title: CELF1 is Up-Regulated in Glioma and Promotes Glioma Cell Proliferation by Suppression of CDKN1B.
abstract: BACKGROUND
  As a member of the CELF family, CELF1 (CUG-binding protein 1, CUGBP1) is involved in cardiac and embryonic development, skeletal muscle differentiation and mammary epithelial cell proliferation. CELF1 is also observed in many kinds of cancer and may play a great role in tumorigenesis and deterioration. However, the expression and mechanism of its function in human glioma remain unclear.
  
  
  METHODS
  We examined CELF1 expression in 62 glioma patients by immunohistochemistry and Western blot. The association between the expression of CELF1 protein and clinicopathological characteristics was analysed using SPSS 17.0. Survival analyses were performed using the Kaplan-Meier method. Small-interfering RNA was utilised to specifically knockdown CELF1 mRNA in U87 and U251 cells. Cell proliferation, cell cycle and cell apoptosis were tested by Cell Counting Kit-8 and flow cytometry. The expression of cell cycle-related gene CDKN1B was investigated by Western blot. The interactions between CELF1 and CDKN1B were detected with immune co-precipitation. Subcutaneous tumour models were used to study the effect of CELF1 on the growth of glioma cells in vivo.
  
  
  RESULTS
  Our results showed that CELF1 protein was frequently up-regulated in human glioma tissues. The expression level of this protein was positively correlated with glioma World Health Organisation grade and inversely correlated with patient survival (P < 0.05). Knockdown of CELF1 inhibited the glioma cell cycle process and proliferation potential, possibly by down-regulating its target, CDKN1B protein.
  
  
  CONCLUSIONS
  Results indicated that CELF1 may be a novel independent prognostic predictor of survival for glioma patients. It may promote glioma cell proliferation and cell cycle process during glioma carcinogenesis.
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Liang
authors.initials: L
authors.lastname: Xia
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Caixing
authors.initials: C
authors.lastname: Sun
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Qinglin
authors.initials: Q
authors.lastname: Li
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Fang
authors.initials: F
authors.lastname: Feng
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Enqi
authors.initials: E
authors.lastname: Qiao
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Limin
authors.initials: L
authors.lastname: Jiang
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Bin
authors.initials: B
authors.lastname: Wu
authors.affiliation: Zhejiang Cancer Hospital, Hangzhou 310022, Zhejiang Province, P.R.C.
authors.forename: Minghua
authors.initials: M
authors.lastname: Ge
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D000067879:CELF1 Protein / Q000235:genetics* / Q000378:metabolism; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics / Q000502:physiology*; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000235:genetics / Q000378:metabolism; D005260:Female; D005910:Glioma / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D000067879:CELF1 Protein; D050760:Cyclin-Dependent Kinase Inhibitor p27
keywords: CELF1; Glioma; Prognosis; Proliferation