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| 1 | Growth inhibition of hepatocellular carcinoma tumor endothelial cells by miR-204-3p and underlying mechanism显示文摘AIM:To investigate the mechanism by which miR-204-3p inhibits the growth of hepatocellular carcinoma(hCC)tumor endothelial cells(TECs).METHODS:Flow cytometry was used to identify hCCTECs and analyze their purity.Differentially expressed miRNAs in hCC TECs as compared to normal hepatic sinusoidal endothelial cells(hSECs)were examined using the hmiOA v4 human miRNA OneArray?microarray.miR-204-3p showed the most significant decrease in expression and was further studied.Over-expression of miR-204-3p was achieved using lentiviral transduction into TECs of hCC.The biological changes in hCC TECs before and after transduction were detected using MTT and apoptosis assays.The association between miR-204-3p and fibronectin 1(FN1)was determined using the dual luciferase activity assay.Changes in FN1protein expression before and after transduction were detected using Western blot analysis.RESULTS:Microarray results showed that compared to normal hSECs,15 miRNAs were differentially expressed in hCC TECs,including 6 miRNAs with increased expression and 9 miRNAs with decreased expression.Among them,miR-204-3p showed the most significant decrease in expression(log2=-1.233477,P=0.000307).Over-expression of miR-204-3p in hCC TECs via lentiviral transduction significantly inhibited the proliferation of hCC TECs and promoted apoptosis.Results from the dual luciferase activity experiment showed that the luciferase intensity in the wild type FN1 group was significantly inhibited(P<0.05),while that in the mutant FN1 group was not obviously affected.This observation indicated that FN1 was one of the potential targets of miR-204-3p.After over-expression of miR-204-3p in hCC TECs,Western blot analysis showed that the expression of FN1 protein was significantly inhibited.CONCLUSION:MiR-204-3p acts on its potential target gene,FN1,and inhibits its expression,thus blocking the adhesion function of FN1 in promoting the growth of TECs. | Zhong-hui Cui Shi-qiang Shen Zu-bing Chen Chao hu | 2014 | World Journal of Gastroenterology2014，20，18： | 9 |
| 2 | Fibroblasts, an inconspicuous but essential player in colon cancer development and progression显示文摘Tumor microenvironments have a crucial role in cancer initiation and progression, and share many molecular and pathological features with wound healing process. Unless treated, tumors, however, do not heal in contrast to wounds that heal within a limited time framework. Wounds heal in coordination of a myriad of types of cells, particularly endothelial cells, leukocytes, and fibroblasts. Similar sets of cells also contribute to cancer initiation and progression, and as a consequence, anti-cancer treatment strategies have been proposed and tested by targeting endothelial cells and/or leukocytes. Compared with endothelial cells and leukocytes, less attention has been paid to the roles of cancer-associated fibroblasts(CAFs), fibroblasts present in tumor tissues, because their heterogeneity hinders the elucidation on them at cellular and molecular levels. Here, we will discuss the origin of CAFs and their crucial roles in cancer initiation and progression, and the possibility to develop a novel type of anti-cancer treatment by manipulating the migration and functions of CAFs. | Naofumi Mukaida Soichiro Sasaki | 2016 | World Journal of Gastroenterology2016，22，23： | 4 |
| 3 | Neuropilin-1在肿瘤发生发展中的作用显示文摘神经菌毛素(neuropilin-1,Nrp-1)是一种多功能的非酪氨酸激酶受体,在内皮细胞及多种肿瘤细胞表面高表达。Nrp-1主要作为血管内皮细胞生长因子165(vascular endothelial growth factor 165,VEGF165)的共受体,可显著提高VEGF165受体(vascular endothelial growth factor receptor 2,KDR)与VEGF165结合,促进肿瘤血管新生及肿瘤迁移。近期的研究表明,Nrp-1还能通过与脑信号蛋白Ⅲ(semaphorin Ⅲ,SEMA3)相互作用、与转化生长因子β(transforming growth factor-β,TGF-β)相互作用从而促进纤连蛋白聚集,改善肿瘤微环境,并介导调节性T细胞到肿瘤组织等多种途径,促进肿瘤的发生发展。由于Nrp-1在于肿瘤发生发展中所起到的病理性促进作用,Nrp-1逐渐成为肿瘤治疗的一个新靶标,本文主要介绍Nrp-1的生物学特征以及其对于肿瘤发生发展中的信号转导作用。 | 戴长松 王美玲 戴华 | 2015 | 中国肿瘤生物治疗杂志2015，22，4： | 4 |
| 4 | Changes in cellular mechanical properties during onset or progression of colorectal cancer显示文摘Colorectal cancer(CRC) development represents a multistep process starting with specific mutations that affect proto-oncogenes and tumour suppressor genes.These mutations confer a selective growth advantage to colonic epithelial cells that form first dysplastic crypts, and then malignant tumours and metastases. All these steps are accompanied by deep mechanical changes at the cellular and the tissue level. A growing consensus is emerging that such modifications are not merely a byproduct of the malignant progression, but they could play a relevant role in the cancer onset and accelerate its progression. In this review, we focus on recent studies investigating the role of the biomechanical signals in the initiation and the development of CRC. We show that mechanical cues might contribute to early phases of the tumour initiation by controlling the Wnt pathway, one of most important regulators of cell proliferation in various systems. We highlight how physical stimuli may be involved in the differentiation of non-invasive cells into metastatic variants and how metastatic cells modify their mechanical properties, both stiffness and adhesion, to survive the mechanical stress associated with intravasation, circulation and extravasation. A deep comprehension of these mechanical modifications may help scientist to define novel molecular targets for the cure of CRC. | Gabriele Ciasca Massimiliano Papi Eleonora Minelli Valentina Palmieri Marco De Spirito | 2016 | World Journal of Gastroenterology2016，22，32： | 3 |
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