Fatty acid transport protein 1 (FATP1), plays a major role in the transport and uptake of fatty acids into cells. The effect of FATP1 on the regulation of skeletal muscle fat uptake and deposition in stressed broiler chickens was investigated both in vivo and in vitro, and the effect of different fatty acid substrates were also included. Dexamethasone (DEX), a synthetic glucocorticoid (GCs), was employed to induce a hyper glucocorticoid milieu and simulate stress. The in vivo results showed that DEX would increase the mRNA expression of FATP1 and fat deposition in muscle tissues (P < 0.05), the very-low-density lipoprotein (VLDL) and insulin (INS) levels were significantly increased in the plasma by DEX (P < 0.05), and the mRNA levels of the glucocorticoid receptor (GR), adiponectin receptor (ADPNR) and peroxisomal proliferator-activated receptor α (PPARα) in thigh were also up-regulated by DEX (P < 0.05). In vitro experiment, DEX did not affect the myoblast fat deposition and PPARα and FATP1 expressions without the external fatty acid (P > 0.05). Under PA pre-treatment, both myoblast fatty acid uptake and fat deposition were promoted by DEX treatment (P < 0.05), and the effects of DEX on the gene expressions of GR, ADPNR, PPARα and FATP1 were upregulated first and then downregulated as the dose of DEX increases; while under OA pre-treatment, the myoblast fat deposition was not affected by DEX (P > 0.05), the fatty acid uptake was decreased by DEX at 500 nM compared to control (P < 0.05). When GR and PPARα were, respectively inhibited by specific inhibitors RU486 and GW6471, the effects of DEX on fatty acid uptake were reversed for PA pre-treated myoblasts (P < 0.05) but not for OA pre-treated myoblasts (P > 0.05). These results indicate that FATP1 regulation by GCs was affected by fatty acid substrate - saturated fatty acids were favorable for fat uptake and deposition, while unsaturated fatty acids were not. GCs may affect the ADPNR-PPARα-FATP1 pathway by binding to its receptors, thus regulating the uptake of saturated fatty acids into myoblasts.

• Gastric cancer
• Intestinal differentiation markers
• Prognostic markers

LI-cadherin belongs to the so called 7D-cadherins, exceptional members of the cadherin superfamily which are characterized by seven extracellular cadherin repeats and a small cytosolic domain. Under physiological conditions LI-cadherin is expressed in the intestine and colon in human and mouse and in the rat also in hepatocytes. LI-cadherin was shown to act as a functional Ca²⁺-dependent adhesion molecule, linking neighboring cells and a lot of biophysical and biochemical parameters were determined in the last time. It is also known that dysregulated LI-cadherin expression can be found in a variety of diseases. Although there are several hypothesis and theoretical models concerning the function of LI-cadherin, the physiological role of LI-cadherin is still enigmatic.

• CDH17
• IC
• LI-cadherin
• cadherin-17
• enterocytes
• osmoregulation

AIM: To investigate the significance of expression of Li-cadherin in gastric adenocarcinoma in Xinjiang Kazakh and Han patients.

METHODS: The mRNA and protein expression of CDH17 was detected by RT-qPCR and immunohistochemisty in 30 gastric adenocarcinoma tissues and 20 normal gastric mucosal tissues from Kazakh patients, as well as 30 gastric adenocarcinoma tissues and 20 normal gastric mucosal tissues from Han patients.

RESULTS: The expression level of CDH17 mRNA was significantly higher in gastric adenocarcinoma than in normal gastric mucosal tissue in Kazakh patients (1.22 ± 0.22 vs 2.37 ± 0.30, P < 0.001). In Kakzkh patients, the positive expression rate of CDH17 protein was 70.0% in gastric adenocarcinoma, and 0 in the normal gastric mucosal tissue. No correlation was found between expression of CDH17 protein and sex, age, or tumor differentiation in gastric adenocarcinoma in Kazakh patients. There was no significant difference in the expression of CDH17 in tumor or normal tissues between Kazakh and Han patients.

CONCLUSION: The expression of CDH17 in gastric adenocarcinoma was significantly higher than that in normal gastric mucosal tissues in Kazakh patients, suggesting that CDH17 may play an important role in the occurrence and development of gastric adenocarcinoma in Xinjiang Kazakh patients. There was no significant difference in the expression of CDH17 between Kazakh and Han patients.

• Gastric adenocarcinoma
• CDH17
• Kazakh
• Han

• li-cadherin
• barrett’s esophagus
• esophageal adenocarcinoma
• intestinal metaplasia
• intraepithelial neoplasia

AIM: To assess BGC823 gastric cancer (GC) cell metastasis after knockdown of liver-intestine cadherin (CDH17) and the therapeutic value of CDH17-RNAi-lentivirus in vivo.

