (D) Statistical analysis of C. (E) Colony number and size were analyzed. (F) Statistical analysis of E. * indicates P

    Journal: Cancer Biology & Medicine

    Article Title: PADI3 induces cell cycle arrest via the Sirt2/AKT/p21 pathway and acts as a tumor suppressor gene in colon cancer

    doi: 10.20892/j.issn.2095-3941.2019.0065

    Figure Lengend Snippet: Effects of Sirt2 on PADI3-expressing HCT116 cells. PADI3-expressing HCT116 cells were transfected with pCDNA3.1-Sirt2-iso1 plasmids (OE-PADI3-Sirt2-iso1) or pCDNA3.1-Sirt2-iso2 plasmids (OE-PADI3-Sirt2-iso2) separately. PADI3-expressing HCT116 cells were used as the positive control, and RFP-expressing HCT116 cells were used as the negative control. (A) Western blot analysis was used to measure the expression of AKT, p-AKT, Snail and p21. (B) A CCK-8 assay was used to measure cell proliferation. (C) The cell cycle was analyzed using FCM. (D) Statistical analysis of C. (E) Colony number and size were analyzed. (F) Statistical analysis of E. * indicates P

    Article Snippet: After culturing for 48 h at 37°C with 5% CO2 , CCK-8 solution (Toyobo, Japan) at a concentration of 10 μL/well was added to the cell culture medium, and culturing was continued for another 2 h. The absorbance was measured at 450 nm with a spectrophotometer (SpectraMax 190, Molecular Devices, USA).

    Techniques: Expressing, Transfection, Positive Control, Negative Control, Western Blot, CCK-8 Assay

    XAV-939 treatment inhibited FAM46B silencing-induced PC cell proliferation and cell cycle process After P69 cells were transfected with siFAM46B-1 with or without XAV-939 treatment (20 μ m ), cell proliferation and cell cycle progression were measured by CCK-8 assay a and flow cytometry b , c , and the expression of C-myc, Cyclin D1, and β-catenin was measured by western blotting d , e . PC-3 cells transfected with pLVX-Puro-FAM46B were treated with MG132 (50 μ m ) for 4 h, and the expression of FAM46B and β-catenin proteins was measured by western blotting f , g . β-catenin was immunoprecipitated and immunoblotted in P69 cells transfected with siFAM46B-1 with or without MG132 (50 μ m ) treatment for 4 h h . * P

    Journal: Experimental & Molecular Medicine

    Article Title: FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

    doi: 10.1038/s12276-018-0184-0

    Figure Lengend Snippet: XAV-939 treatment inhibited FAM46B silencing-induced PC cell proliferation and cell cycle process After P69 cells were transfected with siFAM46B-1 with or without XAV-939 treatment (20 μ m ), cell proliferation and cell cycle progression were measured by CCK-8 assay a and flow cytometry b , c , and the expression of C-myc, Cyclin D1, and β-catenin was measured by western blotting d , e . PC-3 cells transfected with pLVX-Puro-FAM46B were treated with MG132 (50 μ m ) for 4 h, and the expression of FAM46B and β-catenin proteins was measured by western blotting f , g . β-catenin was immunoprecipitated and immunoblotted in P69 cells transfected with siFAM46B-1 with or without MG132 (50 μ m ) treatment for 4 h h . * P

    Article Snippet: After 0, 24, 48, and 72 h, CCK-8 solution (10 μl per well) was added to P69, LNCaP, and PC-3 cells transfected with siFAM46B-1, siFAM46B-2, or pLVX-Puro-FAM46B with or without XAV-939 (20 μm ; Selleck, Houston, TX, USA) treatment.

