Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: NEO212 induces mitochondrial apoptosis and impairs autophagy flux in ovarian cancer

doi: 10.1186/s13046-019-1249-1

Figure Lengend Snippet: NEO212 exerts stronger cytotoxicity than its individual constituents in vitro. a A2780, SK-O-V3 and OVCAR-3 cells were treated with 0, 25, 50, 100, 150, 200, 300 μM TMZ, POH, TMZ + POH and NEO212 respectively for 48 h, DMSO acted as the control, and then subjected to MTT assay. Absorbance value was calculated and standardized to DMSO group. Three independent experiments were performed. b The above cells were treated with 100 μM TMZ, POH, TMZ + POH and NEO212 or DMSO for 48 h, respectively, then drugs were withdrawn and cells grew in normal culture for 14 days, DMSO acted as the control, and subjected to cell colony formation assay Statistical differences of cell colony formation assay were calculated and presented as mean ± SD. c A2780, SK-O-V3 and OVCAR-3 cells were treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO respectively for 48 h, and the cell cycle distributions were analyzed. The results shown are means ± SD; * p < 0.05; ** p < 0.01; *** p < 0.001

Article Snippet: Human ovarian cancer-derived cell lines SK-O-V3 and OVCAR-3 were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA); A2780 were purchased from KeyGEN BioTECH (Jiangsu, China).

Techniques: In Vitro, Control, MTT Assay, Colony Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: NEO212 induces mitochondrial apoptosis and impairs autophagy flux in ovarian cancer

doi: 10.1186/s13046-019-1249-1

Figure Lengend Snippet: NEO212 induces DNA damage and mitochondrial apoptosis. a-c Cells were treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO respectively for 48 h. a Western blot analysis demonstrated p-ATM, p-CHEK1, p-CHEK2, p-H2AFX and ACTB expression in above drug-treated A2780 and SK-O-V3 cells. b Cells were subjected to apoptosis assay using Annexin-V &PI staining. c Lysates from above drug-treated A2780 and SK-O-V3 cells were subjected to western blot using following antibodies against cleaved CASP9, pro-CASP3, cleaved CASP3, Cytochrome C (Cyto C), BAX and ACTB. d A2780 and SK-O-V3 cells were treated with 100 μM NEO212 for 48 h with or without Ac-LEHD or Z-VAD, and then apoptosis assay using Annexin-V &PI staining. The results shown are means ± SD; * p < 0.05; ** p < 0.01

Article Snippet: Human ovarian cancer-derived cell lines SK-O-V3 and OVCAR-3 were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA); A2780 were purchased from KeyGEN BioTECH (Jiangsu, China).

Techniques: Western Blot, Expressing, Apoptosis Assay, Staining

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: NEO212 induces mitochondrial apoptosis and impairs autophagy flux in ovarian cancer

doi: 10.1186/s13046-019-1249-1

Figure Lengend Snippet: NEO212 promotes mitochondrial dysfunction. a A2780 and SK-O-V3 cells treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO for 48 h respectively were stained with MTG. Scale bars: 10 μm. b-c Mitochondria structure in A2780 and SK-O-V3 cells treated with 100 μM NEO212 or DMSO was observed by TEM. Scale bars: 0.5 μm. Mitochondrial shape and area were measured using Fiji Image J. d A2780 and SK-O-V3 cells were treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO for 48 h respectively, and detected using JC-1 flow cytometry. The results shown are means ± SD; * p < 0.05; ** p < 0.01; *** p < 0.001, NS = no significance

Article Snippet: Human ovarian cancer-derived cell lines SK-O-V3 and OVCAR-3 were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA); A2780 were purchased from KeyGEN BioTECH (Jiangsu, China).

