C/EBPβ physical interaction with the <i>CDH3</i> gene promoter.

<p><b>A</b>) Putative C/EBPβ-binding sites within the <i>CDH3</i> gene promoter, where it can be observed their degree of conservation between human and other primates. Grey regions represent total sequence conservation in comparison with human sequence; <b>B</b>) Proximal regulatory region of <i>CDH3</i> promoter displaying the relative localization of the predicted C/EBPβ binding sites (left panel). The right panel illustrates the enrichment (relative to input) of the <i>CDH3</i> promoter DNA-amplified fragments precipitated from DNA-protein complexes obtained by ChIP in MCF-7/AZ breast cancer cells. <b>C</b>) ChIP experiment performed in BT-20 breast cancer cells and on a frozen primary breast tumour, highly positive for P-cadherin and C/EBPβ expression, also showed the same enrichment pattern for all the putative binding sites.</p

Association and regulatory interplay between C/EBPβ and <i>CDH3</i>/P-cadherin expression in breast cancer cells.

<p><b>A</b>) Double immunostaining for C/EBPβ and P-cadherin of an invasive breast carcinoma specimen (basal-like carcinoma, histological grade III), where it can be observed C/EBPβ expression in the nuclei and P-cadherin at the cell membrane of tumour cells (magnification ×200 and ×400-inset); a haematoxylin-eosin staining of this same case is shown to ascertain tissue integrity (magnification ×100); <b>B</b>) Using C/EBPβ-targeted siRNA, a consequent reduction of P-cadherin protein levels was observed in both MCF-7/AZ and BT-20 breast cancer cell lines; <b>C</b>) MCF-7/AZ cells transiently transfected with the different C/EBPβ isoforms (LAP1, LAP2 and LIP) displayed upregulation of P-cadherin protein levels only after induction of the C/EBPβ-LIP isoform; <b>D</b>) Luciferase reporter assays performed in cells transfected with the different C/EBPβ isoforms showed that the promoter activation induced by LIP and LAP1 isoforms was significantly greater compared with the activation induced by LAP2. The co-transfection of both LIP and each LAP1 or LAP2 induced the activation of the <i>CDH3</i> promoter in an additive manner.</p

Association between the presence of gastric H. pylori (detected = positive test; non-detected = negative test) and socio-demographic variables.

<p>Association between the presence of gastric H. pylori (detected = positive test; non-detected = negative test) and socio-demographic variables.</p

Sample characterization.

<p>Sample characterization.</p

<i>H</i>. <i>pylori</i>- specific PCR for DNA extracted from oral cavity.

<p>In this figure, one can see the amplification of <i>VacA</i> in the three cases previously identified as oral cavity positives for H. pylori (Hp positive sample #1 to #3), in comparison with other three cases that are oral cavity H. pylori negatives (Hp negative sample #1 to #3). As a positive control (Hp positive control) PCR for DNA extracted from <i>H</i>. <i>pylori</i> (strain 7354) diluted in saliva was used. Blank—PCR negative control.</p

Highly sensitive PCR for detection of <i>H</i>. <i>pylori</i>.

<p>In order to evaluate the sensitivity of <i>VacA</i>-specific PCR, 50ng of DNA from <i>H</i>. <i>pylori</i> was successively diluted (1 to 1:100000) in saliva from two random cases (#3 and #10) that were shown previously to be negative for the presence of <i>H</i>. <i>pylori</i>. The PCR allowed the amplification of the expected product for all different dilutions.</p