    Techniques: Transfection, CCK-8 Assay, Flow Cytometry, Cytometry, Expressing, Western Blot, Immunoprecipitation

    FAM46B overexpression inhibited cell proliferation and cell cycle progression in LNCaP and PC-3 cells After LNCaP and PC-3 cells were transfected with pLVX-Puro-FAM46B, cell proliferation, cell cycle progression and the expression of C-myc, Cyclin D1, and β-catenin were measured by CCK-8 assay a , b , flow cytometry c – f , and western blotting g , h , respectively. ** P

    Journal: Experimental & Molecular Medicine

    Article Title: FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

    doi: 10.1038/s12276-018-0184-0

    Figure Lengend Snippet: FAM46B overexpression inhibited cell proliferation and cell cycle progression in LNCaP and PC-3 cells After LNCaP and PC-3 cells were transfected with pLVX-Puro-FAM46B, cell proliferation, cell cycle progression and the expression of C-myc, Cyclin D1, and β-catenin were measured by CCK-8 assay a , b , flow cytometry c – f , and western blotting g , h , respectively. ** P

    Article Snippet: After 0, 24, 48, and 72 h, CCK-8 solution (10 μl per well) was added to P69, LNCaP, and PC-3 cells transfected with siFAM46B-1, siFAM46B-2, or pLVX-Puro-FAM46B with or without XAV-939 (20 μm ; Selleck, Houston, TX, USA) treatment.

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

    FAM46B silencing promoted cell proliferation and cell cycle progression in P69 cells After P69 cells were transfected with siFAM46B-1 and siFAM46B-2, cell proliferation, cell cycle progression and the expression of C-myc, Cyclin D1, and β-catenin were measured by CCK-8 assay a , flow cytometry b , c , and western blotting d , respectively. ** P

    Journal: Experimental & Molecular Medicine

    Article Title: FAM46B inhibits cell proliferation and cell cycle progression in prostate cancer through ubiquitination of β-catenin

    doi: 10.1038/s12276-018-0184-0

    Figure Lengend Snippet: FAM46B silencing promoted cell proliferation and cell cycle progression in P69 cells After P69 cells were transfected with siFAM46B-1 and siFAM46B-2, cell proliferation, cell cycle progression and the expression of C-myc, Cyclin D1, and β-catenin were measured by CCK-8 assay a , flow cytometry b , c , and western blotting d , respectively. ** P

    Article Snippet: After 0, 24, 48, and 72 h, CCK-8 solution (10 μl per well) was added to P69, LNCaP, and PC-3 cells transfected with siFAM46B-1, siFAM46B-2, or pLVX-Puro-FAM46B with or without XAV-939 (20 μm ; Selleck, Houston, TX, USA) treatment.

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

    JTC-801 inhibits Hep G2 cell proliferation in the CCK-8 assay. The results indicate that JTC-801 inhibited Hep G2 proliferation in a dose- and time-dependent manner. The relative cell proliferation is plotted following different doses of JTC-801 treatment for 24, 48 and 72 h. *P

    Journal: Oncology Letters

    Article Title: JTC-801 inhibits the proliferation and metastasis of the Hep G2 hepatoblastoma cell line by regulating the phosphatidylinositol 3-kinase/protein kinase B signalling pathway

    doi: 10.3892/ol.2018.9780

    Figure Lengend Snippet: JTC-801 inhibits Hep G2 cell proliferation in the CCK-8 assay. The results indicate that JTC-801 inhibited Hep G2 proliferation in a dose- and time-dependent manner. The relative cell proliferation is plotted following different doses of JTC-801 treatment for 24, 48 and 72 h. *P

    Article Snippet: The cells were cultured in a 5% CO2 incubator at room temperature to detect cell viability once every 24 h. Prior to detection, 10 µl CCK-8 solution (CWBio) was added to each well and incubated at 37°C for 1.5 h. The optical density (OD) was measured with a microplate reader at 450 nm and the growth curve was plotted.

