TY - JOUR
T1 - Oral squamous cell carcinoma cells modulate osteoclast function by RANKL-dependent and -independent mechanisms
AU - Tada, Takeyuki
AU - Shin, Masashi
AU - Fukushima, Hidefumi
AU - Okabe, Koji
AU - Ozeki, Satoru
AU - Okamoto, Masato
AU - Jimi, Eijiro
N1 - Funding Information:
This work was supported by Grant-in-Aids for Scientific Research from the Ministry of Education, Culture, Sports Science and Technology of Japan (No. 18791537) and Frontier Research Grant.
PY - 2009/2/8
Y1 - 2009/2/8
N2 - Oral squamous cell carcinoma (SCC) cells frequently invade mandibular bone, and bone invasion is a common clinical problem. Recent studies have revealed that bone resorption by osteoclasts is an important step in the progress of bone invasion by oral SCCs. We previously reported that oral SCC cells induce osteoclastogenesis by suppressing osteoprotegerin (OPG) in host cells. In the present study, we examined the effects of oral SCCs on osteoclast function. Both BHY cells, a human oral SCC cell line, and its conditioned medium (BHY-CM) stimulated osteoclast survival by suppressing Bim, a pro-apoptotic protein, depending on extracellular signal-regulated kinase (ERK) and multinucleation. Adding BHY cells but not BHY-CM induced pit-forming activity by osteoclasts and adding OPG abrogated the activity. Thus, oral SCC cells regulate not only osteoclastogenesis but also its function.
AB - Oral squamous cell carcinoma (SCC) cells frequently invade mandibular bone, and bone invasion is a common clinical problem. Recent studies have revealed that bone resorption by osteoclasts is an important step in the progress of bone invasion by oral SCCs. We previously reported that oral SCC cells induce osteoclastogenesis by suppressing osteoprotegerin (OPG) in host cells. In the present study, we examined the effects of oral SCCs on osteoclast function. Both BHY cells, a human oral SCC cell line, and its conditioned medium (BHY-CM) stimulated osteoclast survival by suppressing Bim, a pro-apoptotic protein, depending on extracellular signal-regulated kinase (ERK) and multinucleation. Adding BHY cells but not BHY-CM induced pit-forming activity by osteoclasts and adding OPG abrogated the activity. Thus, oral SCC cells regulate not only osteoclastogenesis but also its function.
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U2 - 10.1016/j.canlet.2008.09.015
DO - 10.1016/j.canlet.2008.09.015
M3 - Article
C2 - 18930344
AN - SCOPUS:57749121473
SN - 0304-3835
VL - 274
SP - 126
EP - 131
JO - Cancer Letters
JF - Cancer Letters
IS - 1
ER -