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Dear Editor, We would like to submit the enclosed manuscript entitled “Involement of PAK1 in RIPX-induced gastric cancer cell migration and invasion”, which we wish to be considered for publication in oncotarget. Coordinated regulation of the actin cytoskeleton is responsible for the formation of protrusive structures that are central to tumor cell migration and invasion, including filopodia, lamellipodia and invadopodia. RIPX was reported to play an important role in neuronal development, whereas the role of RIPX in cancer has not been explored. Here, first, we demonstrate that RIPX localizes in F-actin-enriched invadopodia and induces the formation of protrusive structures. Importantly, we found that the overexpression of RIPX promotes gastric cancer cell migration and invasion. Furthermore, p21-activated kinase 1 (PAK1) is involved in RIPX-induced SGC-7901 cell migration and invasion by regulating its expression. Moreover, we showed a positive correlation between PAK1 and RIPX expression in gastric cancer samples. Strikingly, we found that high expression of RIPX is tightly correlated to clinical gastric cancer. These findings revealed a novel function of RIPX in gastric cancer, suggesting that blocking PAK1-RIPX might be a potential therapeutic strategy for metastasis of gastric cancer. Meanwhile, we also declare that there are no conflicts of interests and the content of the study is original and that it has not been published or accepted for publication, either in whole or in part, in any form (other than as an abstract or other preliminary publication). All the authors also declare that no part of the manuscript is currently under consideration for publication elsewhere.If you have any questions, please don't hesitate to contact us. I am looking forward to hearing from you soon. Sincerely yours Guiling Wang&Feng Li Department of Cell Biology, Key Laboratory of Cell Biology of Mini stry of Public Health of China,China Medical University,Shenyang 110001, P.R. China Tel: +86-24-23256666-5348 Fax: +86-24-23261056 E-mail: [email protected]& [email protected] May 8, 2013