    Techniques: CCK-8 Assay

    Both circ_0077837 and circ_0004826 exerted a tumor suppressive effect in BC cells. A, Transgene expression in EJ and 253J‐BV bladder cancer cell lines transduced with lentiviral vectors. Upper panels show phase contrast photomicrograph and lower panels show GFP fluorescence of the same field. B, Overexpression of circ_0077837 and circ_0004826 was confirmed via qRT‐PCR in BC cell lines EJ and 253J‐BV. C, Cell colony formation numbers were counted after transfection with OV‐NC, OV‐circ_7837, or OV‐circ_4826. D, CCK‐8 assays were utilized to detect cell proliferation ability in EJ and 253J‐BV cells transfected with OV‐NC, OV‐circ_7837, or OV‐circ_4826. E and F, The migration potential of EJ and 253J‐BV cells transfected with the OV‐circ_7837 or OV‐circ_4826 than that treated with OV‐NC was damaged by the wound healing assay at 36 h after scratch and transwell migration assay (without Matrigel) at 36 h after incubation. G, Overexpression of OV‐circ_7837 or OV‐circ_4826 all impaired the invasive capacity of EJ and 253J‐BV cells as detected by transwell Matrigel invasion assay. Data are presented as means ± SD; n = 3. SD: standard deviation. OV‐: Overexpression; NC, empty vector; Circ‐7837, hsa_circ_0077837; Circ‐4826, hsa_circ_0004826; CCK‐8: cell counting kit‐8; OD: optical density. * P

    Journal: Cancer Medicine

    Article Title: Downregulated hsa_circ_0077837 and hsa_circ_0004826, facilitate bladder cancer progression and predict poor prognosis for bladder cancer patients, et al. Downregulated hsa_circ_0077837 and hsa_circ_0004826, facilitate bladder cancer progression and predict poor prognosis for bladder cancer patients

    doi: 10.1002/cam4.3006

    Figure Lengend Snippet: Both circ_0077837 and circ_0004826 exerted a tumor suppressive effect in BC cells. A, Transgene expression in EJ and 253J‐BV bladder cancer cell lines transduced with lentiviral vectors. Upper panels show phase contrast photomicrograph and lower panels show GFP fluorescence of the same field. B, Overexpression of circ_0077837 and circ_0004826 was confirmed via qRT‐PCR in BC cell lines EJ and 253J‐BV. C, Cell colony formation numbers were counted after transfection with OV‐NC, OV‐circ_7837, or OV‐circ_4826. D, CCK‐8 assays were utilized to detect cell proliferation ability in EJ and 253J‐BV cells transfected with OV‐NC, OV‐circ_7837, or OV‐circ_4826. E and F, The migration potential of EJ and 253J‐BV cells transfected with the OV‐circ_7837 or OV‐circ_4826 than that treated with OV‐NC was damaged by the wound healing assay at 36 h after scratch and transwell migration assay (without Matrigel) at 36 h after incubation. G, Overexpression of OV‐circ_7837 or OV‐circ_4826 all impaired the invasive capacity of EJ and 253J‐BV cells as detected by transwell Matrigel invasion assay. Data are presented as means ± SD; n = 3. SD: standard deviation. OV‐: Overexpression; NC, empty vector; Circ‐7837, hsa_circ_0077837; Circ‐4826, hsa_circ_0004826; CCK‐8: cell counting kit‐8; OD: optical density. * P

    Article Snippet: Subsequently, each well was supplemented with 10 μL CCK‐8 solution (Boster Bio) and incubated for 3.5 hours in dark.

    Techniques: Expressing, Transduction, Fluorescence, Over Expression, Quantitative RT-PCR, Transfection, CCK-8 Assay, Migration, Wound Healing Assay, Transwell Migration Assay, Incubation, Invasion Assay, Standard Deviation, Plasmid Preparation, Cell Counting

    AGS and MKN28 human gastric cancer cell viability was significantly inhibited by the use of splicing factor 3b subunit 1 (SF3B1) small interfering RNA (siRNA) and pladienolide B. ( A ) The effect of siRNA and pladienolide B on SF3B1 expression was shown by quantitative analysis. ( B ) The chemical structure of pladienolide B, a selective mRNA splicing inhibitor of SF3B1. ( C ) The cell viability AGS and MKN28 human gastric cancer cells with SF3B1 siRNA and ( D ) pladienolide B evaluated by the Cell Counting Kit-8 (CCK-8) assay. The experiments were performed in triplicate. The mean±SD represents the data. * p

