Answers are grounded in this paper and cite their sources.
// Ming Li 4, 5, * , Xinfang Yu 6, * , Wei Li 7, * , Ting Liu 1 , Gang Deng 8 , Wenbin Liu 9 , Haidan Liu 3 and Feng Gao 1, 2 1 Department of Ultrasonography, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China 2 State Key Laboratory of Powder Metallurgy, Central South University, Changsha, Hunan 410006, P.R. China 3 Clinical Center for Gene Diagnosis and Therapy, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China 4 School of Stomatology, Hunan University of Chinese Medicine, Changsha, Hunan 410208, P.R. China 5 Changsha Stomatological Hospital, Changsha, Hunan 410004, P.R. China 6 Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA 7 Department of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China 8 Department of Hepatobiliary and Pancreatic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China 9 Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410013, P.R. China * These authors contributed equally to this work Correspondence to: Haidan Liu, email: lhd1129@126.com Feng Gao, email: gfeng0731@gmail.com Keywords: hepatocellular carcinoma; deguelin; angiogenesis; VEGF; c-Met Received: July 20, 2016 Accepted: October 11, 2017 Published: October 26, 2017 ABSTRACT Angiogenesis plays a crucial role in the development of human hepatocellular carcinoma (HCC). In the present study, we found a natural compound, deguelin, has a profound anti-angiogenesis effect on HCC. Deguelin suppressed vascular endothelial growth factor (VEGF)-induced human umbilical vascular endothelial cells (HUVECs) proliferation, migration, invasion, and capillary-like tube formation in vitro and reduced tumor angiogenesis in vivo . We discovered that VEGF receptor-mediated signal transduction cascades in HUVECs were inhibited by deguelin. Deguelin decreased the autocrine of VEGF in HCC cells in a time- and dose-dependent manner. Additionally, deguelin suppressed HGF-induced activation of the c-Met signaling pathway. Knocking down c-Met or inhibition of c-Met activation impaired HGF-mediated VEGF production. Importantly, we produced patient-derived hepatocellular carcinoma xenografts to evaluate the therapeutic effect of deguelin in vivo . Taken together, these results indicate that deguelin could inhibit HCC through suppression of angiogenesis on vascular endothelial cells and reduction of proangiogenic factors in cancer cells.
No takes yet. Share an insight, caveat, or question.
Li et al. (2017) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: