title: 67kDa laminin receptor regulates the activation of MAPKs through DUSPs in glioma cell line U251.
abstract: OBJECTIVE
  All-trans-retinoic-acid (ATRA), the active derivative of vitamin A, is critical in regulating cell cycle as well as inhibiting tumor growth and angiogenesis. It has been used in the clinical treatment of leukemia. 67kDa laminin receptor (67LR), as one of the receptor of laminin, plays an important role in tumor cells invasion, proliferation and metastasis. Current research indicates that 67LR is highly expressed in glioma and is associated with tumor progression. However, the underlying molecular mechanisms, especially the signaling pathways involved, have not been reported yet. Therefore it is of great importance to clarify its downstream targets.
  
  
  METHODS
  The U251 glioma cell line was used in this study. Cell Counting Kit-8 was used in cell proliferation assay. Quantitative real-time PCR (qRT-PCR) was used to determine the transcription level of dual specificity phosphatases (DUSPs). Western blot analysis was used to detect the expression of mitogen activated protein kinases (MAPKs) and phosphorylated MAPKs.
  
  
  RESULTS
  67LR could influence the transcription of DUSPs and expression of MAPKs. ATRA could enhance the expression of 67LR in U251 cells and this enhancement was dose-dependent. ATRA was able to inhibit the growth of U251 cells.
  
  
  CONCLUSIONS
  ATRA expressed significant therapeutic effect on glioma cells, and 67LR is not the only factor that can influence the proliferation of U251 cells.
authors.affiliation: School of Life Sciences, Shanghai University, Shanghai, .R. China.
authors.forename: Li
authors.initials: L
authors.lastname: Jiang
authors.forename: Can
authors.initials: C
authors.lastname: Zhang
authors.forename: Yue
authors.initials: Y
authors.lastname: Wu
authors.forename: Ying
authors.initials: Y
authors.lastname: Jiang
authors.forename: Yonghua
authors.initials: Y
authors.lastname: Ji
authors.forename: Fuxue
authors.initials: F
authors.lastname: Chen
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D001932:Brain Neoplasms / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D054637:Dual-Specificity Phosphatases / Q000235:genetics / Q000378:metabolism*; D004789:Enzyme Activation; D015971:Gene Expression Regulation, Enzymologic; D015972:Gene Expression Regulation, Neoplastic; D005910:Glioma / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D006801:Humans; D020935:MAP Kinase Signaling System / Q000187:drug effects; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D010766:Phosphorylation; D034622:RNA Interference; D017474:Receptors, Laminin / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D012269:Ribosomal Proteins / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D014158:Transcription, Genetic; D014162:Transfection; D014212:Tretinoin / Q000494:pharmacology
chemical_list: D000970:Antineoplastic Agents; C510624:RPSA protein, human; D017474:Receptors, Laminin; D012269:Ribosomal Proteins; D014212:Tretinoin; D020928:Mitogen-Activated Protein Kinases; D054637:Dual-Specificity Phosphatases