Archives

  • 2018-07
  • 2018-10
  • 2018-11
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • br Acknowledgments This work was supported by Natural Scienc

    2019-10-29


    Acknowledgments This work was supported by Natural Science Foundation of China (No: 81501485). We are particularly grateful to Dr. Dan Yang and Dr. Yi Zhang for their assistance and facilities in helping this experiment and manuscript.
    Oral squamous cell carcinoma (OSCC), the most common malignant neoplasm in the oral cavity, is a significant global public health threat. The management of OSCC varies considerably, but standard procedure includes surgery with or without neck dissection, followed by adjuvant radiotherapy. Despite all efforts and therapeutic developments, the 5-year survival rate for head and neck cancers has not remarkably improved over the last 2 decades., In clinical practice, treatment planning and prognosis for patients with OSCC are mainly based on the TNM classification. At the same time, clinical outcome does not always follow the predictions of those parameters, suggesting that other factors related to the patient or the biologic characteristics of the tumor may be relevant. Chemokines are a superfamily of small cytokines with the ability to chemoattract PIK-90 to target tissues. Recent data indicate that chemokine receptors may direct lymphatic and hematogenous spread and additionally influence the location of metastatic tumor growth. Expression of CXC chemokine receptor CXCR4 is involved in the lymph node or distant metastasis of several types of cancer,, , , , , , including oral cancer., Even so, there have been few reports about the relationship of CXCR-4 expression with survival in OSCC patients. Matrix metalloproteinases (MMPs), a family of zinc-dependent proteinases, are necessary for the degradation of extracellular matrix and can be produced by invasive tumor cells. MMP-2 and MMP-9 are closely associated with malignant potential in OSCCs., Recent studies suggest that the CXCR-4–chemokine ligand 12 (CXCL-12) interaction increases invasiveness through the up-regulation of MMP-2 or MMP-9 in some cancer cells., , , The Ki-67 antibody is reactive with human nuclear proteins associated with cell proliferation. Recently, CXCR-4 has been shown to directly or indirectly regulate proliferation of some ovarian and breast cancer cell lines in culture., However, no reports have examined the relationship between CXCR-4 expression and the expression of MMP-2, MMP-9, and Ki-67 using tissue samples from OSCC patients.
    Introduction Stroke is the primary cause of disability and the second-leading cause of death worldwide. Despite medical advances, clinical outcomes after stroke remain poor, and many patients remain permanently disabled. There are very few effective clinical therapies for acute ischemic stroke. Transplantation therapy using embryonic and adult stem cells is actively being studied to enhance tissue repair and functional recovery after stroke (Andres et al., 2008). Among stem cells that are candidates for transplantation in stroke patients, bone marrow mesenchymal stem cells (BMSCs) are preferred because they are available from autologous donation, which eliminates ethical problems and other concerns related to graft rejection (Malgieri et al., 2010). BMSC transplantation is a promising PIK-90 therapy method and may be effective treatment for various central nervous system diseases. Over the past decade, numerous studies in experimental stroke animal models have demonstrated that small numbers of BMSCs can pass through the blood–brain barrier and migrate into or “home to” the ischemic brain ischemic regions. BMSC transplantation has been shown to have beneficial effects on functional recovery after ischemic stroke or traumatic injury (Chen et al., 2001, Li and Chopp, 2009); however, the mechanism by which BMSCs promote functional benefits after transplantation remains unclear. Stromal cell-derived factor-1 (SDF-1), also known as C-X-C motif chemokine 12 (CXCL12), is a member of the superfamily of chemoattractant cytokines. CXCL12 is found to be expressed by all cell types that are presented in the central nervous system (CNS). It works in conjunction with the G-protein coupled receptor CXCR4, which is found at the surface of a variety of cells including neurons, astrocytes, microglia, bone marrow-derived cells, as well as other progenitor cells (Y. Wang et al. 2012). Studies revealed that SDF-1/CXCR-4 axis plays important roles in controlling cellular migration (Cui et al., 2007) and mediating and proliferation of human and murine progenitor cells (Gillette et al., 2009, Hayakawa et al., 2009, Kyriakou et al., 2008). The SDF-1/CXCR-4 axis is also involved in metastasis, chronic inflammatory disorders, and benign proliferative diseases (Begley et al., 2007). In addition to the CXCR4 receptor, a new receptor termed CXCR-7 (also known as RDC-1) was recently identified (Burns et al., 2006, Balabanian et al., 2005). CXCR-7 is expressed on many different cell types, including neurons, immune cells, tumor cells, and endothelial cells. It can mediate signaling by binding one of its two known ligands, CXCL11 or CXCL12 (Miao et al., 2007). A previous study reported that CXCR-7 promoted cancer cell survival through anti-apoptotic mechanisms (Wang et al., 2011), and CXCR-7 expression was up-regulated following hypoxic preconditioning of cultured mesenchymal stem cells (MSCs) (Liu et al., 2010). However, no reports have described CXCR7-induced chemotaxis, and it is also unknown whether the two SDF-1α receptors are co-expressed in BMSCs. For these reasons, it is unclear whether the SDF-1–CXCR4/CXCR7 axis could affect BMSC transplantation to improve stroke outcome.