    Journal: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research

    Article Title: Inhibition of Splicing Factor 3b Subunit 1 (SF3B1) Reduced Cell Proliferation, Induced Apoptosis and Resulted in Cell Cycle Arrest by Regulating Homeobox A10 (HOXA10) Splicing in AGS and MKN28 Human Gastric Cancer Cells

    doi: 10.12659/MSM.919460

    Figure Lengend Snippet: AGS and MKN28 human gastric cancer cell viability was significantly inhibited by the use of splicing factor 3b subunit 1 (SF3B1) small interfering RNA (siRNA) and pladienolide B. ( A ) The effect of siRNA and pladienolide B on SF3B1 expression was shown by quantitative analysis. ( B ) The chemical structure of pladienolide B, a selective mRNA splicing inhibitor of SF3B1. ( C ) The cell viability AGS and MKN28 human gastric cancer cells with SF3B1 siRNA and ( D ) pladienolide B evaluated by the Cell Counting Kit-8 (CCK-8) assay. The experiments were performed in triplicate. The mean±SD represents the data. * p

    Article Snippet: During detection, 20 μL of CCK-8 solution (KeyGen Biotech Co. Ltd., Nanjing, China) was added into each well, and plates were incubated for a further 2 h. The absorbance at 450 nm was measured with a microplate spectrophotometer reader.

    Techniques: Small Interfering RNA, Expressing, Cell Counting, CCK-8 Assay

    Effects of EGCG on HCC cell proliferation inhibition, S phage arrest, and apoptosis induction. ( A ) HCC cells were cultured with or without EGCG (25, 50, 100, 200 and 400 μM) for 24 h and cell viability was examined using the CCK-8 method. ( B ) EGCG induced cell cycle arrest in HCC-LM3 and HepG2 cells. Cells were treated with the indicated concentrations of EGCG for 24 h, stained with propidium iodide, and analyzed by flow cytometry. ( C ) HCC-LM3 and HepG2 cells were treated with different concentrations of EGCG, and the cell apoptosis rate was examined by flow cytometry. ( D ) Western blot analysis of cleaved-caspase 3 and PARP in HCC cells treated with EGCG (0, 50, and 100 μM). β-actin was used as a loading control. Plotted values represent the mean ± standard error of three independent experiments (n = 3) (*P

    Journal: Scientific Reports

    Article Title: In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity

    doi: 10.1038/srep28479

    Figure Lengend Snippet: Effects of EGCG on HCC cell proliferation inhibition, S phage arrest, and apoptosis induction. ( A ) HCC cells were cultured with or without EGCG (25, 50, 100, 200 and 400 μM) for 24 h and cell viability was examined using the CCK-8 method. ( B ) EGCG induced cell cycle arrest in HCC-LM3 and HepG2 cells. Cells were treated with the indicated concentrations of EGCG for 24 h, stained with propidium iodide, and analyzed by flow cytometry. ( C ) HCC-LM3 and HepG2 cells were treated with different concentrations of EGCG, and the cell apoptosis rate was examined by flow cytometry. ( D ) Western blot analysis of cleaved-caspase 3 and PARP in HCC cells treated with EGCG (0, 50, and 100 μM). β-actin was used as a loading control. Plotted values represent the mean ± standard error of three independent experiments (n = 3) (*P

    Article Snippet: Cell proliferation analysis HCC cells were cultured with the indicated concentrations of EGCG before the addition of 10 μl CCK-8 solution (Peptide Institute Inc., Osaka, Japan) to each well.

    Techniques: Inhibition, Cell Culture, CCK-8 Assay, Staining, Flow Cytometry, Cytometry, Western Blot

    EGCG increased sorafenib induced cell growth inhibition in both sorafenib-resistant HCC cells and nude mice bearing xenograft tumors. ( A ) After sorafenib (5–80 μM) treatment for 24 h, HCC cells (5 × 10 4 ) were harvested and analyzed for cell growth inhibition using the CCK-8 assay. ( B , C ) HCC-LM3 and HepG2 cells were exposed to EGCG (25 μM), sorafenib (5 μM), or combination treatment for 24 h, cell proliferation was analyzed using the CCK-8 assay ( B ), and PFK mRNA expression was tested using qRT-PCR ( C ). ( D – I ) In a xenograft mouse model, mice were treated with EGCG (10 mg/kg BW per day) alone, sorafenib (10 mg/kg BW per day) alone, or combination treatment for 30 days. At the time points indicated, the following measurements were performed: diameter of tumors ( D,E ), changes in the diameter of tumors ( F ), changes in body weight ( G ), and the percent of TUNEL-positive tumor cells ( H , I ). Plotted values represent the mean ± standard error of three independent experiments (n = 3) (*P

