干细胞肿瘤干细胞与肝细胞癌发生关系研究进展

越来越多的实验结果证实肿瘤起源于干细胞,诸如白血病、乳腺癌、脑肿瘤等已成功分离出肿瘤干细胞,有关肝干细胞与肝癌的研究较为成熟,理论上应存在肝癌干细胞,但因缺乏特异性标志物,相关的肝癌干细胞分离尚未成功.     

肝癌干细胞与肝癌的研究进展

肿瘤起源于干细胞的假说已在人类许多实体瘤中得到证实,近来亦发现肝癌中存在肝癌干细胞.肿瘤干细胞被认为是肿瘤产生的根源,对肿瘤的发生、发展、转移、复发及耐药具有关键作用.因此,如何分离鉴定肝癌干细胞对于改善预防方法、促进早期检测以及研发新的治疗方法都是一个非常紧迫的课题.本文就肝癌干细胞的来源、表面标志、分选方法、应用前景及存在的问题作一综述.     

肝癌干细胞研究进展

肿瘤干细胞学说认为肿瘤是一种干细胞疾病,小部分细胞即肿瘤干细胞在肿瘤中发扮演干细胞的角色,在维持肿瘤发生、发展和耐药过程中发挥着主要作用。肝癌是最常见的肿瘤之一,近几年来有文献报道肝癌中也存在肝癌干细胞,本文就其来源、分离鉴定、细胞信号转导通路等方面做一归纳。      

肿瘤干细胞学说与肝癌的相关研究进展

肝癌是世界范围内常见的恶性肿瘤之一,在我国每年大约有25万人死于肝癌,位居恶性肿瘤死亡率的第二位,是严重威胁人们健康乃至生命的恶性疾病。目前对肝癌的治疗主要有手术、放疗、化疗及生物治疗等,总体治疗效果不佳。近年肿瘤干细胞（tumor stem cells,TSC）学说备受人们关注,认为肿瘤起源于干细胞,肿瘤的生长是肿瘤中极少量肿瘤干细胞增殖的结果,     

肝癌干细胞的来源及其研究进展

肿瘤干细胞(CSC)假说认为肿瘤组织是由一小部分具有干细胞特性的细胞分化而来,其在肿瘤发生、发展、转移中起重要作用.现已证实在很多实体肿瘤中存存肿瘤干细胞.肝癌作为最常见的恶性肿瘤之一,越来越多的证据提示有肿瘤干细胞的存在.     

人肝癌干细胞的富集

目的:从人肝癌细胞株中富集癌干细胞(cancer stem cells,CSCs).方法:将肝癌细胞SMMC-7721接种到裸鼠皮下建立动物模型后,荷瘤鼠随机分成4组,每组5只,每周1次腹腔分别注射环磷酰胺(cyclophosphamide, CTX)0、2、5和10 mg/kg,在肿瘤直径达1.5 cm时获取肿瘤,得到经不同剂量CTX富集的肝癌细胞.比较这些肝癌细胞的侧群(side population, SP)细胞含量、软琼脂克隆形成率、细胞增殖能力及致瘤能力.结果:SP细胞含量、软琼脂克隆形成率、细胞增殖能力及致瘤能力经比较均显示,经CTX(10 mg/kg)富集的肝癌细胞表现最强,且均随着CTX的剂量增加而增长(P<0.05).结论:利用低剂量化疗药能够富集肝癌干细胞,且富集效率与化疗剂量呈正比.     

