title: Dexamethasone disrupts cytoskeleton organization and migration of T47D Human breast cancer cells by modulating the AKT/mTOR/RhoA pathway.
abstract: BACKGROUND
  Glucocorticoids are commonly co-administered with chemotherapy to prevent drug-induced allergic reactions, nausea, and vomiting, and have anti-tumor functions clinically; however, the distinct effects of GC on subtypes of tumor cells, especially in breast cancer cells, are still not well understood. In this study, we aimed to clarify the effect of GC on subtypes of T47D breast cancer cells by focusing on apoptosis, cell organization and migration, and underluing molecular mechanisms.
  
  
  METHODS
  The cell scratch test was performed to observe the cell migration rate in T47D cells treated with dexamethasone (Dex). Hoechst and MTT assays were conducted to detect cell survival and rhodamine-labeled phalloidin staining to observe cytoskeleton dynamics. Related factors in the AKT/mTOR pathway were determined by Western blotting.
  
  
  RESULTS
  Dex treatment could effectively inhibit T47D breast cancer cell migration with disruption of the cytoskeletal dynamic organization. Moreover, the effect of Dex on cell migration and cytoskeleton may be mediated by AKT/ mTOR/RhoA pathway. Although Dex inhibited T47D cell migration, it alone may not induce cell apoptosis in T47D cells.
  
  
  CONCLUSIONS
  Dex in T47D human breast cancer cells could effectively inhibit cell migration by disrupting the cytoskeletal dynamic organization, which may be mediated by the AKT/mTOR/RhoA pathway. Our work suggests that glucocorticoid/Dex clinical use may prove helpful for the treatment of breast cancer metastasis.
authors.affiliation: Department of Physical Medicine and Rehabilitation, Qilu Hospital, Shandong University, Jinan, China E-mail : shouweiyue2010@126.com.
authors.forename: Xian-Guo
authors.initials: XG
authors.lastname: Meng
authors.forename: Shou-Wei
authors.initials: SW
authors.lastname: Yue
mesh_terms: D018931:Antineoplastic Agents, Hormonal / Q000494:pharmacology*; D001943:Breast Neoplasms / Q000378:metabolism*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects*; D002470:Cell Survival / Q000187:drug effects; D003599:Cytoskeleton / Q000187:drug effects*; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D006801:Humans; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000187:drug effects* / Q000378:metabolism; D020742:rhoA GTP-Binding Protein / Q000187:drug effects* / Q000378:metabolism
chemical_list: D018931:Antineoplastic Agents, Hormonal; C066737:RHOA protein, human; D003907:Dexamethasone; C546842:MTOR protein, human; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D020742:rhoA GTP-Binding Protein