title: Stathmin destabilizing microtubule dynamics promotes malignant potential in cancer cells by epithelial-mesenchymal transition.
abstract: 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 microtubule-destabilizing 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).
  
  
  METHODS
  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 stathmin-microtubule dynamics-EMT (S-M-E) axis during cancer development. By this axis, stathmin together with its microtubule-destabilizing activity contributes to EMT, which stimulates the malignant potential in cancer cells.
authors.affiliation: Pancreatic Cancer Institute, Fudan University; Department of Pancreatic and Hepatobiliary Surgery, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China. yuxianjun88@hotmail.com.
authors.forename: Yu
authors.initials: Y
authors.lastname: Lu
authors.forename: Chen
authors.initials: C
authors.lastname: Liu
authors.forename: Yong-Feng
authors.initials: YF
authors.lastname: Xu
authors.forename: He
authors.initials: H
authors.lastname: Cheng
authors.forename: Si
authors.initials: S
authors.lastname: Shi
authors.forename: Chun-Tao
authors.initials: CT
authors.lastname: Wu
authors.forename: Xian-Jun
authors.initials: XJ
authors.lastname: Yu
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002453:Cell Cycle; D002454:Cell Differentiation; D002465:Cell Movement; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000378:metabolism* / Q000473:pathology; D019008:Drug Resistance, Neoplasm; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects; D006801:Humans; D008870:Microtubules / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction; D050777:Stathmin / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D050777:Stathmin