Oronto, Toronto, Ontario, Canada. 2Research and Development, Ardea Biosciences, Inc., 4939 Directors

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Pre-publication history The pre-publication history for this paper is often accessed here: http://www.biomedcentral.com/1471-2407/10/515/prepubdoi:ten.1186/1471-2407-10-515 Cite this short article as: Chang et al.: Antitumour activity of a 1315355-93-1 site pubmed ID:http://www.ncbi.nlm.nih.gov/pubmed/27465830 potent MEK inhibitor RDEA119/BAY 869766 combined with rapamycin in human orthotopic main pancreatic cancer xenografts. BMC Cancer 2010, ten:611 http://www.biomedcentral.com/1471-2407/10/RESEARCH ARTICLEOpen AccessPlexin-B1 silencing inhibits ovarian cancer cell migration and invasionShuangmei Ye1, Xing Hao1, Ting Zhou1, Mingfu Wu1, Juncheng Wei1, Yongjun Wang1,two, Li Zhou1, Xuefeng Jiang1, Li Ji1, Yin Chen1, Lanying You1, Yiqun Zhang1, Gang Xu1, Jianfeng Zhou1, Ding Ma1*, Shixuan Wang1*AbstractBackground: Elevated Plexin-B1 expression has been located in diverse human cancers and in non-neoplastic tissues, and it mediates diverse biological and pathological activities. However, whether or not Plexin-B1 expression is involved in human ovarian tumors remains unclear. Within the present study, Plexin-B1 expression was explored in benign and malignant human ovarian tumor tissues. Moreover, the effect of Plexin-B1 expression on ovarian cancer cell proliferation, migration and invasion have been investigated in vitro. Techniques: Plexin-B1 expression was analyzed in normal and benign ovarian tissues and serous ovarian tumors (each borderline and malignant) by immunohistochemical staining, at the same time as in four human ovarian cancer cell lines (A2780, C13*, SKOV3, and OV2008) by RT-PCR and western blot analyses. In addition, endogenous Plexin-B1 expression was suppressed by Plexin-B1 siRNA in SKOV3 cells, which overexpress PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28506461 Plexin-B1.Oronto, Toronto, Ontario, Canada. 2Research and Development, Ardea Biosciences, Inc., 4939 Directors Spot, San Diego, CA, USA. 3Department of Healthcare Oncology and Hematology, Princess Margaret Hospital, Toronto, Ontario, Canada. Authors' contributions QC created the study, carried out the experiments described within the study and drafted the manuscript. MSC, JNM, and DWH conceived, reviewed the study and revised the manuscript. All authors read and authorized the final manuscript. Competing interests MSC and JNM are staff of Ardea Biosciences.Chang et al. BMC Cancer 2010, ten:515 http://www.biomedcentral.com/1471-2407/10/Page 11 ofmitogen-activated protein kinase kinase inhibitor CI-1040 in nude mice bearing human heterotransplants. Cancer Res 2005, 65:2854-2860. 19. Ou DL, Shen YC, Liang JD, Liou JY, Yu SL, Fan HH, Wang DS, Lu YS, Hsu C, Cheng AL: Induction of Bim expression contributes towards the antitumor synergy involving sorafenib and mitogen-activated protein kinase/ extracellular signal-regulated kinase kinase inhibitor CI-1040 in hepatocellular carcinoma. Clin Cancer Res 2009, 15:5820-5828. 20. Huynh H, Ngo VC, Koong HN, Poon D, Choo SP, Toh HC, Thng CH, Chow P, Ong HS, Chung A, et al: AZD6244 enhances the anti-tumor activity of sorafenib in ectopic and orthotopic models of human hepatocellular carcinoma (HCC). J Hepatol 2010, 52:79-87. Pre-publication history The pre-publication history for this paper is usually accessed here: http://www.biomedcentral.com/1471-2407/10/515/prepubdoi:ten.1186/1471-2407-10-515 Cite this article as: Chang et al.: Antitumour activity of a PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27465830 potent MEK inhibitor RDEA119/BAY 869766 combined with rapamycin in human orthotopic primary pancreatic cancer xenografts. BMC Cancer 2010 10:515.Submit your next manuscript to BioMed Central and take complete benefit of:?Handy online submission ?Thorough peer review ?No space constraints or colour figure charges ?Instant publication on acceptance ?Inclusion in PubMed, CAS, Scopus and Google Scholar ?Research which is freely readily available for redistributionSubmit your manuscript at www.biomedcentral.com/submit