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血管生成拟态(vasculogenicmimicry,VM)是实体肿瘤中由肿瘤细胞而非内皮细胞构成的一种微循环结构.体现了恶性肿瘤细胞和/或肿瘤干细胞样细胞的可塑性与多潜能分化性。VM与肿瘤的病理级别及患者的预后有关。随着人们对VM的关注,发现了许多关于VM形成发展的信号通路,本文对VM的起源及VM的分子机制做一综述。 相似文献
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目的:总结肿瘤血管生成拟态(VM)的研究进展,并探讨肿瘤血管生成拟态形成机制。方法:应用PubMed和CNKI期刊全文数据库检索系统,以血管生成拟态为关键词,检索1999-01-01-2011-06-30相关文献,以三维培养模型中VM形态学、分子调节机制及抗肿瘤治疗研究为入选标准,分析文献45篇。结果:VM的生成机制比较复杂,其中VE-cad-herin/EphA2/PI3K/MMP是VM形成的关键通路,同时缺氧的微环境、cAMP和COX-2等对VM结构的形成也起一定的作用。结论:VM与肿瘤的侵袭转移潜能以及较差的临床预后有关,为抗肿瘤治疗提供了新的研究靶点。 相似文献
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血管生成拟态(VM)是近几年来在许多肿瘤中发现的一种全新的肿瘤内血管生成模式,即高度侵袭性肿瘤细胞通过自身变形和基质重塑产生血管样通道而达到自身血液供应的方式,现就其形态特点、分子机制、研究意义等作一综述。 相似文献
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肿瘤微血管包括由血管内皮细胞围成的经典血管结构和由肿瘤细胞围成的血管生成拟态(Vasculogenic mimicry,VM)两种模式。近年研究提示,抗血管生成药能够显著抑制经典的微血管结构,但是不能抑制VM形成,反而促进VM形成。这是影响其临床疗效的原因之一。然而近期研究发现,中成药、基因治疗以及其它靶向VM形成机制的药在抗VM形成中具有独特的优势。本文就目前靶向VM形成治疗肿瘤的研究现状展开综述,为开发既能抗血管生成又能抗VM形成的新一代抗血管生成药提供借鉴。 相似文献
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血管生成拟态(VM)是近年来发现的一种与经典的肿瘤血管生成途径完全不同、不依赖机体内皮细胞的全新肿瘤微循环模式.它描述了在高度侵袭性肿瘤组织中通过肿瘤细胞的自身变形和基质重塑形成类似血管样的通道,通过这种结构有利于肿瘤组织获取营养、侵袭和转移.血管生成拟态的提出为肿瘤研究和治疗提供了新思路. 相似文献
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血管生成拟态是独立于血管生成的一种全新肿瘤血管模式。越来越多的研究发现血管生成拟态的形成机制和肿瘤细胞自身的可塑性及肿瘤干细胞关系密切,另外,肿瘤微环境如细胞外基质重塑、缺氧等在血管生成拟态形成过程中也有很重要的作用。近年来,血管生成拟态形成机制的相关研究已经取得了很大进展,为寻找抑制VM的关键作用靶点、筛选有效的治疗药物提供了新的思路和方向。本文就血管拟态的发现、形成机制及其在肿瘤治疗中的研究现状等方面做一综述。 相似文献
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近几年来,人们先后在黑素瘤、胶质瘤等肿瘤中发现了血管生成拟态。血管生成拟态是肿瘤细胞自身形成的,是肿瘤的微循环特殊形式。血管生成拟态的调节与基质金属蛋白酶、血管上皮钙黏素等的表达相关。血管生成拟态预测低分化、高浸润和低生存率,是预后不良的标志。所以经典抗血管治疗联合抗血管生成拟态治疗在抗肿瘤治疗中成为必要。 相似文献
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Liu XM Zhang QP Mu YG Zhang XH Sai K Pang JC Ng HK Chen ZP 《Journal of neuro-oncology》2011,105(2):173-179
Vasculogenic mimicry (VM) is known as non-endothelial tumor cell-lined microvascular channels in aggressive tumors. We have
previously found the presence of VM in high-grade gliomas. In this study, we aimed to identify VM patterns in gliomas and
to explore their clinical significance. Tumor samples as well as their detailed clinical/prognostic data were collected from
101 patients. Vasculogenic mimicry in the glioma samples was determined by dual staining for endothelial marker CD34 and periodic
acid–Schiff (PAS). Tumor samples were also immunohistochemically stained for Ki-67, VEGF, COX-2 and MMP-9. The association
between VM and the clinical characteristics of the patients were analyzed. A Kaplan–Meier survival analysis and log-rank tests
were performed to compare survival times of the patients. Vasculogenic mimicry was present in 13 out of 101 samples. The higher
grade gliomas had a higher incidence of VM than that of lower grade gliomas (P = 0.006). Vasculogenic mimicry channels were associated with the expression of COX-2 and MMP-9 (P < 0.05). While there was no association between the existence of VM and the sex, age and preoperative epilepsy of the patients,
or expression of Ki-67 and VEGF. However, patients with VM-positive gliomas survived a shorter period of time than those with
VM negative gliomas (P = 0.027). Interestingly, in high-grade gliomas, the level of microvascular density was lower in VM positive tumors than those
