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CD24^+CD44^+胰腺癌细胞的获取及其干细胞特性的初步鉴定
  • ISSN号:1007-3639
  • 期刊名称:《中国癌症杂志》
  • 时间:0
  • 分类:Q51[生物学—生物化学] Q64[生物学—生物物理学]
  • 作者机构:[1]Pancreatic Cancer Institute, Fudan University, [2]Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China
  • 相关基金:supported by grants from the National Natural Science Foundation of China(81172276,81001058,8110156,Sino-German GZ857); the Shanghai Committee of Science and Technology,China(11JC1402500)
中文摘要:

BACKGROUND: Stathmin is a ubiquitous cytosolic regulatory phosphoprotein and is overexpressed in different human malignancies. The main physiological function of stathmin is to interfere with microtubule dynamics by promoting depolymerization of microtubules or by preventing polymerization of tubulin heterodimers. Stathmin plays important roles in regulating many cellular functions as a result of its microtubuledestabilizing activity. Currently, the critical roles of stathmin in cancer cells, as well as in lymphocytes have been valued. This review discusses stathmin and microtubule dynamics in cancer development, and hypothesizes their possible relationship with epithelial-mesenchymal transition(EMT).DATA SOURCES: A PubMed search using such terms as 'stathmin', 'microtubule dynamics', 'epithelial-mesenchymal transition', 'EMT', 'malignant potential' and 'cancer' was performed to identify relevant studies published in English.More than 100 related articles were reviewed.RESULTS: The literature clearly documented the relationship between stathmin and its microtubule-destabilizing activity of cancer development. However, the particular mechanism is poorly understood. Microtubule disruption is essential for EMT, which is a crucial process during cancer development. As a microtubule-destabilizing protein, stathmin may promote malignant potential in cancer cells by initiating EMT.CONCLUSIONS: We propose that there is a stathminmicrotubule dynamics-EMT(S-M-E) axis during cancer development. By this axis, stathmin together with itsmicrotubule-destabilizing activity contributes to EMT, which stimulates the malignant potential in cancer cells.

英文摘要:

BACKGROUND: Stathmin is a ubiquitous cytosolic regulatory phosphoprotein and is overexpressed in different human malignancies. The main physiological function of stathmin is to interfere with microtubule dynamics by promoting depolymerization of microtubules or by preventing polymerization of tubulin heterodimers. Stathmin plays important roles in regulating many cellular functions as a result of its microtubuledestabilizing activity. Currently, the critical roles of stathmin in cancer cells, as well as in lymphocytes have been valued. This review discusses stathmin and microtubule dynamics in cancer development, and hypothesizes their possible relationship with epithelial-mesenchymal transition(EMT).DATA SOURCES: A PubMed search using such terms as "stathmin", "microtubule dynamics", "epithelial-mesenchymal transition", "EMT", "malignant potential" and "cancer" was performed to identify relevant studies published in English.More than 100 related articles were reviewed.RESULTS: The literature clearly documented the relationship between stathmin and its microtubule-destabilizing activity of cancer development. However, the particular mechanism is poorly understood. Microtubule disruption is essential for EMT, which is a crucial process during cancer development. As a microtubule-destabilizing protein, stathmin may promote malignant potential in cancer cells by initiating EMT.CONCLUSIONS: We propose that there is a stathminmicrotubule dynamics-EMT(S-M-E) axis during cancer development. By this axis, stathmin together with itsmicrotubule-destabilizing activity contributes to EMT, which stimulates the malignant potential in cancer cells.

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期刊信息
  • 《中国癌症杂志》
  • 中国科技核心期刊
  • 主管单位:中华人民共和国教育部
  • 主办单位:复旦大学附属肿瘤医院
  • 主编:沈镇宙
  • 地址:上海市徐汇区东安路270号6号楼3楼
  • 邮编:200032
  • 邮箱:zgazzz@163.com
  • 电话:021-64188274 64175590-3574
  • 国际标准刊号:ISSN:1007-3639
  • 国内统一刊号:ISSN:31-1727/R
  • 邮发代号:4-575
  • 获奖情况:
  • 国内外数据库收录:
  • 被引量:19590