METHODS: We evaluated primary tumor growth and assessed local infiltration and systemic tumor dissemination using an orthotopic implantation technique. The therapeutic value of CDH17 knockdown was examined by intratumoral administration of CDH17-RNA interference (RNAi)-lentivirus in an established GC tumor xenograft mouse model. Furthermore, a comparative proteomic approach was utilized to identify differentially expressed proteins in BGC823 and lenti-CDH17-miR-neg cells following CDH17 knockdown.

RESULTS: Metastases in the liver and lung appeared earlier and more frequently in animals with tumors derived from BGC823 or lenti-CDH17-miR-neg cells than in tumors derived from lenti-CDH17-miR-B cells. Average tumor weight and volume in the CDH17-RNAi-lentivirus-treated group were significantly lower than those in the control group (tumor volume: 0.89 ± 0.04 cm³vs 1.16 ± 0.06 cm³, P < 0.05; tumor weight: 1.15 ± 0.58 g vs 2.09 ± 0.08 g, P < 0.05). Fifteen differentially expressed proteins were identified after CDH17 silencing in BGC823 cells, including a variety of cytoskeletal and chaperone proteins as well as proteins involved in metabolism, immunity/defense, cell proliferation and differentiation, cell cycle, and signal transduction.

CONCLUSION: Our data establish a foundation for future studies of the comprehensive protein expression patterns and effects of CDH17 in GC.

• Cadherin
• Gastric cancer
• Intratumoral administration
• Liver
• Orthotopic implantation
• Proteomics

7D-cadherins like LI-cadherin are cell adhesion molecules and represent exceptional members of the cadherin superfamily. Although LI-cadherin was shown to act as a functional Ca²⁺-dependent adhesion molecule, linking neighboring cells together, and to be dysregulated in a variety of diseases, the physiological role is still enigmatic. Interestingly 7D-cadherins occur only in the lateral plasma membranes of cells from epithelia of water transporting tissues like the gut, the liver or the kidney. Furthermore LI-cadherin was shown to exhibit a highly cooperative Ca²⁺-dependency of the binding activity. Thus it is tempting to assume that LI-cadherin regulates the water transport through the epithelium in a passive fashion by changing its binding activity in dependence on the extracellular Ca²⁺.

We developed a simple mathematical model describing the epithelial lining of a lumen with a content of variable osmolarity covering an interstitium of constant osmolarity. The width of the lateral intercellular cleft was found to influence the water transport significantly. In the case of hypertonic luminal content a narrow cleft is necessary to further increase concentration of the luminal content. If the cleft is too wide, the water flux will change direction and water is transported into the lumen. Electron microscopic images show that in fact areas of the gut can be found where the lateral intercellular cleft is narrow throughout the lateral cell border whereas in other areas the lateral intercellular cleft is widened.

Our simple model clearly predicts that changes of the width of the lateral intercellular cleft can regulate the direction and efficiency of water transport through a simple epithelium. In a narrow cleft the cells can increase the concentration of osmotic active substances easily by active transport whereas if the cleft is wide, friction is reduced but the cells can hardly build up high osmotic gradients. It is now tempting to speculate that 7D-cadherins, owing to their location and their Ca²⁺-dependence, will adapt their binding activity and thereby the width of the lateral intercellular cleft automatically as the Ca²⁺-concentration is coupled to the overall electrolyte concentration in the lateral intercellular cleft. This could provide a way to regulate the water resorption in a passive manner adapting to different osmotic conditions.

• Adenocarcinoma/genetics
• Adenocarcinoma/pathology
• Base Sequence
• Cadherins/genetics
• Cell Adhesion
• Cell Cycle
• Cell Line, Tumor
• Cell Movement
• Colorectal Neoplasms/genetics
• Colorectal Neoplasms/pathology
• DNA Primers
• Down-Regulation
• Gene Expression Regulation, Neoplastic
• Gene Knockdown Techniques
• Humans
• Neoplasm Invasiveness/genetics
• Neoplasm Invasiveness/pathology
• Neoplasm Metastasis/genetics
• Neoplasm Metastasis/pathology
• Plasmids/genetics
• Polymerase Chain Reaction
• RNA, Neoplasm/genetics
• Transfection
• Wound Healing

• Animals
• Cadherins/antagonists & inhibitors
• Cadherins/genetics
• Cadherins/physiology
• Cell Line, Tumor
• Cell Proliferation
• Humans
• Lentivirus/genetics
• Mice
• MicroRNAs/physiology
• Neoplasm Invasiveness
• Stomach Neoplasms/pathology
• Stomach Neoplasms/therapy

• Cadherins/genetics
• Cadherins/metabolism
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/virology
• Cell Line, Tumor
• Female
• Hepatitis B/complications
• Humans
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• Liver Neoplasms/virology
• Male
• Microcirculation
• Middle Aged
• Neoplasm Invasiveness
• Prognosis
• RNA, Small Interfering/pharmacology
• Survival Analysis
• Vascular Neoplasms/secondary

• Intestinal metaplasia
• aberrant gene expression
• gastric cancer
• genetic markers.