VM negative tumors (P = 0.039). Our results suggest that VM channels in gliomas correlate with increasing malignancy and higher aggressiveness,
and may provide a complementation to the tumor’s blood supply, especially in less vascularized regions, which may aid in the
identification of glioma patients with a poorer prognosis. 相似文献
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Xiulan Zhao Baocun Sun Yanlei Li Yanrong Liu Danfang Zhang Xudong Wang Qiang Gu Jianmin Zhao Xueyi Dong Zhiyong Liu Na Che 《Oncotarget》2015,6(11):8890-8899
Vasculogenic mimicry (VM) is a functional microcirculation formed by tumor cells. Matrix metalloproteinases (MMPs), especially MMP-2 and MMP-9, promote VM formation. Another specific MMP, collagenase-3 (MMP-13), has broad substrate specificity and potentially affects tumor metastasis and invasion. Here we found that MMP-13 was associated with metastasis and poor survival in 79 patients with melanoma. MMP-13 expression was inversely correlated with VM. These results were confirmed in human and mouse melanoma cell lines. We found that MMP-13 cleaves laminin-5 (Ln-5) into small fragments to accelerate tumor metastasis. Degradation of Ln-5 and VE-cadherin by MMP-13 inhibited VM formation. In conclusion, MMP-13 has a dual effect in melanoma, as it promotes invasion and metastasis but disrupts VM formation. 相似文献
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Long noncoding RNA n339260 promotes vasculogenic mimicry and cancer stem cell development in hepatocellular carcinoma 下载免费PDF全文
Xiulan Zhao Baocun Sun Tieju Liu Bing Shao Ran Sun Dongwang Zhu Yanhui Zhang Qiang Gu Xueyi Dong Fang Liu Nan Zhao Danfang Zhang Yanlei Li Jie Meng Wenchen Gong Yanjun Zheng Xu Zheng 《Cancer science》2018,109(10):3197-3208
Vasculogenic mimicry (VM) refers to the unique capability of aggressive tumor cells to mimic the pattern of embryonic vasculogenic networks. Cancer stem cells (CSC) represent a subpopulation of tumor cells endowed with the capacity for self‐renewal and multilineage differentiation. Previous studies have indicated that CSC may participate in the formation of VM. With the advance of high‐resolution microarrays and massively parallel sequencing technology, long noncoding RNAs (lncRNAs) are suggested to play a critical role in tumorigenesis and, in particular, the development of human hepatocellular carcinoma (HCC). Currently, no definitive relationship between lncRNA and VM formation has been described. In the current study, we demonstrated that expression of the lncRNA, n339260, is associated with CSC phenotype in HCC, and n339260 level correlated with VM, metastasis, and shorter survival time in an animal model. Overexpression of n339260 in HepG2 cells was associated with a significant increase in CSC. Additionally, the appearance of VM and vascular endothelial (VE)‐cadherin, a molecular marker of VM, was also induced by n339260 overexpression. Using a short hairpin RNA approach, n339260 was silenced in tumor cells, and knockdown of n339260 was associated with reduced VM and CSC. The results of this study indicate that n339260 promotes VM, possibly by the development of CSC. The related molecular pathways may be used as novel therapeutic targets for the inhibition of HCC angiogenesis and metastasis. 相似文献