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SEMA3F-deficient colorectal cancer cells promote lymphangiogenesis: fatty acid metabolism replace glycolysis for energy supply during lymphatic endothelial cells proliferation in tumor hypoxia microenvironment

By Xiaoyuan Fu, Miaomiao Tao, Hongbo Ma, Cancan Wang, Yanyan Li, Xiaoqiao Hu, Xiurong Qin, Renming Lv, Gengdou Zhou, Jun Wang, Meiyu Zhou, Guofa Xu, Zexin Wang, Min Chen, Qi Zhou

Posted 09 Dec 2019
bioRxiv DOI: 10.1101/869644

The fuel metabolism in mitochondrial and support proliferation of lymphatic endothelial cells (LECs) remain elusive during lymphangiogenesis in tumor hypoxic microenvironment. Recent studies report that loss of SEMA3F critically contributes to lymphangiogenesis of the CRCs. Here, we silenced SEMA3F expression of CRCs and co-culture with hLECs, the tubulogenesis capacity and hLECs migration were escalated in the hypoxia, the hLECs mainly relied on fatty acid metabolism not aerobic glycolysis during lymphangiogenesis. SEMA3F-deficient CRCs up-regulated PMAKP expression and phosphorylation of hLECs, and activated its peroxisome proliferator-activated receptor (PPARs) and Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1a) facilitated their switched toward fatty acids (FA) catabolism. Furthermore, we observed that activation of the PGCI-PPAR lipid oxidation signaling pathway in hLECs was caused by the secretion of interleukin-6 by tumor cells. Taken together, this study indicates that CRCs with SEMA3F expression depletion significantly promotes lymphangiogenesis in hypoxia and faciliates the secretion of IL-6 in tumor cell, and activates mitochondria fatty acids oxidation (FAO) reaction in the hLECs by PGCI-PPAR signaling pathways to support its growth.

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