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Cancer letters 36건

  1. [해외논문]   Editorial Board   SCI SCIE


    Cancer letters v.414 ,pp. ii - ii , 2018 , 0304-3835 ,

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  2. [해외논문]   IWR-1, a tankyrase inhibitor, attenuates Wnt/β-catenin signaling in cancer stem-like cells and inhibits in vivo the growth of a subcutaneous human osteosarcoma xenograft   SCI SCIE

    Martins-Neves, Sara R. (Pharmacology and Experimental Therapeutics, IBILI - Faculty of Medicine, University of Coimbra, Coimbra, Azinhaga de Sta. Comba, Celas, 3000-354, Portugal ) , Paiva-Oliveira, Daniela I. (Pharmacology and Experimental Therapeutics, IBILI - Faculty of Medicine, University of Coimbra, Coimbra, Azinhaga de Sta. Comba, Celas, 3000-354, Portugal ) , Fontes-Ribeiro, Carlos (Pharmacology and Experimental Therapeutics, IBILI - Faculty of Medicine, University of Coimbra, Coimbra, Azinhaga de Sta. Comba, Celas, 3000-354, Portugal ) , Bové (Department of Pathology, Leiden University Medical Center, P.O.Box 9600, L1-Q, 2300 RC, Leiden, The Netherlands ) , e, Judith V.M.G. (Department of Pathology, Leiden University Medical Center, P.O.Box 9600, L1-Q, 2300 RC, Leiden, The Netherlands ) , Cleton-Jansen, Anne-Marie (Pharmacology and Experimental Therapeutics, IBILI - Faculty of Medicine, University of Coimbra, Coimbra, Azinhaga de Sta. Comba, Celas, 3000-354, Portugal) , Gomes, Cé , lia M.F.
    Cancer letters v.414 ,pp. 1 - 15 , 2018 , 0304-3835 ,

    초록

    Abstract Wnt/β-catenin or canonical Wnt signaling pathway regulates the self-renewal of cancer stem-like cells (CSCs) and is involved in tumor progression and chemotherapy resistance. Previously, we reported that this pathway is activated in a subset of osteosarcoma CSCs and that doxorubicin induced stemness properties in differentiated cells through Wnt/β-catenin activation. Here, we investigated whether pharmacological Wnt/β-catenin inhibition, using a tankyrase inhibitor (IWR-1), might constitute a strategy to target CSCs and improve chemotherapy efficacy in osteosarcoma. IWR-1 was specifically cytotoxic for osteosarcoma CSCs. IWR-1 impaired spheres' self-renewal capacity by compromising landmark steps of the canonical Wnt signaling, namely translocation of β-catenin to the nucleus and subsequent TCF/LEF activation and expression of Wnt/β-catenin downstream targets. IWR-1 also hampered the activity and expression of key stemness-related markers. In vitro , IWR-1 induced apoptosis of osteosarcoma spheres and combined with doxorubicin elicited synergistic cytotoxicity, reversing spheres' resistance to this drug. In vivo , IWR-1 co-administration with doxorubicin substantially decreased tumor progression, associated with specific down-regulation of TCF/LEF transcriptional activity, nuclear β-catenin and expression of the putative CSC marker Sox2. We suggest that targeting the Wnt/β-catenin pathway can eliminate CSCs populations in osteosarcoma. Combining conventional chemotherapy with Wnt/β-catenin inhibition may ameliorate therapeutic outcomes, by eradicating the aggressive osteosarcoma CSCs and reducing drug resistance. Highlights Wnt/β-catenin is specifically active in osteosarcoma cancer stem-like cells. Wnt inhibition induces apoptosis and cell cycle arrest of osteosarcoma CSCs. Wnt/β-catenin disruption impairs osteosarcoma stemness-related features. Wnt inhibition synergizes with doxorubicin against chemoresistant CSCs. IWR-1 abrogates Wnt/β-catenin activity and tumor burden in vivo .

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  3. [해외논문]   Roles of tRNA-derived fragments in human cancers   SCI SCIE

    Sun, Chunxiao (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Fu, Ziyi (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Wang, Siwei (Department of Thoracic Surgery, Nanjing Medical University Affiliated Cancer Hospital, Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Cancer Institute of Jiangsu Province, Nanjing 210009, China ) , Li, Jun (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Li, Yongfei (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Zhang, Yanhong (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Yang, Fan (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Chu, Jiahui (Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China ) , Wu, Hao (Department of Onc) , Huang, Xiang , Li, Wei , Yin, Yongmei
    Cancer letters v.414 ,pp. 16 - 25 , 2018 , 0304-3835 ,

