共查询到19条相似文献,搜索用时 78 毫秒
1.
2.
3.
4.
5.
6.
7.
8.
干细胞、肿瘤干细胞与肿瘤的关系 总被引:8,自引:2,他引:8
干细胞理论认为肿瘤是一种干细胞疾病,该理论为肿瘤的研究及治疗提供了新的方向和靶点。干细胞(stem cell)是一类具有自我更新和增殖分化能力的细胞,肿瘤细胞是一类具有无限增殖和失去分化为成熟细胞能力的细胞,肿瘤干细胞(cancer stem cell)是存在于肿瘤组织中的一小部分具有干细胞性质的细胞群体,能够驱使肿瘤的形成。本文拟综述干细胞、肿瘤干细胞与肿瘤发生发展之间的关系,为肿瘤的研究及临床治疗提供参考。 相似文献
9.
肿瘤治疗新目标——肿瘤干细胞 总被引:3,自引:0,他引:3
肿瘤干细胞是肿瘤细胞的祖细胞,是肿瘤的真正种子,它们虽然仅占肿瘤细胞中极少的一部分,但具有自我更新能力和不定分化潜能,是形成不同分化程度肿瘤和肿瘤不断生长的根源,是肿瘤发生、扩散、复发等过程中的“起始细胞”或“动力细胞”。传统的化疗药物不能有效靶向作用肿瘤干细胞,开发针对肿瘤干细胞的靶向治疗,能给肿瘤治疗模式带来全新的改变,有望彻底改善患者的预后。 相似文献
10.
肿瘤研究的基本问题之一是哪些肿瘤细胞能够无限生长.传统理论认为肿瘤生长是所有肿瘤细胞一起增殖的结果.最近通过对造血系肿瘤的研究发现肿瘤细胞的生长繁殖和干细胞之间有许多惊人的相似之处,提出了肿瘤干细胞学说,认为肿瘤生长是肿瘤组织中极少量具有特殊细胞表面标志的肿瘤干细胞增殖的结果.研究证明人类急性髓性白血病(AML)中的肿瘤干细胞存在于CD34 /CD38亚群中,而人乳腺癌中的肿瘤干细胞属于ESA CD44 CD24-/low亚群.肿瘤干细胞概念的提出,提供了靶向性或选择性杀伤肿瘤干细胞从而根治肿瘤和防止肿瘤复发和转移的可能性.研究肿瘤干细胞特异性的生物学特点,对肿瘤的发生、发展和转归的理论以及肿瘤的诊断、预防和治疗均有重要意义. 相似文献
11.
肿瘤干细胞(cancer stem cell,CSC)能自我更新,分化形成异质性的肿瘤子代细胞群,是肿瘤复发与转移的主要原因。肿瘤转移干细胞(metastatic cancer stem cell,MCSC)具有CSC特性,同时伴有转移能力。肿瘤转移既发生于肿瘤晚期,也发生于早期。MCSC在起源、上皮-间质转变(epithelial-mesenchymal transition,EMT)、间质-上皮转变(mesenchymal-epithelial transition,MET)和靶器官小生境(niche)等方面与CSC不同,因而MCSC是肿瘤转移的基础。杀灭CSC、阻断EMT和MET、抑制MCSC微血管黏附和阻断MCSC依赖的小生境可构建抗肿瘤转移的治疗策略。本文主要介绍MCSC的可能来源,MCSC的生物学特性,MCSC近期研究中可能取得的突破,以及针对MCSC的抗转移策略,为肿瘤转移机制研究和抗转移研究提供参考。 相似文献
12.
Xiaoyan Ning Jianchang Shu Yiqi Du Qiwen Ben Zhaoshen Li 《Cancer biology & therapy》2013,14(4):295-303
Increasing studies have demonstrated a small proportion of cancer stem cells (CSCs) exist in the cancer cell population. CSCs have powerful self-renewal capacity and tumor-initiating ability and are resistant to chemotherapy and radiation. Conventional anticancer therapies kill the rapidly proliferating bulk cancer cells but spare the relatively quiescent CSCs, which cause cancer recurrence. So it is necessary to develop therapeutic strategies acting specifically on CSCs. In recent years, studies have shown that therapeutic agents such as metformin, salinomycin, DECA-14, rapamycin, oncostatin M (OSM), some natural compounds, oncolytic viruses, microRNAs, cell signaling pathway inhibitors, TNF-related apoptosis inducing ligand (TRAIL), interferon (IFN), telomerase inhibitors, all-trans retinoic acid (ATRA) and monoclonal antibodies can suppress the self-renewal of CSCs in vitro and in vivo. A combination of these agents and conventional chemotherapy drugs can significantly inhibit tumor growth, metastasis and recurrence. These strategies targeting CSCs may bring new hopes to cancer therapy. 相似文献
13.