肝癌干细胞研究现状

原发性肝癌是一种常见而恶性度极大的肿瘤,肝癌起源一直存在争议。肝干细胞是肝脏组织中的一类具有自我更新和向前分化为成熟肝细胞、胆管细胞等的不成熟细胞,这类细胞是生理性肝细胞更新和病理性肝损伤修复的起源细胞。传统认为肝癌起源于肝细胞突变和异常增生,目前观点多倾向于肝癌起源于肝干细胞的异常分化和增生。肝干细胞比成熟肝细胞更有可能成为肝癌癌变的靶细胞。现对当前肿瘤干细胞与肝癌干细胞相关方面的最新研究进展作一概述。     

肝癌干细胞的研究进展

肝癌是一种常见的恶性肿瘤,主要分布于亚洲东南部和撒哈拉沙漠以南的非洲地区,近25年,美国和欧洲地区发病率也在持续增加。肝癌的死亡率仅次于肺癌和结肠癌排名世界第三。预计未来20年,其发病率和死亡率还会成倍上升[1-2]。然而目前肝癌的发病     

肝癌干细胞的研究进展

肝癌是一种常见的恶性肿瘤,主要分布于亚洲东南部和撒哈拉沙漠以南的非洲地区,近25年,美国和欧洲地区发病率也在持续增加。肝癌的死亡率仅次于肺癌和结肠癌排名世界第三。预计未来20年,其发病率和死亡率还会成倍上升。然而目前肝癌的发病机制仍不明确,寻找其有效靶点,探明发病机制迫在眉睫。随着研究的深入,     

肝癌干细胞的研究进展

我国是原发性肝癌高发的国家,其发病率、死亡率约占全球的一半以上。尽管目前肝癌的诊断和治疗有了许多新的进展,但是总体疗效仍不满意。近年来的研究表明,肝癌中存在着一群具有干细胞特征、能自我更新、自我无限增殖并具有多向分化潜能的细胞,即肝癌干细胞,这对重新认识肝癌的发生、发展、预后转归以及指导临床治疗将起到极为重要的作用。本文通过复习肝癌干细胞相关文献,就肝癌干细胞起源、分选及相关治疗的研究进展作一综述。     

肝癌干细胞研究进展

近几年,肿瘤起源于干细胞的假说正在人类各种肿瘤中得到证实,包括肝癌。目前认为肿瘤干细胞对肿瘤发生、转移和预后起了关键作用,因此如何分离和鉴定肝癌干细胞对于改善预防方法、促进早期检测以及研发新的治疗方法都是一个非常紧迫的课题。本文就有关肝癌干细胞存在的依据、来源、表面标志物分选等研究进展作一综述。     

肝癌干细胞研究进展

近几年,肿瘤起源于干细胞的假说正在人类各种肿瘤中得到证实,包括肝癌。目前认为肿瘤干细胞对肿瘤发生、转移和预后起了关键作用,因此如何分离和鉴定肝癌干细胞对于改善预防方法、促进早期检测以及研发新的治疗方法都是一个非常紧迫的课题。本文就有关肝癌干细胞存在的依据、来源、表面标志物分选等研究进展作一综述。     

BEX2 is required for maintaining dormant cancer stem cell in hepatocellular carcinoma

Cancer stem cells (CSCs) are responsible for therapy resistance and share several properties with normal stem cells. Here, we show that brain-expressed X-linked gene 2 (BEX2), which is essential for dormant CSCs in cholangiocarcinoma, is highly expressed in human hepatocellular carcinoma (HCC) lesions compared with the adjacent normal lesions and that in 41 HCC cases the BEX2^high expression group is correlated with a poor prognosis. BEX2 localizes to Ki67-negative (nonproliferative) cancer cells in HCC tissues and is highly expressed in the dormant fraction of HCC cell lines. Knockdown of BEX2 attenuates CSC phenotypes, including sphere formation ability and aldefluor activity, and BEX2 overexpression enhances these phenotypes. Moreover, BEX2 knockdown increases cisplatin sensitivity, and BEX2 expression is induced by cisplatin treatment. Taken together, these data suggest that BEX2 induces dormant CSC properties and affects the prognosis of patients with HCC.     