    초록

    Abstract Transfer RNAs (tRNAs) were traditionally considered to participate in protein translation. Recent studies have identified a novel class of small non-coding RNAs (sncRNAs), produced by the specific cleavage of pre- and mature tRNAs, which have been named tRNA-derived fragments. tRNA-derived fragments are classified into diverse subtypes based on the different cleavage positions of the pre- and mature tRNAs. Recently, accumulated evidence has shown that these tRNA-derived fragments are frequently dysregulated in several cancers. Several tRNA-derived fragments were found to participate in cell proliferation, apoptosis, and invasive metastasis in several malignant human tumors. These dysregulated fragments are able to bind both Argonaute proteins and Piwi proteins to regulate gene expression. Some of the newly identified tRNA-derived fragments have been considered as the new biomarkers and therapeutic targets for the treatment of cancer. This review summarizes the biogenesis and biological functions of different subtypes of tRNA-derived fragments and discusses their molecular mechanisms in cancer progression. Highlights tRNA-derived fragments are frequently dysregulated in several cancers. Different types of tRNA-derived fragments have a variety of molecular functions. tRNA-derived fragments are new potential biomarkers and therapeutic targets in cancer. Graphical abstract [DISPLAY OMISSION]

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  4. [해외논문]   Chemoprevention with isothiocyanates – From bench to bedside   SCI SCIE

    Grü (Corresponding authors. Breisacherstr. 115B, 79106 Freiburg, Germany. ) , ndemann, Carsten (Corresponding authors. Breisacherstr. 115B, 79106 Freiburg, Germany.) , Huber, Roman
    Cancer letters v.414 ,pp. 26 - 33 , 2018 , 0304-3835 ,

    초록

    Abstract Isothiocyanates (ITCs) are naturally occurring hydrolization products from glucosinolates (GLSs) in brassicaceae and in epidemiological studies their intake has been weakly to moderately inversely correlated with the risk of colorectal cancer, prostate cancer and lung cancer. Numerous preclinical studies demonstrate chemopreventive mode of actions of ITCs, mainly related to a.) detoxification (induction of phase II enzymes), b.) anti-inflammatory properties by down-regulation of NFkappaB activity, c.) cyclin-mediated cell cycle arrest and d.) epigenetic modulation by inhibition of histone deacetylase activity. First prospective clinical trials were promising in patients with risk of prostate cancer recurrence. The glutathione-S-transferase gene expression seems to play a major role in the individual susceptibility towards ITCs. Safety issues are widely unclear and should be more addressed in future studies because ITCs can, in low concentrations, compromise the function of human immune cells and might impair genome stability. Highlights ITC exhibit multiple chemopreventive actions in vitro , in animals and in humans. Resorption of ITC is excellent but depends on the presence of myrosinase. First prospective clinical study was promising in patients with risk of prostate cancer recurrence. ITC have off-target effects which raise safety concerns.

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  5. [해외논문]   LOX-1 activation by oxLDL triggers an epithelial mesenchymal transition and promotes tumorigenic potential in prostate cancer cells   SCI SCIE

    Gonzá (Biotechnology and Biopharmaceuticals Laboratory, Department of Pathophysiology, School of Biological Science, Universidad de Concepión, Concepción, Chile ) , lez-Chavarrí (Biotechnology and Biopharmaceuticals Laboratory, Department of Pathophysiology, School of Biological Science, Universidad de Concepión, Concepción, Chile ) , a, I. (Biotechnology and Biopharmaceuticals Laboratory, Department of Pathophysiology, School of Biological Science, Universidad de Concepión, Concepción, Chile ) , Fernandez, E. (Biotechnology and Biopharmaceuticals Laboratory, Department of Pathophysiology, School of Biological Science, Universidad de Concepión, Concepción, Chile ) , Gutierrez, N. (Biotechnology and Biopharmaceuticals Laboratory, Department of Pathophysiology, School of Biological Science, Universidad de Concepión, Concepción, Chile ) , Gonzá (Biotechnology and Biopharmaceuticals Laboratory, Department of Pathophysiology, School of Biological Science, Universidad de Concepión, Concepc) , lez-Horta, E.E. , Sandoval, F. , Cifuentes, P. , Castillo, C. , Cerro, R. , Sanchez, O. , Toledo, Jorge R.
    Cancer letters v.414 ,pp. 34 - 43 , 2018 , 0304-3835 ,