Techniques: Staining, Flow Cytometry

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: NEO212 induces mitochondrial apoptosis and impairs autophagy flux in ovarian cancer

doi: 10.1186/s13046-019-1249-1

Figure Lengend Snippet: Relationship of NEO212 induced autophagosome accumulation and apoptosis. a Cells were treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO respectively for 48 h in A2780 and SK-O-V3 cells. Western blot analysis demonstrated BECN1, LC3B and ACTB expression; ( b ) Autophagic vacuoles in A2780 and SK-O-V3 cells treated with 100 μM NEO212 or DMSO were observed by transmission electron microscopy (TEM). The arrow indicates autophagic vacuoles. Scale bars: 0.5 μm. c The above drug-treated cells were inspected under confocal laser microscopy to detect LC3B puncta by immunofluorescence. Scale bars: 10 μm. Number of autophagic vacuoles was calculated using Fiji Image J software. d A2780 and SK-O-V3 cells treated with 100 μM NEO212 or DMSO were subjected to western blot to detected LC3B and ACTB expression in the presence or absence of Baf.A1. e-f A2780 and SK-O-V3 cells were treated with 100 μM NEO212 for 48 h with or without EBSS ( e ) or 3 M, Baf.A1 ( f ), and then apoptosis assay using Annexin-V &PI staining. The results shown are means ± SD; * p < 0.05; ** p < 0.01; *** p < 0.001, NS = no significance

Article Snippet: Human ovarian cancer-derived cell lines SK-O-V3 and OVCAR-3 were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA); A2780 were purchased from KeyGEN BioTECH (Jiangsu, China).

Techniques: Western Blot, Expressing, Transmission Assay, Electron Microscopy, Microscopy, Immunofluorescence, Software, Apoptosis Assay, Staining

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: NEO212 induces mitochondrial apoptosis and impairs autophagy flux in ovarian cancer

doi: 10.1186/s13046-019-1249-1

Figure Lengend Snippet: NEO212 blocks autophagy flux. a A2780 cells expressing mRFP-GFP-LC3 were starved or treated with 1 nm Baf.A1 or 100 μM NEO212 for 48 h and imaged by confocal microscopy. Scale bars: 10 μm. Statistical analysis of the percentage of puncta mRFP signals that were positive for GFP using Fiji Image J. b Cells were treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO respectively for 48 h in A2780 and SK-O-V3 cells. Western blot analysis demonstrated SQSTM1, EEA1, LAMP1, LAMP2, TFEB and ACTB expression. c A2780 cells were either starved or treated with NEO212, and stained with anti-LAMP1 and anti-LC3B antibodies and imaged by confocal microscopy. Scale bars: 10 μm. Statistical analysis of the colocalization coefficient of LAMP1 and LC3B using Fiji Image J. The results shown are means ± SD; *** p < 0.001, NS = no significance

Article Snippet: Human ovarian cancer-derived cell lines SK-O-V3 and OVCAR-3 were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA); A2780 were purchased from KeyGEN BioTECH (Jiangsu, China).

Techniques: Expressing, Confocal Microscopy, Western Blot, Staining

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: NEO212 induces mitochondrial apoptosis and impairs autophagy flux in ovarian cancer

doi: 10.1186/s13046-019-1249-1

Figure Lengend Snippet: NEO212 blocks TFEB nuclear translocation. a-b A2780 and SK-O-V3 cells were treated with 100 μM NEO212 or not and stained with anti-TFEB antibody and imaged by confocal microscopy ( a ). Scale bars: 10 μm. Statistical analysis of the colocalization coefficient of LAMP1 and LC3B using Fiji Image J ( b ). c A2780 cells expressing Flag-TFEB were starved in present or absent with 100 μM NEO212 underwent cytoplasmic and nuclear extraction. Then the cytoplasmic and nuclear lysates were subjected to western blot analysis for demonstrating Flag-TFEB expression using anti Flag antibody. GAPDH acts as control for cytoplasmic protein, Lamin B1 acts as control for nuclear protein; ( d ) Cells were treated with 100 μM TMZ, POH, TMZ + POH, NEO212 or DMSO respectively for 48 h in A2780 and SK-O-V3 cells. Western blot analysis demonstrated p-AKT, AKT, p-ERK, and ACTB expression in above drug treated cells. The results shown are means ±SD, *** p < 0.001

Article Snippet: Human ovarian cancer-derived cell lines SK-O-V3 and OVCAR-3 were purchased from American Type Culture Collection (ATCC, Manassas, VA, USA); A2780 were purchased from KeyGEN BioTECH (Jiangsu, China).

