title: Acquisition of epithelial-mesenchymal transition is associated with Skp2 expression in paclitaxel-resistant breast cancer cells.
abstract: BACKGROUND
  Breast cancer is the most common female malignant disease, and the second leading cause of cancer-related death in the United States. Acquired resistance to chemotherapeutic drugs is a pivotal reason that leads to worse treatment outcome of breast cancer. Therefore, it is urgent to elucidate the mechanism of drug resistance in breast cancer.
  
  
  METHODS
  To investigate the underlying molecular basis of the acquired resistant cells to paclitaxel in breast cancer, we used multiple methods including real-time RT-PCR, western blotting analysis, migration and invasion assays, wound healing assay, and transfection.
  
  
  RESULTS
  We found that epithelial-mesenchymal transition (EMT) is involved in paclitaxel-resistant (PR) breast cancer cells. The resistant cells with EMT features exhibit increased migration and invasion activities. Mechanistically, high expression of Skp2 was found to be associated with EMT in PR cells. Notably, depletion of Skp2 in PR cells led to partial reversal of EMT phenotype.
  
  
  CONCLUSIONS
  These findings suggest that Skp2 was critically involved in PR-mediated EMT. Skp2 could be a potential therapeutic target for breast cancer.
authors.affiliation: Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui 233030, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Yang
authors.affiliation: Clinical Testing and Diagnose Experimental Center of Bengbu Medical College, Anhui 233000, China.
authors.forename: J
authors.initials: J
authors.lastname: Huang
authors.affiliation: Department of Medical Oncology, First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Wu
authors.affiliation: Clinical Testing and Diagnose Experimental Center of Bengbu Medical College, Anhui 233000, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Cai
authors.affiliation: Clinical Testing and Diagnose Experimental Center of Bengbu Medical College, Anhui 233000, China.
authors.forename: L
authors.initials: L
authors.lastname: Zhu
authors.affiliation: Clinical Testing and Diagnose Experimental Center of Bengbu Medical College, Anhui 233000, China.
authors.forename: X
authors.initials: X
authors.lastname: Lu
authors.affiliation: Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui 233030, China.
authors.forename: S
authors.initials: S
authors.lastname: Chen
authors.affiliation: Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui 233030, China.
authors.forename: C
authors.initials: C
authors.lastname: Chen
authors.affiliation: Cyrus Tang Hematology Center, Jiangsu Institute of Hematology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215123, China.
authors.forename: Z
authors.initials: Z
authors.lastname: Wang
mesh_terms: D001943:Breast Neoplasms / Q000188:drug therapy* / Q000235:genetics* / Q000473:pathology; D019008:Drug Resistance, Neoplasm / Q000187:drug effects / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D061986:MCF-7 Cells; D017239:Paclitaxel / Q000008:administration & dosage*; D044786:S-Phase Kinase-Associated Proteins / Q000096:biosynthesis / Q000235:genetics*; D014481:United States
chemical_list: D044786:S-Phase Kinase-Associated Proteins; D017239:Paclitaxel