    초록

    Abstract Obesity is related to an increased risk of developing prostate cancer with high malignancy stages or metastasis. Recent results demonstrated that LOX-1, a receptor associated with obesity and atherosclerosis, is overexpressed in advanced and metastatic prostate cancer. Furthermore, high levels of oxLDL, the main ligand for LOX-1, have been found in patients with advanced prostate cancer. However, the role of LOX-1 in prostate cancer has not been unraveled completely yet. Here, we show that LOX-1 is overexpressed in prostate cancer cells and its activation by oxLDL promotes an epithelial to mesenchymal transition, through of lowered expression of epithelial markers (E-cadherin and plakoglobin) and an increased expression of mesenchymal markers (vimentin, N-cadherin, snail, slug, MMP-2 and MMP-9). Consequently, LOX-1 activation by oxLDL promotes actin cytoskeleton restructuration and MMP-2 and MMP-9 activity inducing prostate cancer cell invasion and migration. Additionally, LOX-1 increased the tumorigenic potential of prostate cancer cells and its expression was necessary for tumor growth in nude mice. In conclusion, our results suggest that oxLDL/LOX-1 could be ones of mechanisms that explain why obese patients with prostate cancer have an accelerated tumor progression and a greater probability of developing metastasis. Highlights The Lectin-like oxidized LDL receptor 1, LOX-1 is overexpressed in prostate cancer and its expression is associated with high Gleason score. The activation of LOX-1 by oxLDL promotes an epithelial to mesenchyme transition, migration and invasion in prostate cancer cells. The activation of LOX-1 enhances tumorigenic potential and its expression is necessary for tumor growth of prostate cancer cells.

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  6. [해외논문]   Hypoxia-induced miR-214 expression promotes tumour cell proliferation and migration by enhancing the Warburg effect in gastric carcinoma cells   SCI SCIE

    Yang, Liuqing (Department of Gastroenterology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China ) , Zhang, Weijie (Department of General Surgery, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China ) , Wang, Yanbo (State Key Laboratory of Pharmaceutical Biotechnology, Collaborative Innovation Center of Chemistry for Life Sciences, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, NJU Advanced Institute for Life Sciences (NAILS), School of Life Sciences, Nanjing University, 163 Xianlin Road, Nanjing, Jiangsu 210023, China ) , Zou, Tianhui (Division of Gastroenterology and Hepatology, Shanghai Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China ) , Zhang, Bin (Department of Gastroenterology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China ) , Xu, Yuanyuan (Department of Gastroenterology, Drum Tower Hospital, Medical School of Nanjing University, Nanjing, Jiangsu 210008, China ) , Pang, Taohong (Department of Gastroenterol) , Hu, Qingqing , Chen, Min , Wang, Lei , Lv, Ying , Yin, Kai , Liang, Hongwei , Chen, Xi , Xu, Guifang , Zou, Xiaoping
    Cancer letters v.414 ,pp. 44 - 56 , 2018 , 0304-3835 ,

    초록

    Abstract miR-214 is an important oncomiRNA and is upregulated in various types of cancer, including gastric cancer. However, the molecular mechanism underlying the ectopic expression and function of miR-214 in gastric cancer is largely undefined. In this study, we found that miR-214 induces the Warburg effect and promotes the migration and proliferation of human gastric cancer cells. According to the mechanistic analysis, miR-214 expression is induced by environmental hypoxia, and miR-214 mediates hypoxia-induced functions. We then explored the molecular mechanism by which miR-214 enhances the Warburg effect in gastric cancer cells and identified the adenosine A2A receptor (A2AR) and PR/SET domain 16 (PRDM16) genes as the direct targets of miR-214. In conclusion, miR-214 inhibits A2AR and PRDM16 expression and enhances the Warburg effect in gastric cancer cells, thus promoting the proliferation and migration of gastric cancer cells. This study highlights an important role for the hypoxia-miR-214-PRDM16/A2AR pathway in the tumourigenesis of gastric cancer and may facilitate the development of new therapeutics against hypoxic tumours.

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  7. [해외논문]   Favorable biodistribution, specific targeting and conditional endosomal escape of RNA nanoparticles in cancer therapy   SCI SCIE

    Xu, Congcong (Division of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, The Ohio State University, Columbus, OH, USA ) , Haque, Farzin (Nanobio Delivery Pharmaceutical Co. Ltd., Columbus, OH, USA ) , Jasinski, Daniel L. (Division of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, The Ohio State University, Columbus, OH, USA ) , Binzel, Daniel W. (Division of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, The Ohio State University, Columbus, OH, USA ) , Shu, Dan (Division of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, The Ohio State University, Columbus, OH, USA ) , Guo, Peixuan (Division of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, The Ohio State University, Columbus, OH, USA)
    Cancer letters v.414 ,pp. 57 - 70 , 2018 , 0304-3835 ,

