PMID- 21129151
OWN - NLM
STAT- MEDLINE
DCOM- 20120410
LR  - 20211020
IS  - 1582-4934 (Electronic)
IS  - 1582-1838 (Print)
IS  - 1582-1838 (Linking)
VI  - 15
IP  - 11
DP  - 2011 Nov
TI  - Menin represses malignant phenotypes of melanoma through regulating multiple 
      pathways.
PG  - 2353-63
LID - 10.1111/j.1582-4934.2010.01222.x [doi]
AB  - Substantial genetic evidence suggests that chromosome 11q is involved in 
      regulating initiation and progression of malignant melanomas. Mutations of the 
      MEN1 gene, located in chromosome 11q13, predispose individuals to the multiple 
      endocrine neoplasia type 1 (MEN1) familial syndrome. MEN1 patients develop 
      primary malignant melanoma, suggesting a potential link between MEN1 syndrome and 
      development of melanomas, but the precise molecular mechanism is poorly 
      understood. Here we show that the MEN1 gene suppresses malignant phenotypes of 
      melanoma cells through multiple signalling pathways. Ectopic expression of menin, 
      the product of MEN1 gene, significantly inhibited melanoma cell proliferation and 
      migration in vitro and in vivo. The inhibition was partly achieved through 
      suppressing expression of growth factor pleiotrophin (PTN) and receptor protein 
      tyrosine phosphatase (RPTP) beta/zeta, accompanied with the reduced expression of 
      phosphatidylinositol 3-kinase (pI3K) and decreased phosphorylation of focal 
      adhesion kinase (FAK) and extracellular signal regulated kinase (ERK1/2). 
      Interestingly, reduced expression of menin was associated with hypermethylation 
      of the CpG islands of the MEN1 promoter in melanoma cells. Taken together, these 
      findings suggest a previously unappreciated function for menin in suppressing 
      malignant phenotypes of melanomas and unravel a novel mechanism involving in 
      regulating PTN signalling by menin in development and progression of melanomas.
CI  - (c) 2011 The Authors Journal of Cellular and Molecular Medicine (c) 2011 Foundation 
      for Cellular and Molecular Medicine/Blackwell Publishing Ltd.
FAU - Gao, Shu-Bin
AU  - Gao SB
AD  - Department of Basic Medical Sciences, Medical College, Xiamen University, Xiamen, 
      Fujian, China.
FAU - Feng, Zi-Jie
AU  - Feng ZJ
FAU - Xu, Bin
AU  - Xu B
FAU - Chen, Yan
AU  - Chen Y
FAU - Zheng, Hong-Hua
AU  - Zheng HH
FAU - Yin, Ping
AU  - Yin P
FAU - Hua, Xianxin
AU  - Hua X
FAU - Jin, Guang-Hui
AU  - Jin GH
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Cell Mol Med
JT  - Journal of cellular and molecular medicine
JID - 101083777
RN  - 0 (Carrier Proteins)
RN  - 0 (Cytokines)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (Men1 protein, mouse)
RN  - 0 (Phosphoinositide-3 Kinase Inhibitors)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 134034-50-7 (pleiotrophin)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 5)
SB  - IM
MH  - Animals
MH  - Carrier Proteins/antagonists & inhibitors/biosynthesis/*metabolism
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Cell Proliferation
MH  - Chromatin Immunoprecipitation
MH  - CpG Islands/genetics
MH  - Cytokines/antagonists & inhibitors/biosynthesis/*metabolism
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Female
MH  - Focal Adhesion Protein-Tyrosine Kinases/metabolism
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/genetics/metabolism
MH  - Melanoma/*metabolism/pathology
MH  - Melanoma, Experimental/*metabolism/pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Phenotype
MH  - Phosphatidylinositol 3-Kinase/biosynthesis/*metabolism
MH  - Phosphoinositide-3 Kinase Inhibitors
MH  - Phosphorylation
MH  - Promoter Regions, Genetic
MH  - Proto-Oncogene Proteins/*metabolism
MH  - Receptor-Like Protein Tyrosine Phosphatases, Class 5/antagonists & 
      inhibitors/biosynthesis/*metabolism
MH  - Signal Transduction
MH  - Transplantation, Heterologous
PMC - PMC3822947
EDAT- 2010/12/07 06:00
MHDA- 2012/04/11 06:00
PMCR- 2011/11/01
CRDT- 2010/12/07 06:00
PHST- 2010/12/07 06:00 [entrez]
PHST- 2010/12/07 06:00 [pubmed]
PHST- 2012/04/11 06:00 [medline]
PHST- 2011/11/01 00:00 [pmc-release]
AID - 10.1111/j.1582-4934.2010.01222.x [doi]
PST - ppublish
SO  - J Cell Mol Med. 2011 Nov;15(11):2353-63. doi: 10.1111/j.1582-4934.2010.01222.x.