肝细胞性肝癌组织CD133+细胞肿瘤干细胞特性的研究

目的 越来越多的研究表明,肝癌细胞系中能检测到肿瘤干细胞(cancer stem cells,CSCs)的存在.本研究旨在探讨从肝细胞性肝癌(hepatocellular carcinoma,HCC)组织样本中分离获得的CD133+细胞是否具有CSCs特性.方法 将2014-02-01-2015-06-30广西医科大学附属肿瘤医院肝胆外科25例手术获得的新鲜HCC组织和对应癌旁组织,采用酶消化法分别消化成单个肝癌细胞和单个肝细胞,利用流式细胞术检测部分单个肝癌细胞和单个肝细胞CD133的表达率.用剩余的单个肝癌细胞进行原代培养,流式细胞术将培养获得的肝癌细胞分选为CD133+和CD133-细胞,通过平板克隆形成实验、肿瘤球形成实验和裸鼠移植瘤形成实验对比分析这两组细胞的CSCs特性.结果 25例HCC组织中CD133的表达率为3.8％～8.3％,平均值为(5.8±1.6)％,而癌旁组织CD133的表达率为0.1％～0.4％,平均值为(0.2±0.1)％,两者比较差异有统计学意义,t=17.12,P＜0.001.CD133+和CD133-细胞的平均克隆率分别为(25.2±0.8)％和(7.6±0.8)％,两者比较差异有统计学意义,t=81.95,P＜0.001.CD133+和CD133-细胞的平均成球率分别为(20.3±0.6)％和(12.5±1.4)％,两者比较差异有统计学意义,t=68.17,P＜0.001.CD133+细胞的裸鼠移植瘤形成能力明显高于CD133-细胞.结论 从HCC组织样本中分离获得的CD133+细胞具有明显的CSCs特性.     

Lung cancer stem cells: Progress and prospects

Epithelial stem cells are critical for tissue generation during development and for repair following injury. In both gestational and postnatal stages, the highly branched and compartmentalized organization of the lung is maintained by multiple, resident stem/progenitor cell populations that are responsible for the homeostatic maintenance and injury repair of pulmonary epithelium. Though lung epithelial injury in the absence of oncogenic mutation is more commonly expressed as chronic lung disease, lung cancer is the most common form of death worldwide and poses a highly significant risk to human health. Cancer is defined by the cell of origin, responsible for initiating the disease. The Cancer Stem Cell Hypothesis proposes that cancer stem cells, identified by stem-like properties of self-renewal and generation of differentiated progeny, are responsible for propagating growth and spread of the disease. In lung cancer, it is hypothesized that cancer stem cells derive from several possible cell sources. The stem cell-like resistance to injury and proliferative potentials of bronchioalveolar stem cells (BASCs) and alveolar epithelial type II cells (AEC2), as well as cells that express the cancer stem cell marker glycoprotein prominin-1 (CD133) or markers for side populations make them potential reservoirs of lung cancer stem cells. The abnormal activation of pathways that normally regulate embryonic lung development, as well as adult tissue maintenance and injury repair, including the Wnt, Hedgehog (Hh) and Notch pathways, has also been identified in lung tumor cells. It is postulated that therapies for lung cancer that specifically target stem cell signaling pathways utilized by lung cancer stem cells could be beneficial in combating this disease.     

Long noncoding RNA n339260 promotes vasculogenic mimicry and cancer stem cell development in hepatocellular carcinoma

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.     

肝细胞癌起源的研究

肝细胞癌是临床常见的难治的恶性肿瘤之一,发病率逐年升高。大量证据表明肝脏干细胞在肝癌的发生发展中起重要作用。有两个关于肝癌干细胞关键问题值得回答：肝细胞癌是否来源于肝干细胞？肝细胞癌是否有肿瘤干细胞的特点？然而到目前为止,肝癌的干细胞仍未被分离,且可靠的表面标志仍未被确认。     

微小RNA在肝细胞癌及肝癌干细胞中的作用

微小RNA (miRNA)是一类约22个核苷酸分子构成的非编码单链小RNA.miRNA能参与一系列重要的生物学活动,如早期胚胎与器官发育、细胞增殖与分化、细胞凋亡等.miRNA在肝细胞癌中表达异常,与肝癌发生发展和浸润转移密切相关.肝癌干细胞可能是肝癌复发和转移的根源,某些miRNA与肝癌干细胞的自我更新、多向分化及成...