    초록

    Abstract The past decades have witnessed the successful transition of several nanotechnology platforms into the clinical trials. However, specific delivery of therapeutics to tumors is hindered by several barriers including cancer recognition and tissue penetration, particle heterogeneity and aggregation, and unfavorable pharmacokinetic profiles such as fast clearance and organ accumulation. With the advent of RNA nanotechnology, a series of RNA nanoparticles have been successfully constructed to overcome many of the aforementioned challenges for in vivo cancer targeting with favorable biodistribution profiles. Compared to other nanodelivery platforms, the physiochemical properties of RNA nanoparticles can be tuned with relative ease for investigating the in vivo behavior of nanoparticles upon systemic injection. The size, shape, and surface chemistry, especially hydrophobic modifications, exert significant impacts on the in vivo fate of RNA nanoparticles. Rationally designed RNA nanoparticles with defined stoichiometry and high homogeneity have been demonstrated to specifically target tumor cells while avoiding accumulation in healthy vital organs after systemic injection. RNA nanoparticles were proven to deliver therapeutics such as siRNA and anti-miRNA to block tumor growth in several animal models. Although the release of anti-miRNA from the RNA nanoparticles has achieved high efficiency of tumor regression in multiple animal models, the efficiency of endosomal escape for siRNA delivery needs further improvement. This review focuses on the advances and perspectives of this promising RNA nanotechnology platform for cancer targeting and therapy. Highlights The novelty of pRNA derived from phi29 DNA packaging motor in RNA nanotechnology is described. Specific targeting of tumors using RNA nanoparticles by different strategies is summarized. Effects of physicochemical properties of RNA nanoparticle on biodistribution are discussed.

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  8. [해외논문]   AGBL2 promotes cancer cell growth through IRGM-regulated autophagy and enhanced Aurora A activity in hepatocellular carcinoma   SCI SCIE

    Wang, Li-Li (State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China ) , Jin, Xiao-Han (State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China ) , Cai, Mu-Yan (State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China ) , Li, Hai-Gang (Department of Pathology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China ) , Chen, Jie-Wei (Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China ) , Wang, Feng-Wei (State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China ) , Wang, Chen-Yuan (State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen Uni) , Hu, Wei-Wei , Liu, Fang , Xie, Dan
    Cancer letters v.414 ,pp. 71 - 80 , 2018 , 0304-3835 ,

    초록

    Abstract AGBL2 has been reported to catalyze α-tubulin detyrosination, by which it promotes tumorigenesis and cancer progression. However, its potential role in the pathogenesis of hepatocellular carcinoma (HCC) has not been revealed yet. In the present study, AGBL2 was frequently found being overexpressed in HCC tissues and cell lines. In a large cohort of clinical HCC tissues, high expression of AGBL2 was positively associated with tumor size, tumor multiplicity and advanced clinical stage ( p in vitro and promoted tumor growth in vivo . In addition, we demonstrated that overexpression of AGBL2 in HCC cells notably inhibited apoptosis by enhancing IRGM-regulated autophagy. Meanwhile, AGBL2 could up-regulate the expression of TPX2 and Aurora A activity to promote cell proliferation in HCC cells. In summary, our findings suggest that up-regulation of AGBL2 plays a critical oncogenic role in the pathogenesis of HCC through modulation on autophagy and Aurora A activity, and it could be a candidate for prognostic marker and therapeutic target in HCC. Highlights AGBL2 is overexpressed in HCC cells and is an independent prognostic biomarker. AGBL2 promotes HCC cell survival and proliferation. AGBL2 enhances autophagy to protect HCC cell from apoptosis by up-regulating IRGM. AGBL2 up-regulates the expression of TPX2 to enhance Aurora A activation, leading to HCC cell proliferation.

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  9. [해외논문]   Emerging role of plexins signaling in glioma progression and therapy   SCI SCIE

    Angelopoulou, Efthalia (Corresponding author. Associate Professor, Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 M. Asias Street - Bldg 16, 11527 Athens, Greece.) , Piperi, Christina
    Cancer letters v.414 ,pp. 81 - 87 , 2018 , 0304-3835 ,