    Journal: Scientific Reports

    Article Title: In vitro and in vivo study of epigallocatechin-3-gallate-induced apoptosis in aerobic glycolytic hepatocellular carcinoma cells involving inhibition of phosphofructokinase activity

    doi: 10.1038/srep28479

    Figure Lengend Snippet: EGCG increased sorafenib induced cell growth inhibition in both sorafenib-resistant HCC cells and nude mice bearing xenograft tumors. ( A ) After sorafenib (5–80 μM) treatment for 24 h, HCC cells (5 × 10 4 ) were harvested and analyzed for cell growth inhibition using the CCK-8 assay. ( B , C ) HCC-LM3 and HepG2 cells were exposed to EGCG (25 μM), sorafenib (5 μM), or combination treatment for 24 h, cell proliferation was analyzed using the CCK-8 assay ( B ), and PFK mRNA expression was tested using qRT-PCR ( C ). ( D – I ) In a xenograft mouse model, mice were treated with EGCG (10 mg/kg BW per day) alone, sorafenib (10 mg/kg BW per day) alone, or combination treatment for 30 days. At the time points indicated, the following measurements were performed: diameter of tumors ( D,E ), changes in the diameter of tumors ( F ), changes in body weight ( G ), and the percent of TUNEL-positive tumor cells ( H , I ). Plotted values represent the mean ± standard error of three independent experiments (n = 3) (*P

    Article Snippet: Cell proliferation analysis HCC cells were cultured with the indicated concentrations of EGCG before the addition of 10 μl CCK-8 solution (Peptide Institute Inc., Osaka, Japan) to each well.

    Techniques: Inhibition, Mouse Assay, CCK-8 Assay, Expressing, Quantitative RT-PCR, TUNEL Assay

    Helicobacter pylori -specific lymphocyte responses and IFN-γ, interleukin-4 (IL-4), and interleukin-17 (IL-17) production in mice immunized with cholera toxin B subunit (CTB)-HUUC or CTB. (A) Assessment on proliferation of specific lymphocytes in mice after immunization with CTB-HUUC, CTB, or PBS. Splenic lymphocytes from mice immunized with CTB-HUUC, CTB, or PBS were stimulated with Concanavalin A (ConA), H. pylori lysates, H. pylori urease, or CTB. Cell proliferation was determined using CCK-8 assay. The results were expressed as stimulation indices (SI) which represents the ratio between the proliferation rates of cells stimulated with antigens and those with the vehicle control. * p

    Journal: Frontiers in Immunology

    Article Title: Protection Against Helicobacter pylori Infection in BALB/c Mouse Model by Oral Administration of Multivalent Epitope-Based Vaccine of Cholera Toxin B Subunit-HUUC

    doi: 10.3389/fimmu.2018.01003

    Figure Lengend Snippet: Helicobacter pylori -specific lymphocyte responses and IFN-γ, interleukin-4 (IL-4), and interleukin-17 (IL-17) production in mice immunized with cholera toxin B subunit (CTB)-HUUC or CTB. (A) Assessment on proliferation of specific lymphocytes in mice after immunization with CTB-HUUC, CTB, or PBS. Splenic lymphocytes from mice immunized with CTB-HUUC, CTB, or PBS were stimulated with Concanavalin A (ConA), H. pylori lysates, H. pylori urease, or CTB. Cell proliferation was determined using CCK-8 assay. The results were expressed as stimulation indices (SI) which represents the ratio between the proliferation rates of cells stimulated with antigens and those with the vehicle control. * p

    Article Snippet: Lymphocyte suspensions were prepared from the mice spleen and cultured with the antigen Concanavalin A (ConA) (Sigma, USA), H. pylori lysates (prepared by our laboratory), H. pylori urease, or CTB in RPMI-1640 for 72 h. After that, 10 µL CCK-8 solution (Cell Counting Kit-8) (Beijing Solarbio Science & Technology Co., Ltd., China) was added into plates and incubated for 4 h. The absorbance was measured at 450 nm using a microplate reader.