Techniques: Translocation Assay, Staining, Confocal Microscopy, Expressing, Extraction, Western Blot, Control

Journal: Oncology Reports

Article Title: miR-1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

doi: 10.3892/or.2020.7623

Figure Lengend Snippet: miR-1299 is downregulated in OC and acts as a negative regulator of NOTCH3. (A) Analysis of miR-1299 expression in OC and normal ovary tissues (NC) using RT-qPCR. (B) miR-1299 expression was significantly lower in OC tissues with high NOTCH3 expression compared to those with low NOTCH3 expression. (C) Correlation between miR-1299 and NOTCH3 levels in OC cell lines. (D) RT-qPCR analysis of NOTCH3 pathway genes after transfection of miR-1299 mimics in A2780 cells. (E) Western blot analysis of NOTCH3 after transfection of miR-1299 mimics in A2780 and CAOV3 cell lines. (F) Putative miR-1299 binding sequence in NOTCH3 3′UTR (untranslated region) (WT) and the mutated 3′UTR sequence (MUT). (G) Relative luciferase activity of reporter plasmids carrying wild-type (WT) or mutant (MUT) NOTCH3 3′UTR in A2780 cells co-transfected with NC or miR-1299 mimics. Means ± SD are shown. Statistical analysis was conducted using Student's t-test. *P<0.05 and **P<0.01; ns, not significant. OC, ovarian cancer; NOTCH3, notch receptor 3; HES1, hairy and enhancer of split-1; HEY1, Hes related family BHLH transcription factor with YRPW motif 1; HEY 2, Hes related family BHLH transcription factor with YRPW motif 2; JAG1, Jagged canonical Notch ligand 1; PBX1, Pre-B-cell leukemia transcription factor 1.

Article Snippet: The human OC cell lines A2780, CAOV3, and SKOV3 were purchased from the National Infrastructure of Cell Line Resources in China (Beijing, China).

Techniques: Expressing, Quantitative RT-PCR, Transfection, Western Blot, Binding Assay, Sequencing, Luciferase, Activity Assay, Mutagenesis

Journal: Oncology Reports

Article Title: miR-1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

doi: 10.3892/or.2020.7623

Figure Lengend Snippet: Upregulation of miR-1299 inhibits cell proliferation, colony formation, EdU incorporation, and cell cycle in OC A2780 and CAOV3 cell lines. (A) RT-qPCR analysis of miR-1299 expression level in OC cells after transfection of NC or miR-1299 mimics for 48 h. (B) Cell proliferation of OC cells after transfection of NC or miR-1299 mimics by CCK-8 assay. (C) Representative photographs and quantifications of the colony formation assay after transfection of NC or miR-1299 mimics. (D) Representative photographs of EdU incorporation assay in OC cells after transfection of NC or miR-1299 mimics. (E) Cell cycle distribution of OC cells after transfection of NC or miR-1299 mimics by flow cytometry. Means ± SD are shown. Statistical analysis was conducted using Student's t-test. *P<0.05 and **P<0.01, miR-1299 mimic compared with the NC mimic; ns, not significant; OC, ovarian cancer.

Article Snippet: The human OC cell lines A2780, CAOV3, and SKOV3 were purchased from the National Infrastructure of Cell Line Resources in China (Beijing, China).

Techniques: Quantitative RT-PCR, Expressing, Transfection, CCK-8 Assay, Colony Assay, Flow Cytometry

