Mouse Anti-Human ITGA1 Hybridoma [UT3/8.2.2]

ITGA2 (Integrin alpha-2) has been detected to be over-expressed in a number of cancers and has been suggested to be involved in cell adhesion and cell-surface mediated signaling. Our previous study using bioinformatic analyses has shown that ITGA2 might be a key gene being involved in the Cadmium-induced malignant transformation of liver cells. In the present study, we firstly aimed to learn the possible functions of ITGA2 via bioinformatics analysis, and then test its expression and clinical significance in liver carcinoma specimens through laboratory experiments. Gene ontology (GO) and pathway enrichment analysis, as well as protein-protein interaction (PPI) analysis has been conducted in Genecards. Then, a tissue microarray containing 90 cases of liver cancer and 90 paired adjacent non-cancerous samples was used for detection of ITGA2 expression by immunohistochemistry assay. Consequently, ITGA2 may be enriched in pathways regarding cell adhesion and migration. PPI analysis suggests that ITGA1, ITGB2, FLT4, LAMB1 and AGRN may have a close relationship with ITGA2. No association between ITGA2 expression and clinical parameters was observed. However, the data showed that ITGA2 might be an independent prognostic factor for liver cancer patients. In conclusion, the data suggest that ITGA2 over-expression might be a potential unfavorable prognostic factor and a potential therapeutic target for liver carcinoma.

Corticosteroids are extensively used in pediatrics, yet the burden of side effects is significant. Availability of a simple, fast, and reliable biochemical read out of steroidal drug pharmacodynamics could enable a rapid and objective assessment of safety and efficacy of corticosteroids and aid development of corticosteroid replacement drugs. To identify potential corticosteroid responsive biomarkers we performed proteome profiling of serum samples from DMD and IBD patients with and without corticosteroid treatment using SOMAscan aptamer panel testing 1,129 proteins in <0.1 cc of sera. Ten pro-inflammatory proteins were elevated in untreated patients and suppressed by corticosteroids (MMP12, IL22RA2, CCL22, IGFBP2, FCER2, LY9, ITGa1/b1, LTa1/b2, ANGPT2 and FGG). These are candidate biomarkers for anti-inflammatory efficacy of corticosteroids. Known safety concerns were validated, including elevated non-fasting insulin (insulin resistance), and elevated angiotensinogen (salt retention). These were extended by new candidates for metabolism disturbances (leptin, afamin), stunting of growth (growth hormone binding protein), and connective tissue remodeling (MMP3). Significant suppression of multiple adrenal steroid hormones was also seen in treated children (reductions of 17-hydroxyprogesterone, corticosterone, 11-deoxycortisol and testosterone). A panel of new pharmacodynamic biomarkers for corticosteroids in children was defined. Future studies will need to bridge specific biomarkers to mechanism of drug action, and specific clinical outcomes.