Examine irrespective of whether Dkk1 is regularly upregulated in human breast cancer patient serums and

Examine irrespective of whether Dkk1 is regularly upregulated in human breast cancer patient serums and malignant tissues with osteolytic bone metastases. In summary, we propose that Dkk1 expression in breast cancer cells contributes to the development and progression of breast osteolytic bone metastases. Breast cancer cells with overactivated Wnt/-catenin signaling make high levels of Dkk1, which blocks osteoblast differentiation, OPG expression and RANKL reduction, and consequently stimulates osteoclastic bone resorption. Therefore, Dkk1 can be a possible therapeutic target in designing pharmacologic interventions for bone metastases in breast cancer.NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptFzAcknowledgmentsThis work was supported in component by a grant from the American Heart Association (0330118N) to Y. L. and grants from the National Institutes of Well being to E.T.K. (P01 CA093900) and to G.B. (RO1 CA100520). We’re grateful to Dr. Gail Johnson for giving the cDNA for E-cadherin and Dr. Jane Knisely for critical reading on the manuscript.AbbreviationsALP CM Dkk1 ECG ER HBM LRP OPG PR RANKL shRNA sFRP1 TCF/LEF alkaline phosphatase conditioned medium Dickkopf1 extracellular matrix oestrogen receptor frizzled higher bone mass the low density lipoprotein receptor-related protein osteoprotegerin progesterone receptor receptor activator of NF-kappaB ligand quick hairpin RNA secreted Frizzled-related protein1 T-cell factor/lymphoid enhancing factor
BMC Cell BiologyResearch articleBioMed CentralOpen AccessHigh glucose upregulates Connective tissue growth aspect expression in human vascular smooth muscle cellsXiaojing Liu1,2, Fengming Luo3, Kejian Pan4, Wenchao Wu2 and Huaiqing Chen1,Address: 1Institute of Biomedical Engineering, West China Center of Healthcare Sciences, Sichuan CRAC Channel medchemexpress University, Chengdu, China, 2Laboratory of Cardiovascular Ailments, West China Hospital, Sichuan University, Chengdu, China, 3Golden-Card Ward, West China Hospital, Sichuan University, Chengdu, China and 4Department of Biochemistry, Chengdu Health-related College, Chengdu, China E-mail: Xiaojing Liu – [email protected]; Fengming Luo – [email protected]; Kejian Pan – [email protected]; Wenchao Wu – [email protected]; Huaiqing Chen – [email protected] Corresponding authorPublished: 16 January 2007 BMC Cell Biology 2007, 8:1 doi:10.1186/1471-2121-8-Received: 31 August 2006 Accepted: 16 JanuaryThis write-up is available from: http://www.biomedcentral.com/1471-2121/8/1 2007 Liu et al; licensee BioMed Central Ltd. This is an Open Access write-up distributed below the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, offered the original operate is correctly cited.AbstractBackground: Connective tissue growth element (CTGF) is really a potent profibrotic element, which is implicated in fibroblast proliferation, angiogenesis and extracellular matrix (ECM) synthesis. It can be a downstream mediator of some of the effects of transforming development factor (TGF) and is potentially induced by hyperglycemia in human renal Neurotensin Receptor Compound mesangial cells. Nevertheless, whether high glucose could induce the CTGF expression in vascular smooth muscle cells (VSMCs) remains unknown. Therefore, this study was created to test whether or not high glucose could regulate CTGF expression in human VSMC. The impact of modulating CTGF expression on VSMC proliferation and migration was additional investigated.