PMID- 16912184
OWN - NLM
STAT- MEDLINE
DCOM- 20071113
LR  - 20161124
IS  - 1538-7445 (Electronic)
IS  - 0008-5472 (Linking)
VI  - 66
IP  - 16
DP  - 2006 Aug 15
TI  - Functional interaction of the retinoblastoma and Ini1/Snf5 tumor suppressors in 
      cell growth and pituitary tumorigenesis.
PG  - 8076-82
AB  - The Ini1 subunit of the SWI/SNF chromatin remodeling complex suppresses formation 
      of malignant rhabdoid tumors in humans and mice. Transduction of Ini1 into 
      Ini1-deficient tumor-derived cell lines has indicated that Ini1 arrests cell 
      growth, controls chromosomal ploidy, and suppresses tumorigenesis by regulating 
      components of the retinoblastoma (Rb) signaling pathway. Furthermore, conditional 
      inactivation of Ini1 in mouse fibroblasts alters the expression of various 
      Rb-E2F-regulated genes, indicating that endogenous Ini1 levels may control Rb 
      signaling in cells. We have reported previously that loss of one allele of Ini1 
      in mouse fibroblasts results only in a 15% to 20% reduction in total Ini1 mRNA 
      levels due to transcriptional compensation by the remaining Ini1 allele. Here, we 
      examine the effects of Ini1 haploinsufficiency on cell growth and immortalization 
      in mouse embryonic fibroblasts. In addition, we examine pituitary tumorigenesis 
      in Rb-Ini1 compound heterozygous mice. Our results reveal that heterozygosity for 
      Ini1 up-regulates cell growth and immortalization and that exogenous Ini1 
      down-regulates the growth of primary cells in a Rb-dependent manner. Furthermore, 
      loss of Ini1 is redundant with loss of Rb function in the formation of pituitary 
      tumors in Rb heterozygous mice and leads to the formation of large, atypical 
      Rb(+/-) tumor cells lacking adrenocorticotropic hormone expression. These results 
      confirm in vivo the relationship between Rb and Ini1 in tumor suppression and 
      indicate that Ini1 plays a role in maintaining the morphologic and functional 
      differentiation of corticotrophic cells.
FAU - Guidi, Cynthia J
AU  - Guidi CJ
AD  - Department of Cell Biology, University of Massachusetts Medical School, 
      Worcester, MA 01655, USA.
FAU - Mudhasani, Rajini
AU  - Mudhasani R
FAU - Hoover, Kathleen
AU  - Hoover K
FAU - Koff, Andrew
AU  - Koff A
FAU - Leav, Irwin
AU  - Leav I
FAU - Imbalzano, Anthony N
AU  - Imbalzano AN
FAU - Jones, Stephen N
AU  - Jones SN
LA  - eng
GR  - 5P30DK32520/DK/NIDDK NIH HHS/United States
GR  - CA95216/CA/NCI NIH HHS/United States
GR  - GM56244/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (Chromosomal Proteins, Non-Histone)
RN  - 0 (DNA Primers)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Retinoblastoma Protein)
RN  - 0 (SMARCB1 Protein)
RN  - 0 (SMARCB1 protein, human)
RN  - 0 (Transcription Factors)
SB  - IM
MH  - Animals
MH  - Cell Division/*physiology
MH  - Chromosomal Proteins, Non-Histone/deficiency/*genetics
MH  - DNA Primers
MH  - DNA-Binding Proteins/deficiency/*genetics
MH  - Embryo, Mammalian
MH  - Fibroblasts/cytology/physiology
MH  - Genotype
MH  - Humans
MH  - Mice
MH  - Pituitary Neoplasms/*pathology
MH  - Retinoblastoma Protein/genetics/*physiology
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - SMARCB1 Protein
MH  - Transcription Factors/deficiency/*genetics
EDAT- 2006/08/17 09:00
MHDA- 2007/11/14 09:00
CRDT- 2006/08/17 09:00
PHST- 2006/08/17 09:00 [pubmed]
PHST- 2007/11/14 09:00 [medline]
PHST- 2006/08/17 09:00 [entrez]
AID - 66/16/8076 [pii]
AID - 10.1158/0008-5472.CAN-06-1451 [doi]
PST - ppublish
SO  - Cancer Res. 2006 Aug 15;66(16):8076-82. doi: 10.1158/0008-5472.CAN-06-1451.