PMID- 15800904
OWN - NLM
STAT- MEDLINE
DCOM- 20050802
LR  - 20160303
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 116
IP  - 2
DP  - 2005 Aug 20
TI  - Oral squamous cell carcinoma cells induce osteoclast differentiation by 
      suppression of osteoprotegerin expression in osteoblasts.
PG  - 253-62
AB  - The invasion of oral squamous cell carcinoma (SCC) cells into the mandibular bone 
      is a common clinical problem. It has been reported that BHY cells, a human oral 
      SCC cell line, are capable of invading mandibular bone of nude mice. These 
      results led us to examine possible mechanisms of osteoclastogenesis induced by 
      BHY cells using in vitro culture systems. When BHY cells were cocultured with 
      mouse bone marrow cells (BMCs), only few osteoclasts were formed, even though BHY 
      cells express the receptor activator of NF-kappaB ligand (RANKL). However, adding 
      BHY cells to a coculture of mouse primary osteoblasts (POBs) and BMCs markedly 
      induced osteoclastogenesis in the absence of osteotropic factors. Furthermore, 
      another oral SCC cell line, HSC-2, which does not express RANKL, also induced 
      osteoclastogenesis in our cocultures. These effects were significantly, but not 
      completely, inhibited by adding osteoprotegerin (OPG). In addition, we also found 
      that TNFalpha released from these cells partially contributes to 
      osteoclastogenesis via a RANKL-independent mechanism. Adding BHY or HSC-2 cells 
      suppressed mouse OPG mRNA expression and protein production by POBs in cocultures 
      of POBs and human oral SCC cells. This finding is consistent with the result that 
      BHY cells and HSC-2 cells did not enhance osteoclastogenesis in cocultures of 
      BMCs and POBs from OPG-deficient mice. Immunohistochemical analysis showed a 
      reduction of OPG expression in osteolytic lesions as compared to normal lesions 
      from oral SCC patients. Therefore, oral SCC-induced suppression of OPG expression 
      in POBs appears critical for osteoclastogenesis, rather than expression of RANKL 
      in SCC cells.
CI  - Copyright 2005 Wiley-Liss, Inc.
FAU - Tada, Takeyuki
AU  - Tada T
AD  - Department of Physiological Science and Molecular Biology, Fukuoka Dental 
      College, Fukuoka, Japan.
FAU - Jimi, Eijiro
AU  - Jimi E
FAU - Okamoto, Masato
AU  - Okamoto M
FAU - Ozeki, Satoru
AU  - Ozeki S
FAU - Okabe, Koji
AU  - Okabe K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (Carrier Proteins)
RN  - 0 (Glycoproteins)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (Osteoprotegerin)
RN  - 0 (RANK Ligand)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor Activator of Nuclear Factor-kappa B)
RN  - 0 (Receptors, Cytoplasmic and Nuclear)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (TNFRSF11A protein, human)
RN  - 0 (TNFRSF11B protein, human)
RN  - 0 (TNFSF11 protein, human)
RN  - 0 (Tnfrsf11a protein, mouse)
RN  - 0 (Tnfrsf11b protein, mouse)
RN  - 0 (Tnfsf11 protein, mouse)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Bone Marrow Cells
MH  - Carcinoma, Squamous Cell/*pathology
MH  - Carrier Proteins/biosynthesis/physiology
MH  - *Cell Communication
MH  - *Cell Differentiation
MH  - Down-Regulation
MH  - Gene Expression Regulation, Neoplastic
MH  - Glycoproteins/*biosynthesis
MH  - Immunohistochemistry
MH  - Membrane Glycoproteins/biosynthesis/physiology
MH  - Mice
MH  - Mouth Neoplasms/*pathology
MH  - Neoplasm Invasiveness/*physiopathology
MH  - Osteoclasts/*physiology
MH  - Osteoprotegerin
MH  - RANK Ligand
MH  - RNA, Messenger/biosynthesis
MH  - Receptor Activator of Nuclear Factor-kappa B
MH  - Receptors, Cytoplasmic and Nuclear/*biosynthesis
MH  - Receptors, Tumor Necrosis Factor/*biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2005/04/01 09:00
MHDA- 2005/08/03 09:00
CRDT- 2005/04/01 09:00
PHST- 2005/04/01 09:00 [pubmed]
PHST- 2005/08/03 09:00 [medline]
PHST- 2005/04/01 09:00 [entrez]
AID - 10.1002/ijc.21008 [doi]
PST - ppublish
SO  - Int J Cancer. 2005 Aug 20;116(2):253-62. doi: 10.1002/ijc.21008.