    Techniques: Mouse Assay, CtB Assay, CCK-8 Assay

    MYCN promotes tumor growth by repressing ELOVL2 in vitro and vivo. a and b BE(2)-C cells stably expressing the negative control or MYCN shRNA were further infected with a lentivirus expressing ELOVL2 shRNA. SK-N-AS cells stably expressing GFP or MYCN were further infected with a lentivirus expressing ELOVL2. The BE(2)-C ( a ) and SK-N-AS ( b ) cell proliferation rate was determined using CCK-8 and a spectrophotometer at OD450. c and d BE(2)-C ( c ) and SK-N-AS ( d ) cells were treated as described in ( a ). Cells were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. e , f and g BE(2)-C were treated as described in ( a ) and injected subcutaneously into nude mice (n = 5 for each group). Tumors were compared ( e ) at the end of the experiment. Tumor growth curves ( f ) were measured starting at 7 days after inoculation. The DHA concentration of tumors ( g ) was measured by ELISA. h , i and j SK-N-AS were treated as described in ( a ) and injected subcutaneously into nude mice (n = 5 for each group). Tumors were compared ( h ) at the end of the experiment. Tumor growth curves ( i ) were measured starting at 7 days after inoculation. The DHA concentration of tumors ( j ) was measured by ELISA. k Representative IHC analysis of ELOVL2 and H2AK119ub protein expression in SK-N-AS cells stably expressing GFP or MYCN (up) and BE(2)-C cells stably expressing the negative control or MYCN shRNA (low). l , m , n and o The results of IHC analysis of ELOVL2 and H2AK119ub protein expression are presented as bar graphs of the mean number of the ELOVL2 and H2AK119ub positive rate. p and q ELOVL2 expression significantly correlated with MYCN expression in ALL (P) and MYCN (Q) amplification clinical tumor samples from the SEQC database. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: MYCN and PRC1 cooperatively repress docosahexaenoic acid synthesis in neuroblastoma via ELOVL2

    doi: 10.1186/s13046-019-1492-5

    Figure Lengend Snippet: MYCN promotes tumor growth by repressing ELOVL2 in vitro and vivo. a and b BE(2)-C cells stably expressing the negative control or MYCN shRNA were further infected with a lentivirus expressing ELOVL2 shRNA. SK-N-AS cells stably expressing GFP or MYCN were further infected with a lentivirus expressing ELOVL2. The BE(2)-C ( a ) and SK-N-AS ( b ) cell proliferation rate was determined using CCK-8 and a spectrophotometer at OD450. c and d BE(2)-C ( c ) and SK-N-AS ( d ) cells were treated as described in ( a ). Cells were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. e , f and g BE(2)-C were treated as described in ( a ) and injected subcutaneously into nude mice (n = 5 for each group). Tumors were compared ( e ) at the end of the experiment. Tumor growth curves ( f ) were measured starting at 7 days after inoculation. The DHA concentration of tumors ( g ) was measured by ELISA. h , i and j SK-N-AS were treated as described in ( a ) and injected subcutaneously into nude mice (n = 5 for each group). Tumors were compared ( h ) at the end of the experiment. Tumor growth curves ( i ) were measured starting at 7 days after inoculation. The DHA concentration of tumors ( j ) was measured by ELISA. k Representative IHC analysis of ELOVL2 and H2AK119ub protein expression in SK-N-AS cells stably expressing GFP or MYCN (up) and BE(2)-C cells stably expressing the negative control or MYCN shRNA (low). l , m , n and o The results of IHC analysis of ELOVL2 and H2AK119ub protein expression are presented as bar graphs of the mean number of the ELOVL2 and H2AK119ub positive rate. p and q ELOVL2 expression significantly correlated with MYCN expression in ALL (P) and MYCN (Q) amplification clinical tumor samples from the SEQC database. * P

    Article Snippet: At 0, 24, 48, and 72 h, spent medium was carefully removed and 100 μL DMEM containing 10% CCK-8 solution (TaKaRa) was added to each well and incubated for 3 h at 37 °C with 5% CO2, the relative cell number was recorded by a Benchmark Microplate Reader at 450 nm (Bio-Rad Laboratories).

