PMID- 20616437
OWN - NLM
STAT- MEDLINE
DCOM- 20110211
LR  - 20190907
IS  - 1348-4540 (Electronic)
IS  - 0918-8959 (Linking)
VI  - 57
IP  - 9
DP  - 2010
TI  - Caspase 8 and menin expressions are not correlated in human parathyroid tumors.
PG  - 825-32
AB  - Menin is lost by the sequential inactivation of both MEN1 alleles in subsets of 
      non-hereditary endocrine tumors as well as those associated with multiple 
      endocrine neoplasia type 1 (MEN1), an autosomal dominant hereditary cancer 
      syndrome characterized by multiple tumors including parathyroid, pituitary and 
      enteropancreatic endocrine tumors. Loss of menin has been reported to be 
      associated with lowered caspase 8 expression and resistance to apoptosis in 
      murine fibroblasts and in pancreatic islet tumors arising in heterozygous MEN1 
      gene knockout mice, the animal model of the human MEN1 syndrome. We confirmed by 
      menin-knockdown experiments with specific siRNA that menin is crucial for caspase 
      8 expression in human culture cells while overexpression of menin did not 
      increase caspase 8 protein over basal levels. We then examined expression of 
      menin, caspase 8 and cyclin-dependent kinase inhibitors p27(Kip1) and p15(Ink4b) 
      by Western blotting in human parathyroid tumors surgically resected from patients 
      with MEN1 and those with non-hereditary primary hyperparathyroidism. The menin 
      and p27(Kip1) expression levels were correlated with MEN1 mutation status that 
      was confirmed by DNA analysis. The caspase 8 and p15(Ink4b) protein levels were 
      variable among tumors, and were not correlated with menin protein levels. These 
      findings suggest that human endocrine tumors lacking menin may not always exhibit 
      lowered caspase 8 expression and hence may not be resistant to apoptosis-inducing 
      therapy.
FAU - Yu, Dong
AU  - Yu D
AD  - Tumor Endocrinology Project, National Cancer Center Research Institute, Tokyo, 
      Japan.
FAU - Nagamura, Yuko
AU  - Nagamura Y
FAU - Shimazu, Satoko
AU  - Shimazu S
FAU - Naito, Junko
AU  - Naito J
FAU - Kaji, Hiroshi
AU  - Kaji H
FAU - Wada, Seiki
AU  - Wada S
FAU - Honda, Munehiro
AU  - Honda M
FAU - Xue, Lian
AU  - Xue L
FAU - Tsukada, Toshihiko
AU  - Tsukada T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100703
PL  - Japan
TA  - Endocr J
JT  - Endocrine journal
JID - 9313485
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p15)
RN  - 0 (MEN1 protein, human)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - Caspase 8/*biosynthesis
MH  - Cyclin-Dependent Kinase Inhibitor p15/metabolism
MH  - Cyclin-Dependent Kinase Inhibitor p27/biosynthesis
MH  - HEK293 Cells
MH  - Humans
MH  - Multiple Endocrine Neoplasia Type 1/genetics/*metabolism
MH  - Parathyroid Neoplasms/*physiopathology
MH  - Proto-Oncogene Proteins/*biosynthesis/genetics
EDAT- 2010/07/10 06:00
MHDA- 2011/02/12 06:00
CRDT- 2010/07/10 06:00
PHST- 2010/07/10 06:00 [entrez]
PHST- 2010/07/10 06:00 [pubmed]
PHST- 2011/02/12 06:00 [medline]
AID - JST.JSTAGE/endocrj/K10E-085 [pii]
AID - 10.1507/endocrj.k10e-085 [doi]
PST - ppublish
SO  - Endocr J. 2010;57(9):825-32. doi: 10.1507/endocrj.k10e-085. Epub 2010 Jul 3.