    초록

    Abstract Gliomas are highly invasive brain tumors with increased resistance to chemotherapy and high recurrence rate. Neoplastic cells commonly infiltrate into the surrounding tissue even at low grade tumors. Cell migration is often ceased at white and grey matter junctions indicating the involvement of tropic and axon guidance molecules in glioma growth and invasion. Emerging evidence implicates plexin-semaphorin signaling in the pathobiology of gliomas. Plexins are transmembrane receptors divided into four subfamilies (Plexins-A to -D) with differential specificity and functionality. They are involved in cell adhesion and motility, vascular growth and organogenesis, as well as tumor progression. In gliomas, plexins-A serve as coreceptors of neuropilins and transduce signals of class 3 semaphorins to PI3K/Akt pathway promoting cell growth, migration and invasion. Plexins-B1 and -B2 bind class 4 semaphorins to regulate RhoGTPases and induce glioma invasiveness and angiogenesis while, plexins-B3 interact with class 5 semaphorins to inhibit cell invasion and promote astrocytic cell differentiation via glial fibrillary acidic protein (GFAP) regulation. This review focuses on the biological roles of plexin-semaphorin signaling in glioma pathogenesis and discusses their potential as prognostic biomarkers and therapeutic targets. Highlights Plexin-Semaphorin signaling is involved in glioma pathogenesis. Plexin-A1-Sema3F interaction promotes glioma growth and invasion via PI3K pathway. Plexin-B1-Sema4D and Plexin-B2-Sema4C induce glioma invasiveness and angiogenesis. Plexins-B3-Sema5A inhibit cell invasion and promote astrocytic differentiation.

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  10. [해외논문]   NRPa-308, a new neuropilin-1 antagonist, exerts in vitro anti-angiogenic and anti-proliferative effects and in vivo anti-cancer effects in a mouse xenograft model   SCI SCIE

    Liu, Wang-Qing (INSERM U648, Laboratory of Molecular and Cellular Pharmacochemistry, Université) , Lepelletier, Yves (Paris Descartes, Sorbonne Paris Cité, UFR Biomédicale des Saints Pères, 45 rue des Saints Pères, 75270, Paris cedex 06, France ) , Montè (INSERM UMR 1163, Laboratory of cellular and Molecular basis of normal hematopoiesis and hematological disorders, 24 boulevard Montparnasse, 75015, Paris, France ) , s, Matthieu (Conservatoire National des Arts et Métiers, Chaire de Bioinformatique, Laboratoire Génomique, Bioinformatique et Applications, EA 4627, 292 rue Saint Martin, 75003 Paris, France ) , Borriello, Lucia (INSERM U648, Laboratory of Molecular and Cellular Pharmacochemistry, Université) , Jarray, Rafika (Paris Descartes, Sorbonne Paris Cité, UFR Biomédicale des Saints Pères, 45 rue des Saints Pères, 75270, Paris cedex 06, France ) , Gré (Sup'Biotech, 66 Rue Guy Môquet, 94800, Villejuif, France ) , pin, Renaud (Centre Scientifique de Monaco, Biomedical Department, 8 Quai Antoine Ier, MC-98000, Mona) , Leforban, Bertrand , Loukaci, Ali , Benhida, Rachid , Hermine, Olivier , Dufour, Sylvie , Pagè , s, Gilles , Garbay, Christiane , Raynaud, Franç , oise , Hadj-Slimane, Reda , Demange, Luc
    Cancer letters v.414 ,pp. 88 - 98 , 2018 , 0304-3835 ,

    초록

    Abstract Neuropilin-1 (NRP-1) is an extra-cellular receptor for the main Vascular Endothelial Growth Factor over-expressed in tumour tissues, VEGF-A 165 . Consequently, NRP-1 is involved in angiogenesis and in tumour growth, and its over-expression is related to a clinical poor prognosis. NRP-1 appears as a major target in oncology, which remains poorly exploited. Herein, we report a new series of 18 small-sized fully organic VEGF-A 165 /NRP-1 antagonists (NRPas). These compounds share an original scaffold, including two linkers (sulphonamide and amide) and three aromatic cores. Among them, 2a (renamed NRPa-308 ) emerges as a promising “hit”. In vitro, 2a exerts not only potent anti-angiogenic activity, but also significant effects on cell viability of large panel of human solid and haematological cancer cell lines. Importantly, 2a is less cytotoxic on healthy tissues than the marketed anti-angiogenic drug sunitinib. Lastly, in a mouse xenograft model (human MDA-MB-231 breast cancer cells), 2a improves the median survival and reduces the tumour growth, but does not exert visible acute toxicity. Altogether, these results highlight its huge potential for a further “hit-to-lead” optimization, leading to new anti-cancer drugs. Highlights A new series of 18 neuropilin antagonists is disclosed. NRPa-308 ( 2a ) exerts in vitro anti-angiogenic activity. NRPa-308 ( 2a ) exerts in vitro anti-proliferative effects against a panel of cancer cells. NRPa-308 ( 2a ) appears less toxic than sunitinib on healthy tissues. NRPa-308 ( 2a ) improves median survival and reduces in vivo tumour growth in a mice xenograft model.

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