中国肺癌杂志
中國肺癌雜誌
중국폐암잡지
Chinese Journal of Lung Cancer
2015年
10期
633-639
,共7页
肺干细胞%肺肿瘤%表面标志%信号通路%靶向治疗
肺榦細胞%肺腫瘤%錶麵標誌%信號通路%靶嚮治療
폐간세포%폐종류%표면표지%신호통로%파향치료
Lung stem cells%Lung neoplasms%Surface markers%Signal pathway%Targeted therapy
癌干细胞是目前癌症研究的热点之一。肺癌干细胞与正常肺干细胞有许多共同之处，包括自我更新能力和多分化潜能。许多癌干细胞分子标志为肺癌干细胞所共有，如CD133、CD44、乙醛脱氢酶（aldehyde dehydrogenase, ALDH）以及ATP结合转运蛋白G超家族成员2（ATP-binding cassette sub-family G member 2, ABCG2）。肺癌干细胞的扩增与作用不仅受胚胎干细胞途径如Notch、Hedgehog和Wnt调控，也受肿瘤信号途径如表皮生长因子受体（epidermal growth factor receptor, EGFR）、信号传导转录激活因子3（signal transducer and activator of transcription 3, STAT3）和磷脂酰肌醇3激酶（phosphatidylinositol 3 kinase, PI3K）等的调控。由于癌干细胞在肿瘤复发、转移和耐药性等方面发挥着重要作用，揭示肺癌干细胞与正常干细胞的区别，鉴定并靶向癌干细胞特异性表面标志物及其介导的信号通路，将有望改善肺癌治疗效果和提高患者生存率。
癌榦細胞是目前癌癥研究的熱點之一。肺癌榦細胞與正常肺榦細胞有許多共同之處，包括自我更新能力和多分化潛能。許多癌榦細胞分子標誌為肺癌榦細胞所共有，如CD133、CD44、乙醛脫氫酶（aldehyde dehydrogenase, ALDH）以及ATP結閤轉運蛋白G超傢族成員2（ATP-binding cassette sub-family G member 2, ABCG2）。肺癌榦細胞的擴增與作用不僅受胚胎榦細胞途徑如Notch、Hedgehog和Wnt調控，也受腫瘤信號途徑如錶皮生長因子受體（epidermal growth factor receptor, EGFR）、信號傳導轉錄激活因子3（signal transducer and activator of transcription 3, STAT3）和燐脂酰肌醇3激酶（phosphatidylinositol 3 kinase, PI3K）等的調控。由于癌榦細胞在腫瘤複髮、轉移和耐藥性等方麵髮揮著重要作用，揭示肺癌榦細胞與正常榦細胞的區彆，鑒定併靶嚮癌榦細胞特異性錶麵標誌物及其介導的信號通路，將有望改善肺癌治療效果和提高患者生存率。
암간세포시목전암증연구적열점지일。폐암간세포여정상폐간세포유허다공동지처，포괄자아경신능력화다분화잠능。허다암간세포분자표지위폐암간세포소공유，여CD133、CD44、을철탈경매（aldehyde dehydrogenase, ALDH）이급ATP결합전운단백G초가족성원2（ATP-binding cassette sub-family G member 2, ABCG2）。폐암간세포적확증여작용불부수배태간세포도경여Notch、Hedgehog화Wnt조공，야수종류신호도경여표피생장인자수체（epidermal growth factor receptor, EGFR）、신호전도전록격활인자3（signal transducer and activator of transcription 3, STAT3）화린지선기순3격매（phosphatidylinositol 3 kinase, PI3K）등적조공。유우암간세포재종류복발、전이화내약성등방면발휘착중요작용，게시폐암간세포여정상간세포적구별，감정병파향암간세포특이성표면표지물급기개도적신호통로，장유망개선폐암치료효과화제고환자생존솔。
Cancer stem cells (CSCs) are emerging as a hot topic for cancer research. Lung CSCs share many char-acteristics with normal lung stem cells (SCs), including self-renewal and multi-potency for differentiation. Many molecular markers expressed in various types of CSCs were also found in lung CSCs, such as CD133, CD44, aldehyde dehydrogenase (ALDH) and ATP-binding cassette sub-family G member 2 (ABCG2). Similarly, proliferation and expansion of lung CSCs are regulated not only by signal transduction pathways functioning in normal lung SCs, such as Notch, Hedgehog and Wnt path-ways, but also by those acting in tumor cells, such as epidermal growth factor receptor (EGFR), signal transducer and activator of transcription 3 (STAT3) and phosphatidylinositol 3 kinase (PI3K) pathways. As CSC plays an critical role in tumor recur-rence, metastasis and drug-resistance, understanding the difference between lung CSCs and normal lung SCs, identifying and targeting CSC markers or related signaling pathways may increase the effcacy of therapy on lung cancer and improved survival of lung cancer patients.
