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Results: 5

1.
Figure 1

Figure 1. From: An oncogenic role for the multiple endocrine neoplasia type 1 gene in prostate cancer.

Fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC) examples. (a) FISH validation of 11q13.1 copy number gain in soft tissue (left) and lung (right) metastases from the same patient. Green signals represent the probe spanning the multiple endocrine neoplasia I (MEN1) locus, red signals represent the reference probe. (b) Representative IHC staining demonstrating MEN1 expression in the cytoplasm of benign prostate tissue (left) and nuclear MEN1 expression in a tumor sample (right) from different patients.

PL Paris, et al. Prostate Cancer Prostatic Dis. ;12(2):184-191.
2.
Figure 5

Figure 5. From: An oncogenic role for the multiple endocrine neoplasia type 1 gene in prostate cancer.

(a) DU145 expression array results of selected genes. The gene and the corresponding expression array fold change are listed. Fold change is calculated as the ratio of the expression in multiple endocrine neoplasia I (MEN1) knocked down DU145 cells compared to the controls (no siRNA and scramble combined). (b) TaqMan validation of DU145 expression array results. Every gene’s expression was measured relative to that of the house keeping gene BGUS. TaqMan results are shown for ITGβ1 (light gray), CASP8 (dark gray) and PERP.34 Each result is plotted as the percent expression relative to untreated DU145. Reg represents DU145 cells without siRNA, scramble are DU145 cells that were treated with siRNAs that share no homology to known cDNAs, MEN1 siRNAs are the DU145 cells treated with siRNA. Each bar represents two biological replicates that were each run in triplicate before averaging the results.

PL Paris, et al. Prostate Cancer Prostatic Dis. ;12(2):184-191.
3.
Figure 2

Figure 2. From: An oncogenic role for the multiple endocrine neoplasia type 1 gene in prostate cancer.

Results of Oncomine database query for multiple endocrine neoplasia I expression in prostate cancer (differential expression P<0.05). The shades of gray within an analysis are to help distinguish each tissue type represented. The corresponding table legend describes each analysis.
Analysis numberClass 1Class 2Class 3Class 4P-valueReferences1Normal adjacent prostate (N = 2), normal adult prostate (N = 7), normal pubertal prostate (N = 3)Prostate cancer (N = 25)8.9E–9192Normal prostate (N = 6), benign prostatic hyperplasia (N = 16)Primary prostate cancer (N = 59)Metastatic prostate cancer (N = 20)4.1E–5183Benign prostate (N = 6)Prostate carcinoma (N = 7)Hormone refractory metastatic prostate carcinoma (N = 6)1E–4224Prostate cancer (N = 25)Metastatic prostate cancer (N = 6)0.002195Atrophic epithelium (N = 5), benign prostate (N = 22)Prostatic intraepithelial neoplasia (N = 13)Prostate carcinoma (N = 30)Metastatic prostate cancer (N = 19)0.006206Normal prostate (N = 8)Prostate adenocarcinoma (N = 27)Metastatic prostate cancer (N = 5)0.009217Benign prostatic hyperplasia (N = 9)Prostate carcinoma (N = 16)0.01338Benign (N = 8)Gleason score 6 (N = 12)Gleason score 9 (N = 15)Metastatic (N = 5)0.051219Naive (N = 3)Refractory (N = 16)0.05820

PL Paris, et al. Prostate Cancer Prostatic Dis. ;12(2):184-191.
4.
Figure 3

Figure 3. From: An oncogenic role for the multiple endocrine neoplasia type 1 gene in prostate cancer.

Phenotypic effects of multiple endocrine neoplasia I (MEN1) siRNA silencing. (a) In vitro cell proliferation assay using an ACEA instrument showing decreased cell proliferation of DU145 cells transfected with four different MEN1 siRNAs (M1-4). Transfections were carried out in serum starved conditions; cells were rescued and maintained in serum media subsequently for 48 h. Controls include nontransfected (SFM), transfection reagent alone (HP) and scrambled siRNAs (AF, S5). (b) shows corresponding TaqMan data for the same samples confirming knockdown of MEN1 expression in cells with the siRNA, 72 h posttransfection. (c) DU145 cells were transfected in serum-free conditions and then rescued with serum media, 48 h later. Cell viability was quantified using the MTS assay, after 72 h of rescue. Samples include DU145 cells transfected with three different MEN1 siRNAs (M1, M3 and M4). Controls include nontransfected (SFM), transfection reagent alone (NC) and scramble siRNA (AF). Doxorubicin treated DU145 cells were included as an additional control (Dox500).

PL Paris, et al. Prostate Cancer Prostatic Dis. ;12(2):184-191.
5.
Figure 4

Figure 4. From: An oncogenic role for the multiple endocrine neoplasia type 1 gene in prostate cancer.

Fluorescence-activated cell sorter (FACS) analysis. (a) Cell cycle distribution of multiple endocrine neoplasia I (MEN1) siRNA treated DUI45 cells. Transfected cells were analyzed by FACS to ascertain the effects of MEN1 knockdown on the cell cycle. DU145 cells were transfected and starved in serum-free media for 48 h before rescue with serum –media. 48 h later, cells were fixed in ethanol and stained with PI. Samples include DU145 cells transfected with 2 different MEN1 siRNAs (M1 and M4). Controls include DU145 cells (REG), nontransfected (SFM), transfection reagent alone (NC) and scrambled siRNA (AF). Light gray bars represent cells in G1 phase, dark gray bars represent S phase, and G2 phase cells are represented by white bars. Each sample was run in duplicate and the average is shown. (b) Transfected cells were analyzed by FACS to study the effects of MEN1 silencing on the induction of apoptosis. DU145 cells were transfected and starved in serum-free media for 48 h before rescue with serum media. After 48 h, cells were stained with Annexin to track phosphatidyl serine flipping in cell membranes that is a hallmark of early apoptosis. Samples include DU145 cells transfected with two different MEN1 siRNAs (M1 and M4). Controls include DU145 cells (Reg), nontransfected (SFM), transfection reagent alone (NC) and scramble siRNA (AF). Two different concentrations of doxorubicin treated DU145 cells were included as additional controls. Each sample was run in duplicate and the average is shown.

PL Paris, et al. Prostate Cancer Prostatic Dis. ;12(2):184-191.

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