Sterculic Acid Alters Adhesion Molecules Expression and Extracellular Matrix Compounds to Regulate Migration of Lung Cancer Cells

Sterculic acid (SA) is a cyclopropenoid fatty acid isolated from Sterculia foetida seeds. This molecule is a well-known inhibitor of SCD1 enzyme, also known as ∆9-desaturase, which main function is related to lipid metabolism. However, recent studies have demonstrated that it also modifies many other pathways and the underlying gene expression. SCD overexpression, or up-regulated activity, has been associated with tumor aggressiveness and poor prognosis in many cancer types. Scd1 down-regulation, with different inhibitors or molecular strategies, reduces tumor cell survival and cell proliferation, as well as the chemoresistance associated with cancer stem cell presence. However, SA effects over cancer cell migration and extracellular matrix or adhesion molecules have not been described in cancer cells up to now. We used different migration assays and qPCR gene expression analysis to evaluate the effects of SA treatment in cancer cells. The results reveal that SA induces tumoral cell death at high doses, but we also observed that lower SA-treatments induce cell adhesion-migration capacity reduction as a result of modifications in the expression of genes related to integrins and extracellular matrix compounds. Overall, the functional and transcriptomic findings suggest that SA could represent a new inhibitor activity of epithelial to mesenchymal transition.

Alterations in hepatic microsomal protein levels in rainbow trout fed cyclopropenoid fatty acids analyzed by two-dimensional gel electrophoresis

Two-dimensional gel electrophoresis was used to analyze the effect of dietary cyclopropenoid fatty acids on hepatic microsomal polypeptide distribution patterns. Antibodies against rainbow trout type-LM2 cytochrome P-450 were employed to localize the corresponding polypeptide(s) by immunochemical staining. The LM2 antigen was purified from trout that had been fed β-naphthoflavone. Microsomes from trout fed β-naphthoflavone showed a decrease in a cytochrome P-450 polypeptide, detected with antibody against LM2. In contrast, microsomes from control fish contained two distinct cytochrome P-450 polypeptides, differing in their isoelectric points. Cyclopropenoid fatty acid treatment caused a preferential decrease in the additional isozyme seen in control samples. The distribution of concanavalin-A-binding glycopolypeptides was also assessed. Surprisingly, the two P-450 isozymes localized from control microsomes were found to bind concanavalin A. In addition to this, the cyclopropenoid fatty acid treatment generated a shift in a closely related group of microsomal glycopolypeptides, labelled gp80, gp82, gp801, and gp821. A decrease in the levels of gp80 and gp82 and a corresponding increase in gp801 and gp821 was observed.

Liver Fat and Protein Metabolism in Rainbow Trout (Salmo gairdneri) Fed Cyclopropenoid Fatty Acids

Effects of cyclopropenoid fatty acid (CPFA) ingestion on fat and protein metabolism in the liver of rainbow trout (Salmo gairdneri) were studied. Three dietary regimens were used: experimental group fed 0.5 mg CPFA/kg body weight per day, pair-fed control, and ad lib. control. CPFA ingestion did not cause a reduction in body weight gain; however, the ratio of liver weight to body weight was elevated. Livers of CPFA-fed trout had higher fat and lower protein levels. Incorporation of 14C labelled amino acids into livers was reduced in CPFA-fed trout. Of the amino acids incorporated into the livers, a higher proportion was found in the liver proteins of CPFA-fed trout than pair-fed controls. The percentage of 14C labelled acetate incorporation into liver fat of CPFA-fed trout was similar to that of the pair-fed controls, whereas acetate incorporation into liver proteins was reduced. Activities of glutamate dehydrogenase (EC 1.4.1.3) and alanine aminotransferase (EC 2.6.1.2) were lower in CPFA-fed trout after 36 days on the diet; acetyl-CoA carboxylase (EC 6.4.1.2) activity was unaffected by the treatment.