Biglycan (BGN), a key member of the small leucine-rich proteoglycan family, is an important component of the extracellular matrix. Clinical studies have demonstrated that upregulation of BGN is associated with poor prognosis in patients with various types of solid cancer. The present study analyzed the mRNA expression levels of BGN in various types of solid cancer when compared with that in normal tissues via the Oncomine database. The UALCAN, OncoLnc and Kaplan-Meier Plotter databases were additionally used to evaluate the prognostic values of BGN in patients with solid cancer and co-expression gene analysis was conducted using the protein-protein interaction networks of BGN. The present study observed that the mRNA expression levels of BGN were increased in bladder, brain and central nervous system, breast, colorectal, esophageal, gastric, head and neck, lung, ovarian and 28 subtypes of cancer compared with normal tissues. The increased expression of BGN was identified to be associated with a poor outcome in ovarian and gastric cancer. Based on the co-expression network, BGN was identified as the key gene in a 43-gene network. The present findings of increased expression of BGN in solid tumors and its positive association with poor outcome on patient survival indicate that BGN may serve as a prognostic marker and as a target for novel therapeutics for multiple types of cancer.

BackgroundThe integrin β1 subunit and its downstream molecules such as integrin-linked kinase (ILK) and focal adhesion kinase (FAK) are indispensable to the inhibition of postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure. As a component of the integrin pathway, C3G (Crk SH3-domain-binding guanine nucleotide exchange factor) protein may also participate in postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure.Material/MethodsExperimental myocardial infarction (MI) and sham-operation (sham) models were set up in Sprague-Dawley rats. C3G protein expression in the myocardium in the sham group and in the non-infarcted myocardium of the peri-infarct zones in the MI group was examined by Western blot.ResultsThe C3G protein expression in the myocardium was 0.22±0.06, n=8 in the post-sham 24-hour group; 0.29±0.10, n=8 in the post-MI 24-hour group; 0.22±0.07, n=8 in the post-sham 12-week group; and 0.56±0.14, n=8 in the post-MI 12-week group. The C3G protein expression in the myocardium in the post-MI 12-week group was significantly elevated compared to that in the post-sham 12-week group (p=0.0002), in the post-sham 24-hour group (p=0.0002), and in the post-MI 24-hour group (p=0.0006).ConclusionsC3G protein expression exhibits in the myocardium of rats. Furthermore, C3G protein expression is significantly elevated in the non-infarcted myocardium of the peri-infarct zones. The elevated C3G protein expression could participate in postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure.

The integrin β1 subunit and its downstream molecule focal adhesion kinase have been identified as critical molecules for the inhibition of postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure. However, as a component of the integrin pathway, it is still unclear whether Dock180 (dedicator of cytokinesis 1) protein is expressed in the noninfarcted myocardium of the peri-infarct zones. In this study, experimental myocardial infarction (MI) and sham-operation (sham) models were established in Sprague Dawley rats and the expression of Dock180 protein in the myocardium of the sham group and in the noninfarcted myocardium of the peri-infarct zones of the MI group was detected by Western blot technique. The Dock180 protein expression in the myocardium was as follows: postsham 24-hour group, 0.10 ± 0.04 (n = 8); post-MI 24-hour group, 0.13 ± 0.03 (n = 8); postsham 12-week group, 0.11 ± 0.05 (n = 8); and post-MI 12-week group 0.17 ± 0.04 (n = 8). The Dock180 protein expression in the myocardium in the post-MI 12-week group was significantly higher than that in the postsham 12-week group (p = 0.019), in the postsham 24-hour group (p = 0.004), and in the post-MI 24-hour group (p = 0.040). We conclude that Dock180 protein is expressed in the myocardium in rats. Furthermore, its expression is significantly increased in the noninfarcted myocardium of the peri-infarct zones.

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