title: The effects of GLUT1 on the survival of head and neck squamous cell carcinoma.
abstract: OBJECTIVE
  Cancer cells require increased nutrient uptake to support a high rate of proliferation, and the overexpression of glucose transporters, in particular GLUT1, is a common characteristic of human malignancies. Here, we investigated the relationship between the expression of GLUT1 and cell viability, colony forming ability and apoptosis of head and neck squamous cell carcinoma (HNSCC) in vitro and in a xenograft mouse model in vivo.
  
  
  METHODS
  Lentiviral mediated overexpression and knock-down of GLUT1 was performed in two oral cancer cell lines (CAL27 and SCC25). QRT-PCR and Western blot analysis were used to detect the mRNA and protein expression of GLUT1 and nuclear factor-kappa B (NFκB) p65 subunit. Cell viability and apoptosis were assessed by MTT and flow cytometry analyses, respectively. Colony formation assays were performed by staining with 0.5% crystal violet. The role of GLUT1 in HNSCC was examined in vivo through the generation of a CAL27 (or CAL27 with different transfections) nude mice xenograft model of HNSCC.
  
  
  RESULTS
  GLUT1 overexpression promoted cell viability and colony formation whereas GLUT1 silencing had the opposite effect. GLUT1 knock-down significantly increased the number of Annexin V positive cells in both cell lines and GLUT1 overexpression had the opposite effect, indicating that GLUT1 modulates apoptosis. Xenograft mouse models of GLUT1 knockdown and overexpression showed that GLUT1 expression was associated with poor survival and increased tumor growth. GLUT1 overexpression significantly upregulated the expression of NFκB-p65, and this effect was reversed by inhibition of GLUT1 expression.
  
  
  CONCLUSIONS
  GLUT1 expression plays an important role in the survival of HNSCC, and its effects may be associated with the activation of the NFκB pathway.
authors.affiliation: Department of Oral and Maxillofacial Surgery, Stomatology Hospital, Tongji University, Shanghai, China.
authors.forename: Shengjiao
authors.initials: S
authors.lastname: Li
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Yang
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.forename: Xing
authors.initials: X
authors.lastname: Ran
mesh_terms: D000818:Animals; D017209:Apoptosis; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D002470:Cell Survival; D002945:Cisplatin / Q000627:therapeutic use; D019008:Drug Resistance, Neoplasm; D005260:Female; D005822:Genetic Vectors / Q000378:metabolism; D051272:Glucose Transporter Type 1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D006258:Head and Neck Neoplasms / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D006801:Humans; D016086:Lentivirus / Q000235:genetics; D051379:Mice; D008819:Mice, Nude; D034622:RNA Interference; D012333:RNA, Messenger / Q000378:metabolism; D034741:RNA, Small Interfering / Q000378:metabolism; D000077195:Squamous Cell Carcinoma of Head and Neck; D051996:Transcription Factor RelA / Q000378:metabolism; D014183:Transplantation, Heterologous
chemical_list: D051272:Glucose Transporter Type 1; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D051996:Transcription Factor RelA; D002945:Cisplatin