Rabbit Anti-Mouse AKT Pan monoclonal antibody, clone K.425.5

The influence of chia (Salvia hispanica L.) flour and oil on glucose metabolism (GM) in insulin resistant (IR) Wistar rats and the effect of chia hydrolyzed phenolics extract (CHPE) on GM in IR HepG2 cells were evaluated. In vivo study: animals were divided into four groups: AIN-93M, high-fat and high-fructose (HFHF), HFHF with chia flour (14.7%) or chia oil (4%). In vitro study: IR HepG2 cells were treated with CHPE (80 ppm). In vivo, chia flour and oil reduced adiposity and increased AMPK mRNA. Chia oil improved glucose tolerance, increased AKT1[pS473] protein level, mRNA of insulin receptor, FOXO1 and glycolysis enzymes. In vitro, CHPE decreased gluconeogenesis enzymes mRNA. Chia flour and oil decreased adiposity, but only chia oil was able to improve glucose tolerance and restore energy fuel system in liver of rats fed HFHF diet. CHPE decreased mRNA levels of gluconeogenesis enzymes.

Background: Oral Squamous Cell Carcinoma (OSCC) is a major sub-type of oral cancer that shares 90% proportion of oral cavity cancers. It is declared as the sixth most frequent cancer among all cancer types throughout the world. Higher morbidity in Asian countries is reported due to frequent use of Smokeless Tobacco (SLT) products besides exposure to other risk factors. Hyper-activation of epidermal growth factor receptors is a molecular event in many solid tumors including oral cancer making them potential therapeutic targets. Objective: Current study was designed to explore the effect of varlitinib, a pan-HER inhibitor, on oral cancer cell line. We investigated key regulatory genes in downstream pathway in response to drug treatment. Furthermore, we also examined expression profile of these genes in malignant and healthy oral tissue. Methods: Gene expression pattern in drug treated and untreated cancer cell line along with OSCC tumor samples (n=45) and adjacent normal tissues was studied using real time PCR. Results: In response to varlitinib treatment, significant suppression of oncogenes (IGF1R, MAPK1, SFN and CDK2) was observed. Interestingly, mRNA expression level of CDKN1A and Akt1 was found to be the opposite of what was expected. In case of malignant tissue, over expression of oncogenes (IGF1R, Akt1, MAPK1, SFN and CDK2) with simultaneous down expression of tumor suppressor genes (Tp53 and CDKN1A) was noted. STRING analysis indicated a strong association among differentially expressed genes suggesting their combined role in carcinogenesis. Conclusion: In summary, our results indicate that varlitinib can be considered as a potential therapeutic agent in oral cancer due to its antitumor potential.