Chinese Med J 2003, 116:301–304. 109. Wang HS, Chard T: IGFs and IGF-binding proteins in the regulation of human ovarian and endometrial function. J Endocrinol 1999, 161:1–13.PubMedCrossRef 110. Fowler DJ, Nicolaides
KH, Miell JP: Insulin-like growth factor binding protein-1 (IGFBP-1): a multifunctional role in the human female reproductive tract. Hum Reprod Update 2000, 6:495–504.PubMedCrossRef Competing interests The authors indicate no potential conflicts of interest. TSA HDAC supplier Author contribution RS, JFL, and HB provided conceptual input. RS, XL, and YF participated in tissue collection and funded the experiments. RS and YF prepared the figures. RS and XL performed the literature search. RS drafted the manuscript. All authors participated in the discussion and approved the final submitted version of the manuscript.”
“Background Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer with an annual incidence of over 560,000 cases worldwide [1]. Despite various advances in combined modality therapy, the survival rate of HNSCC patients has not improved over the past two decades, due largely to the uncontrollable metastasis to lymph nodes selleck and distant organs [2]. Cervical lymph node metastasis in particular has been considered the most important adverse prognostic factor in HNSCC [3–5].
More effective strategies based on a better understanding Phospholipase D1 of the molecular mechanisms that lead to metastasis are thus indispensable. Recent progress in tumor biology indicates that the initial steps during the sequential process of metastasis are notably analogous to
the epithelial-to-mesenchymal transition (EMT) in which cells lose epithelial features including cell adhesion and gain mesenchymal traits including cell motility during embryogenesis and wound healing [6, 7]. In the tumor context, the acquisition of the EMT, Forskolin in vitro accompanied by functional loss of E-cadherin that maintains intercellular adhesion, stimulates the dissemination of single tumor cells from primary sites through the loss of cell-to-cell contact, thereby endowing cells with metastatic abilities [6–8]. At the transcriptional level, E-cadherin is downregulated by several transcriptional repressors including snail, slug, DeltaEF1/ZEB1, SIP1 (Smad interacting protein 1)/ZEB2, E12/E47, and twist, by binding to E-box promoter elements of CDH-1, a gene encoding human E-cadherin [6–8]. We recently reported that SIP1 expression was inversely correlated with E-cadherin expression in HNSCC cells, and that the downregulation of E-cadherin and upregulated nuclear localization of SIP1 were independently correlated with delayed neck metastasis in stage I/II tongue squamous cell carcinoma (TSCC) [9]. However, a practical therapeutic approach that leads to the suppression of the EMT has not been developed to control the progression of cancers, including HNSCC.