Journal: International Journal of Cancer

Article Title: Identification of a novel zinc finger gene,zf5-3, as a potential mediator of neuroblastoma differentiation

doi: 10.1002/(sici)1097-0215(19990611)81:6<970::aid-ijc21>3.0.co;2-9

Figure Lengend Snippet: FIGURE 5 – Northern blot analysis of RNA samples from a variety of pediatric tumor-derived cell lines probed with zf5-3 (upper panel, visualized as a 7.0/7.2-kb doublet) and the housekeeping gene GAPDH (lower panel, visualized as a 1.8-kb band). Cell lines were derived from a hepatoblastoma (HEPG2), neuroblastomas (NUB-7, SK-N-SH, NBL-S, NUB-6, IMR-32, LAN-2, LAN-5, GOTO, NB1), a neuroepithelioma (EW-2, formerly NUB-20), a teratocarcinoma (TERA-2) and its derived clone (NT2D1), Wilms’ tumor (WT13, SK-NEP; note MT13 is a non-tumorigenic fibroblast cell line derived from patient WT13) and malignant rhabdoid tumor of kidney (G401, Tm87–16), as well as an SV40-transformed cell line of mesenchymal origin derived from kidney (56A1).

Article Snippet: Williams (Cleveland Clinic Foundation Research Institute, Cleveland, OH); Tm87-16 was provided by Dr. T. Triche (UCLA School of Medicine); SK-N-SH (ATCC HTB-11), IMR-32 (ATCC CCL 127), HEPG2 (ATCC HTB 8065), TERA-2 (ATCC HTB 106) and its clone NT2D1, G401 (ATCC CRL 1441) and SK-NEP (ATCC HTB 48) were obtained from the ATCC (Rockville, MD).

Techniques: Northern Blot, Derivative Assay, Wilms Tumor Assay, Transformation Assay

Journal: PloS one

Article Title: Reduced selenium-binding protein 1 in breast cancer correlates with poor survival and resistance to the anti-proliferative effects of selenium.

doi: 10.1371/journal.pone.0063702

Figure Lengend Snippet: Figure 1. The Expression of SELENBP1 in Normal and Tumor Breast Tissues. Breast cancer tissue arrays were stained by immunohistochemistry using anti-human SELENBP1 antibody at 1:100 dilution. Positive stained cells are shown in dark brown color. (A) Strong positive staining of SELENBP1 in normal breast tissue under low power view (200X). (B–C) Weak positive to negative staining of SELENBP1 in breast cancer tissues under high power view (400X). (D) The Allred scoring distributions of SELENBP1 expression in normal and tumor tissue groups. Inside lines represent means and standard deviations. *p,0.05. (E) Statistical results for the difference between normal and tumor tissues as analyzed by Kruskal-Wallis test. doi:10.1371/journal.pone.0063702.g001

Article Snippet: Breast Cancer Tissue Array Slides Three sets of breast cancer tissue arrays (including normal, primary tumor, and metastases) were obtained from Imgenex or Biomax Inc.

Techniques: Expressing, Staining, Immunohistochemistry, Negative Staining

Journal: PloS one

Article Title: Reduced selenium-binding protein 1 in breast cancer correlates with poor survival and resistance to the anti-proliferative effects of selenium.

doi: 10.1371/journal.pone.0063702

Figure Lengend Snippet: Figure 2. SELENBP1 Expression is Progressively Reduced in Advancing Clinical Stages in Breast Cancer Tissues. (A) The scoring distributions of SELENBP1 expression in normal tissues and tumor tissues at stage II and stage III. Inside lines represent means and standard deviations. **p,0.01. (B) Statistical results for the difference between normal and tumor tissues as analyzed by Kruskal-Wallis test. (C) Survival curves of breast cancer patients with respect to different SELENBP1 expression levels are shown at stage II and (D) stage III. Blue and red lines represent the SELENBP1-high and SELENBP1-low groups, respectively. doi:10.1371/journal.pone.0063702.g002

Article Snippet: Breast Cancer Tissue Array Slides Three sets of breast cancer tissue arrays (including normal, primary tumor, and metastases) were obtained from Imgenex or Biomax Inc.

