O resolve structure: SHELXS97 (Sheldrick, 2008); system(s) used to refine structure
O resolve structure: SHELXS97 (Sheldrick, 2008); system(s) used to refine structure: SHELXL97 (Sheldrick, 2008); molecular graphics: ORTEP-3 for Windows (Farrugia, 2012)and PLATON (Spek, 2009); application utilised to prepare material for publication: WinGX (Farrugia, 2012).Connected literatureFor the functionalization of camphor, see: Jennings Herschbach (1965); Pastran et al., (2011). For transition metal complexes of camphor, see: Spannenberg et al. (2002); Harrad et al. (2010); Ait Ali et al. (2006); Gaudo et al. (2011). For ringpuckering parameters, see: Cremer Pople (1975).The authors thank Professor Daniel Avignant for the X-ray measurements.Supplementary data and figures for this paper are obtainable in the IUCr electronic archives (Reference: BT6921).
Wang et al. BMC Cancer 2014, 14:442 http:biomedcentral1471-240714RESEARCH ARTICLEOpen AccessSrc-homology 2 domain-containing tyrosine phosphatase 2 promotes oral cancer invasion and metastasisHsueh-Chun Wang1,two, Wei-Fan Chiang3, Hsin-Hsiu Huang4, Ying-Ying Shen5 and Hung-Che Chiang4,IGFBP-3, Human 6AbstractBackground: Tumor invasion and metastasis represent a major unsolved trouble in cancer pathogenesis. Recent research have indicated the involvement of Src-homology 2 domain-containing tyrosine phosphatase two (SHP2) in various malignancies; on the other hand, the role of SHP2 in oral cancer progression has but to be elucidated. We propose that SHP2 is involved inside the progression of oral cancer toward metastasis. Methods: SHP2 expression was evaluated in paired oral cancer tissues by using MAX Protein Storage & Stability immunohistochemical staining and real-time reverse transcription polymerase chain reaction. Isogenic highly invasive oral cancer cell lines from their respective low invasive parental lines had been established working with a Boyden chamber assay, and changes in the hallmarks from the epithelial-mesenchymal transition (EMT) had been assessed to evaluate SHP2 function. SHP2 activity in oral cancer cells was lowered working with si-RNA knockdown or enforced expression of a catalytically deficient mutant to analyze migratory and invasive capability in vitro and metastasis toward the lung in mice in vivo. Outcomes: We observed the important upregulation of SHP2 in oral cancer tissues and cell lines. Following SHP2 knockdown, the oral cancer cells markedly attenuated migratory and invasion ability. We observed comparable final results in phosphatase-dead SHP2 C459S mutant expressing cells. Enhanced invasiveness was related with significant upregulation of E-cadherin, vimentin, SnailTwist1, and matrix metalloproteinase-2 inside the hugely invasive clones. Also, we determined that SHP2 activity is expected for the downregulation of phosphorylated ERK12, which modulates the downstream effectors, Snail and Twist1 at a transcript level. In lung tissue sections of mice, we observed that HSC3 tumors with SHP2 deletion exhibited substantially lowered metastatic capacity, compared with tumors administered handle si-RNA. Conclusions: Our data recommend that SHP2 promotes the invasion and metastasis of oral cancer cells. These benefits provide a rationale for additional investigating the effects of small-molecule SHP2 inhibitors around the progression of oral cancer, and indicate a previously unrecognized SHP2-ERK12-SnailTwist1 pathway that is definitely likely to play a important function in oral cancer invasion and metastasis. Key phrases: Extracellular signal-related kinase, Invasion, Metastasis, Oral cancer, Src-homology 2 domain-containing tyrosine phosphatase Correspondence: hcchiangnhri.org.t.