    Techniques: In Vitro, Stable Transfection, Expressing, Negative Control, shRNA, Infection, CCK-8 Assay, Spectrophotometry, Staining, Flow Cytometry, Cytometry, Injection, Mouse Assay, Concentration Assay, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Amplification

    ELOVL2 inhibits cell proliferation in vitro. a Relative DHA concentrations of IMR32 and BE(2)-C cells stably expressing GFP or ELOVL2 were measured by ELISA (fold-change over GFP control ± SD). b and c The proliferation rate of IMR32 and BE(2)-C cells stably expressing GFP or ELOVL2 was assayed using CCK-8 and a spectrophotometer at OD450. d and e IMR32 and BE(2)-C cells stably expressing GFP or ELOVL2 were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. f IMR32 and BE(2)-C stably expressed GFP or ELOVL2. Colony growth in soft agar is shown for representative cultures after staining with crystal violet. Scale bar, 25 μm. g and h The results of the soft agar assays of ( f ) are presented as bar graphs of the mean number of colonies (±SD) forming. i Relative DHA concentration of SK-N-AS cells stably expressing the negative control or ELOVL2 shRNA was measured by ELISA (fold-change over negative control ± SD). j SK-N-AS cells stably expressing the negative control or ELOVL2 shRNA were treated with DHA 50 nM. The proliferation rate was assayed using CCK-8 and a spectrophotometer at OD450. k SK-N-AS cells stably expressing the negative control or ELOVL2 shRNA were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. l SK-N-AS cells stably expressed the negative control or ELOVL2 shRNA. Colony growth in soft agar is shown for representative cultures after staining with crystal violet. Scale bar, 25 μm. m The results of the soft agar assays of (L) are presented as bar graphs of the mean number of colonies (±SD) forming. * P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: MYCN and PRC1 cooperatively repress docosahexaenoic acid synthesis in neuroblastoma via ELOVL2

    doi: 10.1186/s13046-019-1492-5

    Figure Lengend Snippet: ELOVL2 inhibits cell proliferation in vitro. a Relative DHA concentrations of IMR32 and BE(2)-C cells stably expressing GFP or ELOVL2 were measured by ELISA (fold-change over GFP control ± SD). b and c The proliferation rate of IMR32 and BE(2)-C cells stably expressing GFP or ELOVL2 was assayed using CCK-8 and a spectrophotometer at OD450. d and e IMR32 and BE(2)-C cells stably expressing GFP or ELOVL2 were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. f IMR32 and BE(2)-C stably expressed GFP or ELOVL2. Colony growth in soft agar is shown for representative cultures after staining with crystal violet. Scale bar, 25 μm. g and h The results of the soft agar assays of ( f ) are presented as bar graphs of the mean number of colonies (±SD) forming. i Relative DHA concentration of SK-N-AS cells stably expressing the negative control or ELOVL2 shRNA was measured by ELISA (fold-change over negative control ± SD). j SK-N-AS cells stably expressing the negative control or ELOVL2 shRNA were treated with DHA 50 nM. The proliferation rate was assayed using CCK-8 and a spectrophotometer at OD450. k SK-N-AS cells stably expressing the negative control or ELOVL2 shRNA were stained with PI for 72 h, and the change in the cell cycle was measured by flow cytometry. l SK-N-AS cells stably expressed the negative control or ELOVL2 shRNA. Colony growth in soft agar is shown for representative cultures after staining with crystal violet. Scale bar, 25 μm. m The results of the soft agar assays of (L) are presented as bar graphs of the mean number of colonies (±SD) forming. * P

    Article Snippet: At 0, 24, 48, and 72 h, spent medium was carefully removed and 100 μL DMEM containing 10% CCK-8 solution (TaKaRa) was added to each well and incubated for 3 h at 37 °C with 5% CO2, the relative cell number was recorded by a Benchmark Microplate Reader at 450 nm (Bio-Rad Laboratories).