肿瘤干细胞(cancer stem cell,CSC)是肿瘤发生和转移的种子细胞,CSC具有自我更新、增殖和不完全分化的能力。CSC对化疗/放疗的抵抗以及免疫逃逸成为肿瘤复发的根源,要提高肿瘤治愈率必须彻底清除CSC。认识CSC的标记特征和"干性"调节关键分子才能有效和特异地攻击CSC。免疫治疗具有抗原识别的靶向性和时空效应性,是以CSC为靶的治疗的基础;以单克隆抗体和致敏的免疫细胞为主要治疗技术的免疫治疗清除CSC具有可实践性和挑战性。 相似文献
14.
15.
目的: 观察慢病毒-胸苷激酶(lentivirus-thymidine kinase,Lenti-TK)/间充质干细胞(mesenchymal stem cell,MSC)对鼻咽癌CD133+干细胞的靶向迁移及杀伤作用。 方法: 构建包含TK基因的重组慢病毒表达载体Lenti-TK,感染MSC后得到Lenti-TK-MSC,RT-PCR及Western blotting检测Lenti-TK-MSC中HA-TK的表达。免疫磁珠法从鼻咽癌5-8F细胞中分选CD133+细胞;Transwell小室迁移实验检测Lenti-TK-MSC对CD133+5-8F细胞的趋向性;Lenti-TK-MSC联合更昔洛韦(ganciclovir,Lenti-TK-MSC/GCV)与CD133+5-8F细胞共培养,CCK-8试剂盒检测其对细胞的杀伤作用和旁观者效应。 结果: 成功构建重组慢病毒载体Lenti-TK,其滴度为1×108UT/ml,Lenti-TK(MOI=50)感染MSC 72 h时,感染效率达(95.1±01)%。Lenti-TK-MSC迁移至CD133+5-8F细胞组的细胞数明显多于CD133-5-8F细胞组、未分选5-8F细胞组\[(83.0±8.7) vs (29.6±53)、(38.3±5.2),P=0.000\]。Lenti-TK-MSC/GCV处理组与单独GCV处理组、Lenti-TK-MSC/GCV条件培养液(即Lenti-TK-MSC加入1 mg/L GCV培养48 h的培养上清)处理组相比,CD133+5-8F细胞的存活率明显降低\[(37.2±2.3)% vs (98.5±3.1)%、(83.8±34)%,P=0.000\]。Lenti-TK-MSC数量达到混合细胞总数(Lenti-TK-MSC和CD133+5-8F细胞)的20%时,CD133+5-8F细胞存活率为(68.2±2.3)%,表现出明显的旁观者杀伤效应。 结论: Lenti-TK感染后MSC对鼻咽癌CD133+5-8F细胞具有靶向迁移及杀伤作用。 相似文献
16.
Eiji Sugihara Hideyuki Saya 《International journal of cancer. Journal international du cancer》2013,132(6):1249-1259
Heterogeneity of tumor tissue has been accounted for in recent years by a hierarchy‐based model in which cancer stem cells (CSCs) have the ability both to self‐renew and to give rise to differentiated tumor cells and are responsible for the overall organization of a tumor. Research into CSCs has progressed rapidly and concomitantly with recent advances in the biology of normal tissue stem cells, resulting in the identification of CSCs in a wide range of human tumors. Studies of mouse models of human cancer have provided further insight into the characteristics of CSCs as well as a basis for the development of novel therapies targeted to these cells. However, recent studies have revealed complexities, such as plasticity of stem cell properties and clonal diversity of CSCs, in certain tumor types that have led to revision of the original CSC model. In this review, we summarize the history of the discovery and characterization of CSCs, as well as address recent advances that have revealed the complexity of these cells and their therapeutic implications. 相似文献
17.
