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10.1038/onc.2014.143 http://scihub22266oqcxt.onion/10.1038/onc.2014.143 C4254377!4254377!24882582     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24882582&cmd=llinks): Failed to open stream: HTTP request failed! 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Activation of mTOR Pathway in Myeloid-derived Suppressor Cells Stimulates Cancer Cell Proliferation and Metastasis in lal?/? Mice |pdf=|usr=}}{{24882582}} gab.com Text Activation of mTOR Pathway in Myeloid-derived Suppressor Cells Stimulates Cancer Cell Proliferation and Metastasis in lal / Mice JO: Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=24882582 #FOAvip Inflammation critically contributes to cancer metastasis, in which myeloid-derived suppressor cells (MDSCs) are an important participant. Although MDSCs are known to suppress immune surveillance, their roles in directly stimulating cancer cell proliferation and metastasis currently remain unclear. Lysosomal acid lipase (LAL) deficiency causes systemic expansion and infiltration of MDSCs in multiple organs and subsequent inflammation. In the LAL-deficient (lal?/?) mouse model, melanoma metastasized massively in allogeneic lal?/? mice, which was suppressed in allogeneic lal+/+ mice due to immune rejection. Here we report for the first time that MDSCs from lal?/? mice directly stimulated B16 melanoma cell in vitro proliferation, and in vivo growth and metastasis. Cytokines i.e., IL-1? and TNF? from MDSCs are required for B16 melanoma cell proliferation in vitro. Myeloid-specific expression of human LAL (hLAL) in lal?/? mice rescues these malignant phenotypes in vitro and in vivo. The tumor-promoting function of lal?/? MDSCs is mediated, at least in part, through over-activation of the mammalian target of rapamycin (mTOR) pathway. Knockdown of mTOR, Raptor or Rictor in lal?/? MDSCs suppressed their stimulation on proliferation of cancer cells, including B16 melanoma, LLC and Tramp-C2 cancer cells. Our results indicate that LAL plays a critical role in regulating MDSCs ability to directly stimulate cancer cell proliferation, and overcome immune rejection of cancer metastasis in allogeneic mice through modulation of the mTOR pathway, which provides a mechanistic basis for targeting MDSCs to reduce the risk of cancer metastasis. Therefore, MDSCs possess dual functions to facilitate cancer metastasis: suppress immune surveillance, and stimulate cancer cell proliferation and growth. Twit Text FOAVip Activation of mTOR Pathway in Myeloid-derived Suppressor Cells Stimulates Cancer Cell Proliferation and Metastasis in lal / Mice ????Oncogene http://www.kidney.de/pget.php?&tw=1&pmid=24882582 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24882582 #FOAvip English Wikipedia <ref>{{Cite pmid|24882582}}</ref> Activation of mTOR Pathway in Myeloid-derived Suppressor Cells Stimulates Cancer Cell Proliferation and Metastasis in lal?/? Mice #MMPMID24882582 Zhao T; Du H; Ding X; Walls K; Yan C Oncogene 2015[Apr]; 34 (15): 1938-48 PMID24882582show ga Inflammation critically contributes to cancer metastasis, in which myeloid-derived suppressor cells (MDSCs) are an important participant. Although MDSCs are known to suppress immune surveillance, their roles in directly stimulating cancer cell proliferation and metastasis currently remain unclear. Lysosomal acid lipase (LAL) deficiency causes systemic expansion and infiltration of MDSCs in multiple organs and subsequent inflammation. In the LAL-deficient (lal?/?) mouse model, melanoma metastasized massively in allogeneic lal?/? mice, which was suppressed in allogeneic lal+/+ mice due to immune rejection. Here we report for the first time that MDSCs from lal?/? mice directly stimulated B16 melanoma cell in vitro proliferation, and in vivo growth and metastasis. Cytokines i.e., IL-1? and TNF? from MDSCs are required for B16 melanoma cell proliferation in vitro. Myeloid-specific expression of human LAL (hLAL) in lal?/? mice rescues these malignant phenotypes in vitro and in vivo. The tumor-promoting function of lal?/? MDSCs is mediated, at least in part, through over-activation of the mammalian target of rapamycin (mTOR) pathway. Knockdown of mTOR, Raptor or Rictor in lal?/? MDSCs suppressed their stimulation on proliferation of cancer cells, including B16 melanoma, LLC and Tramp-C2 cancer cells. Our results indicate that LAL plays a critical role in regulating MDSCs ability to directly stimulate cancer cell proliferation, and overcome immune rejection of cancer metastasis in allogeneic mice through modulation of the mTOR pathway, which provides a mechanistic basis for targeting MDSCs to reduce the risk of cancer metastasis. Therefore, MDSCs possess dual functions to facilitate cancer metastasis: suppress immune surveillance, and stimulate cancer cell proliferation and growth. äActivation of mTOR Pathway in Myeloid-derived Suppressor Cells Stimula(epmc).pdf DeepDyve Pubget Overpricing