Journal: Oncology Reports

Article Title: miR-1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

doi: 10.3892/or.2020.7623

Figure Lengend Snippet: lncRNA TUG1 functions as a sponge of miR-1299 and promotes cell proliferation in OC. (A) Screening methods for regulatory lncRNAs of miR-1299 in OC. (B) The two highest scoring putative miR-1299 binding sites in the TUG1 sequence (WT) and the point mutations in either binding site (MUT). (C) Relative luciferase activity of reporter plasmids carrying wild-type (WT) or mutant (MUT) TUG1 binding sites in A2780 cells co-transfected with NC or miR-1299 mimics. (D) Confirmation of TUG1 knockdown in A2780 cells transfected with TUG1 shRNA by RT-qPCR analysis. (E) RT-qPCR analysis of miR-1299 level in A2780 cells transfected with TUG1 shRNA or scrambled shRNA. Results of the (F) cell proliferation, (G) colony formation, (H) EdU incorporation assays, and (I) cell cycle analysis of A2780 cells transfected with NC-sh, TUG1-sh1, TUG1-sh2, and TUG1-sh+miR-1299 inhibitors. (J) Representative blot image of NOTCH3 protein level in A2780 cells transfected with NC-sh, TUG1-sh1, TUG1-sh2, and TUG1-sh+miR-1299 inhibitors by western blotting. Means ± SD are shown. Statistical analysis was conducted using Student's t-test and one-way ANOVA with Tukey post hoc test. *P<0.05 and **P<0.01; ns, not significant; OC, ovarian cancer; NOTCH3, notch receptor 3; TUG1, lncRNA taurine upregulated gene 1.

Article Snippet: The human OC cell lines A2780, CAOV3, and SKOV3 were purchased from the National Infrastructure of Cell Line Resources in China (Beijing, China).

Techniques: Binding Assay, Sequencing, Luciferase, Activity Assay, Mutagenesis, Transfection, Knockdown, shRNA, Quantitative RT-PCR, Cell Cycle Assay, Western Blot

Journal: Oncology Reports

Article Title: miR-1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

doi: 10.3892/or.2020.7623

Figure Lengend Snippet: TUG1 is a potential downstream target of NOTCH3. (A) Schematic diagram showing RBP Jκ motifs around the transcriptional start site (TSS) of the TUG1 gene. (B and C) TUG1 expression was inversely correlated with NOTCH3 mRNA in fresh OC tissues (B) and in the TCGA database (C). (D) RT-qPCR analysis of TUG1 level in A2780 cells treated with DAPT. (E) Diagrams showing the miR-1299/NOTCH3/TUG1 feedback loop in the development of OC. Statistical analysis was conducted using one-way ANOVA with Tukey post hoc test and Pearson's correlation analysis. **P<0.01; ns, not significant; OC, ovarian cancer; NOTCH3, notch receptor 3; TUG1, lncRNA taurine upregulated gene 1; NICD3, NOTCH3 intracellular domain; HES1, hairy and enhancer of split-1; HEY1, Hes related family BHLH transcription factor with YRPW motif 1; HEY 2, Hes related family BHLH transcription factor with YRPW motif 2.

Article Snippet: The human OC cell lines A2780, CAOV3, and SKOV3 were purchased from the National Infrastructure of Cell Line Resources in China (Beijing, China).

Techniques: Expressing, Quantitative RT-PCR

Journal: Bioscience Reports

Article Title: The role of Rho GTPases’ substrates Rac and Cdc42 in osteoclastogenesis and relevant natural medicinal products study

doi: 10.1042/BSR20200407

Figure Lengend Snippet: The source, structure, cells or animal models and mechanisms of ten natural compounds

Article Snippet: Panacis Japonici Rhizoma , Panax japonicus C. A. Meyer , , A2780 cell line , N/A , N/A , Cdc42 , Chen [ ] .