目的:在原位移植瘤模型上验证CD44+胃癌细胞的肿瘤干细胞特性.方法:选取MKN-45胃癌细胞株,通过流式细胞仪分选为CD44+和CD44-两组,以未分选的MKN-45胃癌细胞为对照.体外部分,通过MTT法和克隆形成实验验证CD44+胃癌细胞体外增殖能力,通过Transwell实验验证其侵袭力.体内部分,将上述细胞通过原位移植法接种至裸鼠,同等条件下饲养8周后处死裸鼠,检验其成瘤率;分离肝脏,检测肝转移瘤数目;H-E染色观察胃肿瘤和肝转移瘤形态;通过免疫荧光法检测两处肿瘤CD44+细胞数量.结果:CD44+胃癌细胞相比CD44‘胃癌细胞具有明显增强的细胞增殖力(P<0.01)和侵袭力(P<0.01),更容易成瘤且更容易发生转移(P<0.05),但和MKN-45未分选组相比差异无统计学意义(P>0.05).不论是在原发肿瘤还是转移瘤中,CD44+胃癌细胞均能产生CD44‘细胞,但后者不能产生CD44+细胞.结论:CD44+ MKN-45胃癌细胞相比CD44-胃癌细胞具备更强的增殖力和侵袭力、更容易成瘤和发生转移,符合肿瘤干细胞部分特征,值得进一步研究. 相似文献
18.
Tumor cells actively contribute to constructing their own microenvironment during tumorigenesis and tumor progression. The tumor microenvironment contains multiple types of stromal cells that work together with the extracellular matrix and local and systemic factors to coordinately contribute to tumor initiation and progression. Tumor cells and their stromal compartments acquire many genetic and/or epigenetic alternations to facilitate tumor growth and metastasis. The cancer stem cell (CSC) concept has been widely applied to interpreting tumor initiation, growth, metastasis, dormancy and relapse. CSCs have differentiation abilities to generate the original lineage cells that are similar to their normal stem cell counterparts. Interestingly, recent evidence demonstrates that CSCs also have the potential to transdifferentiate into vascular endothelial cells and pericytes, indicating that CSCs can transdifferentiate into other lineage cells for promoting tumor growth and metastasis in some tissue contexts instead of only recruiting stromal cells from local or distant tissues. Although the transdifferentiation of CSCs into tumor stromal cells provides a new dimension that explains tumor heterogeneity, many aspects of CSC transdifferentiation remain elusive. In this review, we summarize the multi-lineage differentiation and transdifferentiation potentials of CSCs as well as discuss their potential contributions to tumor heterogeneity and tumor microenvironment in tumor progression. 相似文献
19.
目的: 探讨小白菊内酯(parthenolide,PTL)对小鼠乳腺癌肿瘤干细胞(cancer stem cell,CSC)的杀伤作用,为临床应用PTL治疗乳腺癌提供实验依据。 方法: 采用5-氟尿嘧啶(5-fluorouracil, 5-FU)化疗法制备富含CSC的小鼠4T1细胞乳腺癌模型,随机分为对照组、5-FU组、PTL组。4周后脱颈处死小鼠,检测各组小鼠肿瘤的体积和重量,流式细胞术检测小鼠肿瘤组织中CD44+CD24-/low细胞比例,Hoechst33342染色法检测侧群(side population,SP)细胞的比例,免疫组化法检测CD55和乙醛脱氢酶1(aldehyde dehydrogenase1,ALDH1)蛋白的表达,倒置显微镜观察乳腺癌细胞微球体的形成。 结果: 成功制备富含CSC的小鼠乳腺癌细胞移植瘤模型,PTL可下调小鼠肿瘤组织中CD44+CD24-/low细胞的比例\[(42.5±3.7)% vs (68.7±32)%,P<0.05\],有效降低荷瘤小鼠肿瘤组织中SP细胞的比例\[(39.2±1.8)% vs (61.3±2.6)%,P<0.05\],下调小鼠移植瘤组织中CD55和ALDH1蛋白的表达\[(18.9±1.5)% vs (30.1±1.3)%,(8.1±2.3)% vs (18.0±1.4)%;均P<0.05\],抑制小鼠肿瘤细胞在无血清培养条件下形成微球体,并可抑制小鼠移植瘤的体积和重量\[(0.625±0.159)cm3 vs (1.715±0184)cm3,(1.467±0.373)g vs (3.367±0.398)g;均P<0.05\]。 结论: PTL在荷瘤小鼠体内可以明显降低肿瘤组织CSC含量,提示PTL可用来靶向杀伤乳腺癌CSC。 相似文献