<i>SSTR1, SSTR2, SSTR3, SSTR4 and SSTR5</i> gene expression analysis.

<p><i>SSTR1-5</i> gene expression analysis was performed by QRT-PCR on total RNA from five human NET cell lines: CNDT2.5, KRJ-1, QGP-1, NCI-H720 and NCI-H727. The absolute mRNA copy numbers are adjusted by <i>β-actin</i> mRNA copy number. Results were plotted using the 2^−ΔΔCt method with <i>β-actin</i> expression (set to 1) from each individual sample as endogenous reference.</p

ANXA1, ARHGAP18, EMP1, GDF15, TGFBR2 and TNFSF15 Western blot analysis.

<p>CNDT2.5 cells cultured in the absence or presence of 1 µM octreotide were collected at 1 week (wk), 4 months, 10 months and 16 months (mo) to prepare total lysates. Octreotide induces protein expression level of octreotide treated CNDT2.5 cells for 10 and 16 months compared to untreated cells (5A). β-actin was used as endogenous control. Fold changes are illustrated in 5B.</p

Gene expression of CNDT2.5 cells and 1 µM octreotide treated cells.

<p>Microarray analysis detected 25 differentially expressed genes in octreotide treated CNDT2.5 cells compared to CNDT2.5 untreated cells (control). Upregulated genes are in yellow and downregulated genes are in blue. Genes were clustered according to Euclidian distance, as indicated in the figure. Of the 25 genes, 6 were selected for further analysis and they are indicated by a red asterisk.</p

Gene ontology of 25 selected genes from microarray analyses.

<p>Log₂ ratio expression between octreotide (Oct) treated CNDT2.5 cells and untreated CNDT2.5 cells (control). Bolded genes were further analyzed.</p

Result of Immunohistochemistry on paraffin embedded SI-NET specimens.

<p>Primary tumour (P); Liver metastases (L); Mesentery metastases (M); Untreated (UT); Treated (T).</p><p>Intensity in >50% of tumour cells: +++ strong, ++ moderate, + weak, – negative.</p

CNDT2.5 cells growth in the presence of 1 µM octreotide was kinetically evaluated.

<p>Cells were cultured in the absence or presence of 1 µM octreotide (oct). WST-1 assay was used to evaluate cell growth. Cell proliferation ratio for each time point was converted to a percentage of the mean value relative to CNDT2.5 cells growth, set to 100%. Plotted results are means ± SD from triplicate wells. Significance was calculated by using Two-Way ANOVA followed by Bonferroni test; comparing with untreated CNDT2.5 cells. *** = <i>p</i><0.001.</p

Expression profile of insulin 1 and insulin 2 (panels A and B, respectively) in the whole pancreas of cort+/+ and cort−/− male mice fed a low fat (LF) or high fat diet (HFD).

<p>C, plasma insulin level obtained from cort+/+ and cort−/− animals fed a LF- or HF-diet. Values represent mean ± SEM of copy number adjusted by normalization factor (NF) per 100 ng of cDNA obtained from 4–7 animals per experimental group. (*: p<0,05).</p

Expression level of different ghrelin system components in the whole pancreas of cort+/+ and cort−/− male mice fed a low fat (LF) or high fat diet (HFD).

<p>Values represent mean ± SEM of copy number adjusted by normalization factor (NF) per 100 ng of cDNA obtained from 3–7 animals per experimental group. (*: p<0,05; **: p<0,01; ***: p<0,001).</p

Evaluation of in vitro CORT action on glucose induced-Insulin release in cultured pancreatic islets from cort−/− mice.

<p>Values represent mean ± SEM obtained from 3 independent experiments. Different letters stand for statistical differences (p<0,05).</p

Expression level of different ghrelin system components in pancreatic islets of cort+/+ and cort−/− male mice fed a low fat (LF) or high fat diet (HFD).

<p>Values represent mean ± SEM of copy number adjusted by normalization factor (NF) per 100 ng of cDNA obtained from 4–7 animals per experimental group. (*:p<0,05; **: p<0,01; ***: p<0,001).</p