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失巢凋亡与上皮间充质转变和肿瘤干细胞
引用本文:蒋雪梅,陶彩云,万淑芳. 失巢凋亡与上皮间充质转变和肿瘤干细胞[J]. 中国临床康复, 2011, 0(40): 7585-7588
作者姓名:蒋雪梅  陶彩云  万淑芳
作者单位:[1]三峡大学医学院,湖北省宜昌市443002 [2]宜昌市兴山县人民医院,湖北省宜昌市443002
摘    要:背景:上皮起源的肿瘤干细胞可能经历上皮到间充质的转变导致间充质特征的癌干细胞的产生,癌干细胞与失巢凋亡抵抗和肿瘤转移性疾病的起始相关.目的:综述癌干细胞的生物学特点及其与上皮间充质的转变、失巢凋亡的关系.方法:由第一作者采用电子检索的方式在PubMed数据及万方数据库中检索1990-01/2010-12有关肿瘤干细胞的研究,关键词为"上皮间充质转变,癌干细胞".结果与结论:上皮细胞到间充质状态转变的诱导作用已经牵涉到肿瘤细胞的迁移和广泛转移的增强,并且可能促成凋亡和失巢凋亡抵抗.癌干细胞与间充质细胞有关联,并且在肿瘤的开始,生长、转移和治疗抵抗方面起一个关键的作用.有效针对靶向癌干细胞的策略对于监测癌症治疗的进展和评估新的治疗因子是很关键的,间充质状态转变在肿瘤发生和转移方面产生和维持癌干细胞,提供治疗干扰这种新途径起到了调控作用,并且治疗干扰具有超越传统抗癌疗法的潜力.

关 键 词:上皮间充质转变  癌干细胞  失巢凋亡  肿瘤干细胞

Association of anoikis with epithelial mesenchymal transition and cancer stem cells
Jiang Xue-mei,Tao Cai-yun,Wan Shu-fang. Association of anoikis with epithelial mesenchymal transition and cancer stem cells[J]. Chinese Journal of Clinical Rehabilitation, 2011, 0(40): 7585-7588
Authors:Jiang Xue-mei  Tao Cai-yun  Wan Shu-fang
Affiliation:1Medical School, China Three Gorges University, Yichang 443002, Hubei Province, China; 2People’s Hospital of Xingshan County, Yichang 443002, Hubei Province, China
Abstract:BACKGROUND: Epithelial originated epithelial cancer stem cells (eCSCs) may undergo epithelial to mesenchymal transition (EMT) leading to the production of CSCs with mesenchymal features (mCSCs) that have been associated with anoikis resistance and the onset of metastatic diseases. OBJECTIVE: To review the biological feature of CSCs and their relationship between CSCs and EMT, anoikis. METHODS: The first author retrieved PubMed database and Wanfang database (1990-01/2010-12) for publications of cancer stem cells research with the keywords of "epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs)". RESULTS AND CONCLUSION: The induction of transition from an epithelial to a mesenchymal state has been implicated in enhanced migration and metastatic spread of tumor cells and may contribute to apoptosis and anoikis resistance. CSCs normally have characteristics associated with mesenchymal cells and also play a critical role in tumor initiation, growth, metastasis, and therapeutic resistance. Strategies aiming at efficiently targeting CSCs are critical for monitoring the progress of cancer treatment and for evaluating new therapeutic agents. EMT may provide useful information to uncover the roles of these EMT regulators in generating and maintaining CSCs in tumorigenesis and metastasis and offer new avenues of therapeutic intervention with the potential to go beyond traditional anticancer approaches.
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