    Techniques: In Vitro, Stable Transfection, Expressing, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Spectrophotometry, Staining, Flow Cytometry, Cytometry, Concentration Assay, Negative Control, shRNA

    Effect of D206008 on cell viability and morphology. Notes: ( A ) The effect of different concentrations (0–100 µM) of D206008 on B16 melanoma cell viability was measured by CCK-8 assay. The data are expressed as the mean ± SD (* P

    Journal: Drug Design, Development and Therapy

    Article Title: Amine derivatives of furocoumarin induce melanogenesis by activating Akt/GSK-3β/β-catenin signal pathway

    doi: 10.2147/DDDT.S180960

    Figure Lengend Snippet: Effect of D206008 on cell viability and morphology. Notes: ( A ) The effect of different concentrations (0–100 µM) of D206008 on B16 melanoma cell viability was measured by CCK-8 assay. The data are expressed as the mean ± SD (* P

    Article Snippet: Cell viability assay Viability of B16 cells was measured by CCK-8 solution (Promega, Madison, MA, USA) assay.

    Techniques: CCK-8 Assay

    CAP sensitizes MCF-7/TxR cells to Tx. ( A ) The effect of CAP on the sensitivity of MCF-7 and MCF-7/TxR to Tx was examined by colony formation. The area of colonies is represented by a bar graph. ( B ) Effect of Tx on the growth rate of MCF-7/TxR vs. MCF-7. Cell growth was examined by CCK-8 assay. ( C ) Effect of CAP on growth rate of MCF-7/TxR in presence of Tx. All assays were performed in triplicate, and the results are expressed as mean ± SE. * p

    Journal: Cancers

    Article Title: Cold Atmospheric Plasma Restores Paclitaxel Sensitivity to Paclitaxel-Resistant Breast Cancer Cells by Reversing Expression of Resistance-Related Genes

    doi: 10.3390/cancers11122011

    Figure Lengend Snippet: CAP sensitizes MCF-7/TxR cells to Tx. ( A ) The effect of CAP on the sensitivity of MCF-7 and MCF-7/TxR to Tx was examined by colony formation. The area of colonies is represented by a bar graph. ( B ) Effect of Tx on the growth rate of MCF-7/TxR vs. MCF-7. Cell growth was examined by CCK-8 assay. ( C ) Effect of CAP on growth rate of MCF-7/TxR in presence of Tx. All assays were performed in triplicate, and the results are expressed as mean ± SE. * p

    Article Snippet: The cell growth rate was monitored at specific time points using CCK-8 solution (Enzo, New York, NY, USA) following the supplier’s protocol.

    Techniques: CCK-8 Assay

    LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using CCK-8 assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments

    Journal: Cell Death & Disease

    Article Title: LAMB3 mediates apoptotic, proliferative, invasive, and metastatic behaviors in pancreatic cancer by regulating the PI3K/Akt signaling pathway

    doi: 10.1038/s41419-019-1320-z

    Figure Lengend Snippet: LAMB3 is expressed in pancreatic ductal adenocarcinoma (PDAC) cells and promotes PDAC cell proliferation in vitro. a LAMB3 mRNA expression levels in a normal pancreatic cell line and seven different established PDAC cell lines. b LAMB3 mRNA expression was examined by quantitative PCR (qPCR) in PANC-1 and MIA PaCa-2 cells stably transfected with overexpressing LAMB3 overexpression (LAMB3U), LAMB3 knockdown (LAMB3D), or empty vector plasmids (NC). c Cell lysates were prepared from a normal pancreatic cell line and three pancreatic cancer cell lines (PANC-1, BXPC-3, and MIA PaCa-2) and examined by western blot analysis. d LAMB3 protein levels were examined by western blot analysis in transfected PANC-1 and MIA PaCa-2 cells. e Cell proliferation was compared using CCK-8 assays in the LAMB3D, LAMB3U, and NC groups. f Colony formation assays were performed in the LAMB3D, LAMB3U, and NC groups. Each figure is representative of three independent experiments

    Article Snippet: CCK-8 solution (Abcam, MA, USA) was added to each well.

    Techniques: In Vitro, Expressing, Real-time Polymerase Chain Reaction, Stable Transfection, Transfection, Over Expression, Plasmid Preparation, Western Blot, CCK-8 Assay