PMID- 25778325
OWN - NLM
STAT- MEDLINE
DCOM- 20150430
LR  - 20150317
IS  - 1107-0625 (Print)
IS  - 1107-0625 (Linking)
VI  - 20
IP  - 1
DP  - 2015 Jan-Feb
TI  - 67kDa laminin receptor regulates the activation of MAPKs through DUSPs in glioma 
      cell line U251.
PG  - 253-60
AB  - PURPOSE: 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.
FAU - Jiang, Li
AU  - Jiang L
AD  - School of Life Sciences, Shanghai University, Shanghai, .R. China.
FAU - Zhang, Can
AU  - Zhang C
FAU - Wu, Yue
AU  - Wu Y
FAU - Jiang, Ying
AU  - Jiang Y
FAU - Ji, Yonghua
AU  - Ji Y
FAU - Chen, Fuxue
AU  - Chen F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Cyprus
TA  - J BUON
JT  - Journal of B.U.ON. : official journal of the Balkan Union of Oncology
JID - 100883428
RN  - 0 (Antineoplastic Agents)
RN  - 0 (RPSA protein, human)
RN  - 0 (Receptors, Laminin)
RN  - 0 (Ribosomal Proteins)
RN  - 5688UTC01R (Tretinoin)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
RN  - EC 3.1.3.48 (Dual-Specificity Phosphatases)
SB  - IM
MH  - Antineoplastic Agents/pharmacology
MH  - Brain Neoplasms/*enzymology/genetics/pathology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Dual-Specificity Phosphatases/genetics/*metabolism
MH  - Enzyme Activation
MH  - Gene Expression Regulation, Enzymologic
MH  - Gene Expression Regulation, Neoplastic
MH  - Glioma/*enzymology/genetics/pathology
MH  - Humans
MH  - *MAP Kinase Signaling System/drug effects
MH  - Mitogen-Activated Protein Kinases/*metabolism
MH  - Phosphorylation
MH  - RNA Interference
MH  - Receptors, Laminin/drug effects/genetics/*metabolism
MH  - Ribosomal Proteins/drug effects/genetics/*metabolism
MH  - Transcription, Genetic
MH  - Transfection
MH  - Tretinoin/pharmacology
EDAT- 2015/03/18 06:00
MHDA- 2015/05/01 06:00
CRDT- 2015/03/18 06:00
PHST- 2015/03/18 06:00 [entrez]
PHST- 2015/03/18 06:00 [pubmed]
PHST- 2015/05/01 06:00 [medline]
PST - ppublish
SO  - J BUON. 2015 Jan-Feb;20(1):253-60.