The cholesterol-hydroxyecdysone-vitellogenin pathway is involved in the longevity of trophocytes and oenocytes of queen honey bees (Apis mellifera)

International audienceAbstractTrophocytes and oenocytes in the abdomen of honey bees do not divide after eclosion; however, trophocytes and oenocytes of queen bees have a longer lifespan and maintain better cellular function than those of worker bees. To explore this phenomenon, we assayed the molecules involved in the cholesterol-hydroxyecdysone-vitellogenin (Vg) pathway in the trophocytes and oenocytes of young and old worker and queen bees. The results showed that Vg and cholesterol levels in hemolymph and cholesterol levels, 20-hydroxyecdysone (20E) levels, and the messenger RNA levels of cytochrome P450 314A1 20-hydroxylase (Cyp314A1), ecdysone receptor isoform A (EcR-A), ecdysone receptor isoform B1 (EcR-B1), ultraspiracle (USP), ecdysone-induced protein 74 (E74), ecdysone-induced protein 75 (E75), broad-complex (BR-C), Vg, and Vg receptor (VgR) in trophocytes and oenocytes were increased in queen bees compared with worker bees. These findings indicated that queen bees have higher expression of molecules in the cholesterol-hydroxyecdysone-Vg pathway than worker bees

An On-Line Personalized Promotion Decision Support System for Electronic Commerce

With the development of the Internet and Electronic Commerce (EC), enterprises have overcome the space and time barriers and are now capable of serving customers electronically. However, it is a great challenge to attract and retain the customers over Internet. One approach is to provide the responsive personalized service to satisfy the customer demand and promote sales at the first time. Hence, in this paper, we propose a decision support system which develops best promotion products based on combinations of different marketing strategies, pricing strategies, and customer behaviors evaluated in terms of multiple criteria. Data mining techniques are utilized to help the business discover patterns to develop on-line sales promotion products for each customer for enhancing customer satisfaction and loyalty. The proposed system consists of four components: (1) establishing marketing strategies, (2) promotion pattern model, (3) personalized promotion products, and (4) on-line transaction model. A simple example is given to illustrate the implementation and application of proposed decision support system

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

Chemokine (C-C motif) ligand 3 (CCL3), also known as macrophage inflammatory protein-1α, is a cytokine involved in inflammation and activation of polymorphonuclear leukocytes. CCL3 has been detected in infiltrating cells and tumor cells. Chondrosarcoma is a highly malignant tumor that causes distant metastasis. However, the effect of CCL3 on human chondrosarcoma metastasis is still unknown. Here, we found that CCL3 increased cellular migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells. Pre-treatment of cells with the MMP-2 inhibitor or transfection with MMP-2 specific siRNA abolished CCL3-induced cell migration. CCL3 has been reported to exert its effects through activation of its specific receptor, CC chemokine receptor 5 (CCR5). The CCR5 and AMP-activated protein kinase (AMPK) inhibitor or siRNA also attenuated CCL3-upregulated cell motility and MMP-2 expression. CCL3-induced expression of MMP-2 and migration were also inhibited by specific inhibitors, and inactive mutants of AMPK, p38 mitogen activated protein kinase (p38 or p38-MAPK), and nuclear factor κB (NF-κB) cascades. On the other hand, CCL3 treatment demonstrably activated AMPK, p38, and NF-κB signaling pathways. Furthermore, the expression levels of CCL3, CCR5, and MMP-2 were correlated in human chondrosarcoma specimens. Taken together, our results indicate that CCL3 enhances the migratory ability of human chondrosarcoma cells by increasing MMP-2 expression via the CCR5, AMPK, p38, and NF-κB pathways

Overexpression of Nuclear Protein Kinase CK2 α Catalytic Subunit (CK2α) as a Poor Prognosticator in Human Colorectal Cancer

BACKGROUND: Colorectal cancer (CRC) is one of the most common malignancies but the current therapeutic approaches for advanced CRC are less efficient. Thus, novel therapeutic approaches are badly needed. The purpose of this study is to investigate the involvement of nuclear protein kinase CK2 α subunit (CK2α) in tumor progression, and in the prognosis of human CRC. METHODOLOGY/PRINCIPAL FINDINGS: Expression levels of nuclear CK2α were analyzed in 245 colorectal tissues from patients with CRC by immunohistochemistry, quantitative real-time PCR and Western blot. We correlated the expression levels with clinicopathologic parameters and prognosis in human CRC patients. Overexpression of nuclear CK2α was significantly correlated with depth of invasion, nodal status, American Joint Committee on Cancer (AJCC) staging, degree of differentiation, and perineural invasion. Patients with high expression levels of nuclear CK2α had a significantly poorer overall survival rate compared with patients with low expression levels of nuclear CK2α. In multi-variate Cox regression analysis, overexpression of nuclear CK2α was proven to be an independent prognostic marker for CRC. In addition, DLD-1 human colon cancer cells were employed as a cellular model to study the role of CK2α on cell growth, and the expression of CK2α in DLD-1 cells was inhibited by using siRNA technology. The data indicated that CK2α-specific siRNA treatment resulted in growth inhibition. CONCLUSIONS/SIGNIFICANCE: Taken together, overexpression of nuclear CK2α can be a useful marker for predicting the outcome of patients with CRC

Cyclooxygenase-2 enhances α2β1 integrin expression and cell migration via EP1 dependent signaling pathway in human chondrosarcoma cells

<p>Abstract</p> <p>Background</p> <p>Cyclooxygenase (COX)-2, the inducible isoform of prostaglandin (PG) synthase, has been implicated in tumor metastasis. Interaction of COX-2 with its specific EP receptors on the surface of cancer cells has been reported to induce cancer invasion. However, the effects of COX-2 on migration activity in human chondrosarcoma cells are mostly unknown. In this study, we examined whether COX-2 and EP interaction are involved in metastasis of human chondrosarcoma.</p> <p>Results</p> <p>We found that over-expression of COX-2 or exogenous PGE₂increased the migration of human chondrosarcoma cells. We also found that human chondrosarcoma tissues and chondrosarcoma cell lines had significant expression of the COX-2 which was higher than that in normal cartilage. By using pharmacological inhibitors or activators or genetic inhibition by the EP receptors, we discovered that the EP1 receptor but not other PGE receptors is involved in PGE₂-mediated cell migration and α2β1 integrin expression. Furthermore, we found that human chondrosarcoma tissues expressed a higher level of EP1 receptor than normal cartilage. PGE₂-mediated migration and integrin up-regulation were attenuated by phospholipase C (PLC), protein kinase C (PKC) and c-Src inhibitor. Activation of the PLCβ, PKCα, c-Src and NF-κB signaling pathway after PGE₂treatment was demonstrated, and PGE₂-induced expression of integrin and migration activity were inhibited by the specific inhibitor, siRNA and mutants of PLC, PKC, c-Src and NF-κB cascades.</p> <p>Conclusions</p> <p>Our results indicated that PGE₂enhances the migration of chondrosarcoma cells by increasing α2β1 integrin expression through the EP1/PLC/PKCα/c-Src/NF-κB signal transduction pathway.</p