ABSTRACT
For lack of the biomarker, early diagnosis of prostate cancer is often difficult. Caveolin-1 (Cav-1) is an important oncogene and a major structural coat protein of caveolae, which is involved in multiple cellular functions including molecular transport, cell adhesion, and signal transduction, as well as in the development and progression of prostate cancer. Cav-1 is secreted as a biologically active molecule that promotes cell survival and angiogenesis within the tumor microenvironment, and is overexpressed in the metastatic and primary sites of human prostate cancer. Secreted Cav-1 can be detected in the peripheral blood, and its expression level has an indicative value in the diagnosis and prognosis of prostate cancer. This review focuses on the structure and biological characteristics of Cav-1 and its correlation with prostate cancer.
Subject(s)
Humans , Male , Biomarkers, Tumor , Caveolin 1 , Prostatic Neoplasms , DiagnosisABSTRACT
<p><b>BACKGROUND</b>Inflammation and immunity play a vital role in the pathogenesis of early brain injury after subarachnoid hemorrhage (SAH). Nuclear factor-kappa B (NF-kappaB) regulates many genes essential for inflammation and immunity and is activated by toll-like receptor (TLR). This study aimed to detect the expression of the toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-kappaB) signaling in the rat brain after early SAH.</p><p><b>METHODS</b>The rats were decapitated and their brains were removed at 0, 2, 4, 6, 12, 24 and 48 hours after a single injection of blood into the prechiasmatic cistern. mRNA expression of TLR4 was measured by Taqman real-time RT-PCR, and protein expression by immunohistochemistry and Western blotting. NF-kappaB activity and concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay (ELISA).</p><p><b>RESULTS</b>TaqMan real-time RT-PCR and Western blotting identified a biphasic change in TLR4 expression in both mRNA and protein: an initial peak (2 - 6 hours) and a sustained elevation (12 - 48 hours). Immunohistochemical staining showed the inducible expression of TLR4-like immunoreactions predominantly in glial cells and vascular endothelium. A similar biphasic change in the activation of NF-kappaB subunit p65 as well as the production of NF-kappaB-regulated proinflammatory cytokines (TNF-alpha, IL-1beta and IL-6) were detected by ELISA.</p><p><b>CONCLUSIONS</b>These data suggest that experimental SAH induces significant up-regulation of TLR4 expression and the NF-kappaB signaling in early brain injury. Activation of the TLR4/NF-kappaB signaling may regulate the inflammatory responses after SAH.</p>