Human chorionic gonadotropin β (HCGβ) down‐regulates E‐cadherin and promotes human prostate carcinoma cell migration and invasion

Abstract

People are not equally disabled by combined anterior cruciate ligament (ACL)/medial collateral ligament (MCL) injuries, nor do they all develop osteoarthritis (OA). Although biological/biomechanical causes are not clear, some association presumably exists between joint instability and OA development. We hypothesized that degree of OA development following standardized complete ACL/MCL injuries will vary directly with the degree of biomechanical abnormality between individuals. Three groups of sheep were used to test the hypothesis: 17 normal, 9 ACL/MCL transected, and 7 sham animals. Normal joints were assessed morphologically while sham and experimental animals had gait assessment pre‐ and at 4 and 20 weeks post‐surgery, with cartilage and bone changes being mapped and graded at sacrifice at 20 weeks. Sham joints were morphologically normal and had only one minor kinematic change at 20 weeks. Although variable, ACL/MCL deficient animals showed significant kinematic abnormalities in 4/6 degrees of freedom (DOFs), as well as cartilage/bone damage by 20 weeks (p < 0.05). Linear regression analysis revealed that changes in medial–lateral (ML) translation were related to the current level of joint degradation as represented by total gross OA score (p = 0.0044, R2 = 0.71) in the ACL/MCL transected group. Even identical ACL/MCL injuries result in inter‐animal variations in instability and OA, however significant kinematic abnormalities in ML translation do relate to early OA in sheep. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:384–392, 2012

KCl Cotransporter-3 Down-regulates E-Cadherin/β-Catenin Complex to Promote Epithelial-Mesenchymal Transition

“…Down-regulation or loss of E-cadherin has been implicated in the gain of invasive potential by carcinomas (34)(35)(36)(37). h-Catenin also functions as a component of adherent cell-cell junctions that promote cell adhesion by binding to the intracellular domain of E-cadherin and linking E-cadherin to the cytoskeleton through the adaptor Figure 3.…”

Sulforaphane inhibits invasion by phosphorylating ERK1/2 to regulate E-cadherin and CD44v6 in human prostate cancer DU145 cells

“…EMT is a reversible process, whereby the epithelial cells lose their junctions and polarity, reorganize their cytoskeleton, gain ability of motility, transit into mesenchymal cells and develop an invasive phenotype (30). The functional loss of E-cadherin is the typical characteristic of EMT and this contributes to the destabilization of adheren junctions, as well as tumor invasion and metastasis (20,30,47,48). Therefore, SFN is capable of suppressing the process of EMT by inducing E-cadherin.…”

Is garlic a promising food for benign prostatic hyperplasia and prostate cancer?

“…It was also shown that the inhibitory effect of the prostate cancer cell invasion was mediated via restoration of Ecadherin expression [15]. In previous studies, it was suggested that inactivation of E-cadherin was one of the main characteristics of metastatic prostate cancer [16][17][18][19]. Chu et al showed that E-cadherin expression was induced by the garlic derivatives in some other human cancer cell lines including ovarian, nasopharyngeal and esophageal cancer cell lines [15].…”