Techniques: Expressing

Journal: PloS one

Article Title: Reduced selenium-binding protein 1 in breast cancer correlates with poor survival and resistance to the anti-proliferative effects of selenium.

doi: 10.1371/journal.pone.0063702

Figure Lengend Snippet: Figure 3. The Correlation of SELENBP1 Expression with ER, PR, and TP53 in Breast Cancer Tissues. (A) The scoring distributions of SELENBP1 expression in normal tissues and tumor tissues with ER+ and ER– status. The inside lines represent means and standard deviations. **p,0.01. The difference between normal and ER+ and ER– tumor tissues was analyzed by Kruskal-Wallis test and statistical results are shown (B). Survival curves of breast cancer patients with respect to different SELENBP1 expression are shown in ER+ group in (C). The blue line is the SELENBP1- high group and the red line is the SELENBP1-low group. The scoring distributions of SELENBP1 expression in normal and tumor tissues with PR+/PR–

Article Snippet: Breast Cancer Tissue Array Slides Three sets of breast cancer tissue arrays (including normal, primary tumor, and metastases) were obtained from Imgenex or Biomax Inc.

Techniques: Expressing

Journal: Journal of Clinical Investigation

Article Title: BVES regulates EMT in human corneal and colon cancer cells and is silenced via promoter methylation in human colorectal carcinoma

doi: 10.1172/jci44228

Figure Lengend Snippet: Figure 1 BVES expression is significantly downregulated, and it is mislocalized in human colon carcinoma. (A) A human BVES hydrolysis probe was used to perform qPCR on an Origene cDNA array (TissueScan Cancer Survey I). Ct values were normalized to β-actin and then presented as fold reduction from matched normal (N) (n = 3 per tissue type) and tumor (T) tissue (n = 9 per tissue type). ***P < 0.001, 2-tailed unpaired t test. (B) Analysis of the combined Moffit Cancer Center and Vanderbilt Medical Center colon tumor expression array data set (10, normal samples; 6, adenomas; 33, stage I; 76, stage 2; 82, stage 3; and 59, stage 4; for combined total of 250 CRC samples). For whisker plots, the bottom and top of the boxes are the 25th and 75th percentile, respectively (the lower and upper quartiles, respectively), and the band near the middle of the box is the 50th percentile (median). The whiskers extend to the most extreme data points, which are no more than 1.5 times the interquartile range from the box. *P = 0.04, ***P = 0.001, ****P = 0.0001. (C) Representative immunofluorescence images from normal colon or adenocarci- noma (original magnification, ×400) of H&E, BVES (green), ZO-1 (red), DAPI (blue), and merged images.

Article Snippet: BVES TaqMan qRT-PCR was performed on a multicancer tissue cDNA array (TissueScan Cancer Survey I, OriGene) according to the manufacturers protocol.

Techniques: Expressing, Whisker Assay, Immunofluorescence

Journal: Genes to Cells

Article Title: Functional Role of COP1 Gene in Hepatocellular Carcinoma Lipid Metabolism and Stemness

doi: 10.1111/gtc.70108

Figure Lengend Snippet: COP1 knockdown reduces motility, and stemness in HCC cells. (a‐b) Migration (a) or invasion (b) assay showing reduced motility in Huh7 and HepG2 cells treated with COP1‐siRNA, as quantified by the relative migration or invaded area. Statistical significance: *, p < 0.05; ** p < 0.01; *** p < 0.001 vs. control. (c) Sphere formation assay images and quantitative data from Huh7 and HepG2 cells, demonstrating a decrease in both the number and size of spheres in COP1‐siRNA‐treated cells. (d) Sphere formation assay images and quantitative data from PLC/PRF/5 CD133+ cells. Compared to the control grpup, both the sphere number and size decreased upon COP1‐siRNA treatment. Scale bar, 100 μm Statistical significance: *, p < 0.05; *** p < 0.001 vs. control.

Article Snippet: The cells were treated with FcR Blocking Reagent and CD133 MicroBeads (130‐100‐857, Miltenyi Biotec, Bergisch Gladbach, Germany) according to the manufacturer's instructions and incubated for 15 min at 4°C in the dark.

Techniques: Knockdown, Migration, Control, Tube Formation Assay