title: Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
abstract: BACKGROUND
  The role of CTGF varies in different types of cancer. The purpose of this study is to investigate the involvement of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC).
  
  
  METHODS
  CTGF expression levels were examined in NPC tissues and cells, nasopharynx (NP) tissues, and NP69 cells. The effects and molecular mechanisms of CTGF expression on cell proliferation, migration, invasion, and cell cycle were also explored.
  
  
  RESULTS
  NPC cells exhibited decreased mRNA expression of CTGF compared to immortalized human nasopharyngeal epithelial cell line NP69. Similarly, CTGF was observed to be downregulated in NPC compared to normal tissues at mRNA and protein levels. Furthermore, reduced CTGF was negatively associated with the progression of NPC. Knocking down CTGF expression enhanced the colony formation, cell migration, invasion, and G1/S cell cycle transition. Mechanistic analysis revealed that CTGF suppression activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs. Finally, DNA methylation microarray revealed a lack of hypermethylation at the CTGF promoter, suggesting other mechanisms are associated with suppression of CTGF in NPC.
  
  
  CONCLUSIONS
  Our study demonstrates that reduced expression of CTGF promoted cell proliferation, migration, invasion and cell cycle progression through FAK/PI3K/AKT, EMT and MMP pathways in NPC.
authors.affiliation: Cancer Research Institute of Basic Medicine School, Southern Medical University, Guangzhou, PR China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhen
authors.forename: Yanfen
authors.initials: Y
authors.lastname: Ye
authors.forename: Xiaoli
authors.initials: X
authors.lastname: Yu
authors.forename: Chunping
authors.initials: C
authors.lastname: Mai
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhou
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Huiling
authors.initials: H
authors.lastname: Yang
authors.forename: Xiaoming
authors.initials: X
authors.lastname: Lyu
authors.forename: Ye
authors.initials: Y
authors.lastname: Song
authors.forename: Qiangyun
authors.initials: Q
authors.lastname: Wu
authors.forename: Qiaofen
authors.initials: Q
authors.lastname: Fu
authors.forename: Mengyang
authors.initials: M
authors.lastname: Zhao
authors.forename: Shengni
authors.initials: S
authors.lastname: Hua
authors.forename: Hao
authors.initials: H
authors.lastname: Wang
authors.forename: Zhen
authors.initials: Z
authors.lastname: Liu
authors.forename: Yajie
authors.initials: Y
authors.lastname: Zhang
authors.forename: Weiyi
authors.initials: W
authors.lastname: Fang
mesh_terms: D002277:Carcinoma; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation; D002999:Clone Cells; D055513:Connective Tissue Growth Factor / Q000235:genetics* / Q000378:metabolism; D019175:DNA Methylation / Q000235:genetics; D018450:Disease Progression; D015536:Down-Regulation / Q000235:genetics; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics; D004848:Epithelium / Q000378:metabolism / Q000473:pathology; D016193:G1 Phase; D015972:Gene Expression Regulation, Neoplastic; D055785:Gene Knockdown Techniques; D006801:Humans; D000077274:Nasopharyngeal Carcinoma; D009303:Nasopharyngeal Neoplasms / Q000235:genetics* / Q000473:pathology*; D009305:Nasopharynx / Q000473:pathology; D009361:Neoplasm Invasiveness; D011379:Prognosis; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D011401:Promoter Regions, Genetic / Q000235:genetics; D016196:S Phase; D015398:Signal Transduction / Q000235:genetics
chemical_list: C526317:CCN2 protein, human; D018809:Proliferating Cell Nuclear Antigen; D055513:Connective Tissue Growth Factor