Abstract
Abstract The deregulated expression of cytokines and the aberrant activation of their downstream signaling pathways would give tumor cells the abnormal proliferation and survival. Therefore identification and understanding of deregulated cytokines in certain tumor would provide an opportunity of better targeted therapies of the cancer. MIF, a proinflammatory cytokine has been known to play a role in proliferation, survival and apoptosis in several tumors. In our studies it was found that MIF expression in Ewing tumors is pretty high and it is secreted out of the cells. Ewing tumor cell lines deficient of MIF showed morphological change, deregulation of differentiation, decrease of proliferation and increase of apoptosis. Through the investigation of several signaling pathways it was found that JAK2/STATs pathways are involved in the MIF dependent survival and proliferation of Ewing tumors and in addition, MIF is involved in the autophagy of Ewing tumors through the activation of AMPK. It has been reported that CD74 is the main receptor of MIF and in our study it was found that CD74 is expressed in Ewing tumors even though the expression is much less than MIF. The decreased expression of CD74 in Ewing tumor cell lines caused the morphological change and inhibition of proliferation, which are the similar phenotypes of MIF deficient Ewing tumor cell lines. It is known that CD74 is associated with CD44 which is involved in the signaling pathways of cellular survival and proliferation. In our study it was found that decreased expression of CD44 in Ewing tumor cell lines caused the inhibition of cell survival and proliferation. In conclusion, our data implies that MIF and its downstream signaling pathways such as JAK/STATs, AMPK, CD74 and CD44 might be involved in growth, survival, proliferation and metastasis of Ewing tumors. Therefore MIF and its downstream signaling pathways could be promising targets of Ewing tumors therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4336. doi:1538-7445.AM2012-4336
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