Techniques: In Vitro

Journal: bioRxiv

Article Title: Oncogene-like addiction to aneuploidy in human cancers

doi: 10.1101/2023.01.09.523344

Figure Lengend Snippet: (A) Chromosomal engineering strategies for the targeted deletion of chromosome arms: (1) ReDACT-NS: using CRISPR-Cas9 homology-directed repair, we integrated a positive-negative selection cassette encoding a fluorescent reporter, a positive selection marker, and a negative selection marker (HSV thymidine kinase) at a centromere-proximal region on chromosome 1q. We induced arm loss by generating a dsDNA break centromere-proximal to the cassette with Cas9, and isolated clonal populations of cells that were ganciclovir-resistant. (2) ReDACT-TR: We induced arm loss by generating a dsDNA break at a centromere-proximal location with Cas9 while providing cells with an ectopic telomere seed sequence for repair. (3) ReDACT-CO: We induced arm loss by generating a dsDNA break at a centromere-proximal location with Cas9, and isolated clonal populations of cells. For all three approaches, we screened clonal populations of cells for targeted chromosome loss through TaqMan CNV assays and validated their karyotypes through SMASH sequencing. (B) Representative SMASH karyotypes of the 1q-disomic clones generated from the 1q-trisomic cancer cell lines A2780, AGS, and A2058. Chromosome 1q is highlighted in blue. A complete list of aneuploidy-loss clones is included in . (C) 1q-disomic clones display decreased RNA expression and protein expression of genes encoded on chromosome 1q. RNA expression data was obtained through bulk RNA-seq and represents the average expression of genes by chromosome arm across multiple 1q-disomic clones for each cell line. Protein expression data was obtained through mass spectrometry, and representative data from one 1q-disomic clone is shown for each cell line. Data are log2 transformed, normalized to the parental cell line, and adjusted so that the mean expression across all chromosomes is 0. (D) 1q-disomic clones exhibit decreased anchorage-independent growth. The micrographs display representative images of colony formation for 1q-trisomic and 1q-disomic clones. (E) 1q-disomic clones exhibit impaired xenograft growth in vivo . 1q-trisomic and 1q-disomic cells were injected contralaterally and subcutaneously into immunocompromised mice. The graphs display the mean ± SEM for each trial. Representative mice are shown on the right. (F) SMASH karyotype of a 1q-disomic clone generated from the mammary epithelial cell line MCF10A. Chromosome 1q is highlighted in blue. (G) 1q-disomic MCF10A clones transduced with HRAS G12V exhibit decreased anchorage-independent growth relative to 1q-trisomic MCF10A cells. (H) 1q disomic MCF10A clones transduced with HRAS G12V clones exhibit impaired xenograft growth in vivo . 1q-trisomic and 1q-disomic cells were injected contralaterally and subcutaneously into immunocompromised mice. The graphs display the mean ± SEM for each trial. Representative mice are shown below. For anchorage-independent growth assays in D and G, the boxplots represent the 25th, 50th, and 75th percentiles of colonies per field, while the whiskers represent the 10th and 90th percentiles. Unpaired t-test, n = 15 fields of view, data from representative trial. Representative images are shown below. **p < 0.005, ***p < 0.0005

Article Snippet: A2780 samples were sent to Cell Line Genetics Inc. ( www.clgenetics.com ), and AGS and A2058 samples were sent to Karyologic Inc. ( www.karyologic.com ) for G-banding karyotyping.

Techniques: CRISPR, Selection, Marker, Isolation, Sequencing, Clone Assay, Generated, RNA Expression, Expressing, RNA Sequencing, Mass Spectrometry, Transformation Assay, In Vivo, Injection, Transduction

Journal: bioRxiv

Article Title: Oncogene-like addiction to aneuploidy in human cancers

doi: 10.1101/2023.01.09.523344

Figure Lengend Snippet: (A) GSEA analysis of A2780 RNA-seq data reveals upregulation of the p53 pathway in the 1q-disomic clones, relative to the parental trisomy. (B) A heatmap displaying the upregulation of 10 p53 target genes in A2780 1q-disomic clones. The TK+ clone indicates a clone that harbors the CRISPR-mediated integration of the HSV-TK transgene but that was not treated to induce chromosome 1q-loss. (C) Western blot analysis demonstrating activation of p53 signaling in 1q-disomic clones. GAPDH was analyzed as a loading control. The TK+ clone indicates a clone that harbors the CRISPR-mediated integration of the HSV-TK transgene but that was not treated to induce chromosome 1q-loss. (D) A waterfall plot highlighting the most-significant instances of mutual exclusivity between chromosome arm gains and mutations in cancer-associated genes. The complete dataset for mutual exclusivity and co-occurrence is included in . (E) Boxplots displaying the TP53-mutation phenocopy signature in cancers from the TCGA, split based on whether the cancers harbor a non-synonymous mutation in TP53. (F) A scatterplot comparing the association between chromosome arm gains and the TP53-mutation phenocopy signature in TP53-wildtype cancers from TCGA. Cancers with chromosome 1q gains are highlighted in blue. (G) Boxplots displaying the TP53-mutation phenocopy signature in cancers from the TCGA, split based on whether tumors harbor a gain of chromosome 1q. Only TP53-wildtype cancers are included in this analysis. (H) Boxplots displaying the expression of three p53 target genes – CDKN1A (p21), RRM2B, and GADD45A – in cancers from TCGA split based on the copy number of chromosome 1q. Only TP53-wildtype cancers are included in this analysis. (I) A CRISPRi competition assay demonstrates that gRNAs targeting MDM4 drop out over time in A2780 cells. In contrast, gRNAs targeting AAVS1 and PIP5K1A, another gene encoded on chromosome 1q, exhibit minimal depletion. (J) A schematic displaying the strategy for using paired CRISPR gRNAs to delete a single copy of MDM4 in a cell line with a trisomy of chromosome 1q. (K) SMASH karyotype demonstrating maintenance of the chromosome 1q trisomy in an MDM4 +/+/KO clone. Chromosome 1q is highlighted in blue. (L) 1q-disomic clones and MDM4 +/+/KO clones in A2780 exhibit comparable upregulation of p53 transcriptional targets, as determined through TaqMan gene expression assays. (M) MDM4 +/+/KO clones exhibit decreased anchorage-independent growth relative to the MDM4 +/+/+ parental cell line. (N) Induction of MDM4 cDNA in 1q-disomic clones in A2780 increases anchorage-independent growth. For the graphs in E, G, H, M, and N, the boxplots represent the 25th, 50th, and 75th percentiles of the indicated data, while the whiskers represent the 10th and 90th percentiles of the indicated data. For the soft agar experiments in M and N, the data are from n = 15 fields of view, and a representative trial is shown. ***p < 0.0005

Article Snippet: A2780 samples were sent to Cell Line Genetics Inc. ( www.clgenetics.com ), and AGS and A2058 samples were sent to Karyologic Inc. ( www.karyologic.com ) for G-banding karyotyping.

Techniques: RNA Sequencing, Clone Assay, CRISPR, Western Blot, Activation Assay, Control, Mutagenesis, Expressing, Competitive Binding Assay, Gene Expression

Journal: bioRxiv

Article Title: Oncogene-like addiction to aneuploidy in human cancers

doi: 10.1101/2023.01.09.523344

Figure Lengend Snippet: (A) A schematic of the metabolism of two pyrimidine analogs, RX-3117 and 3-deazauridine. UCK2, a kinase encoded on chromosome 1q, phosphorylates these compounds to produce cytotoxic derivatives that can poison DNA and RNA synthesis. (B) Boxplots displaying the expression of UCK2 in cancer cell lines (left) and human cancers (right), divided based on the copy number of chromosome 1q. The boxplots represent the 25th, 50th, and 75th percentiles of the indicated data, while the whiskers represent the 10th and 90th percentiles of the indicated data. (C) Expression of UCK2 protein in cancer cell lines with 1q trisomies or following aneuploidy-elimination. (D) Cellular sensitivity of A2780 and MCF10A treated with different concentrations of RX-3117 or 3-deazauridine. (E) A schematic displaying cellular competition between trisomic and disomic cells. Under normal conditions, certain trisomies enhance cellular fitness, allowing these cells to overtake the population and enhance malignant growth (top). However, treatment with an “anti-trisomy” compound could selectively impair the growth of the aneuploid cells, keeping the population in a low-malignant state (bottom). (F) A cellular competition between fluorescently-labeled A2780 1q-trisomic and unlabeled 1q-disomic cells. These cells were mixed at a ratio of 10% to 90% and then cultured in either DMSO or RX-3117. While the trisomic cells quickly dominate the population in drug-free media, treatment with RX-3117 prevents the outgrowth of the 1q-trisomy subpopulation. *p < 0.05, ** p < 0.005, *** p < 0.0005

Article Snippet: A2780 samples were sent to Cell Line Genetics Inc. ( www.clgenetics.com ), and AGS and A2058 samples were sent to Karyologic Inc. ( www.karyologic.com ) for G-banding karyotyping.

Techniques: Expressing, Labeling, Cell Culture