抄録
It is known that there are close relationships between bone destruction and tumor growth in bone metastasis. RANKL is a central factor in bone metastasis, inducing osteoclastogenesis mediated by its receptor RANK. Recent reports demonstrate that RANKL has important roles in organogenesis stimulating proliferation and differentiation of epithelial and stroma cells. RANKL is induced not only by cytokines and hormones but also by UV-irradiation, inflammation and carcinogens. Expression of RANK and RANKL is found in several human cancer cell lines, and RANK signaling stimulates proliferation, migration and epithelial-mesenchymal transition of cancer cells, which may be involved in metastasis via an autocrine/paracrine mechanism. RANKL regulates the number of Tregs that produce RANKL, which may affect cancer metastasis. In this review we discuss the multifunctional roles of RANKL/RANK in osteoclastogenesis, organogenesis, and the metastasis and tumorigenesis of cancer cells.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 1609-1622 |
| ページ数 | 14 |
| ジャーナル | Future Oncology |
| 巻 | 9 |
| 発行部数 | 11 |
| DOI | |
| 出版物ステータス | 出版済み - 11 1 2013 |
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All Science Journal Classification (ASJC) codes
- Oncology
- Cancer Research
これを引用
Multifunctional properties of RANKL/RANK in cell differentiation, proliferation and metastasis. / Kukita, Akiko; Kukita, Toshio.
：: Future Oncology, 巻 9, 番号 11, 01.11.2013, p. 1609-1622.研究成果: ジャーナルへの寄稿 › 評論記事
}
TY - JOUR
T1 - Multifunctional properties of RANKL/RANK in cell differentiation, proliferation and metastasis
AU - Kukita, Akiko
AU - Kukita, Toshio
PY - 2013/11/1
Y1 - 2013/11/1
N2 - It is known that there are close relationships between bone destruction and tumor growth in bone metastasis. RANKL is a central factor in bone metastasis, inducing osteoclastogenesis mediated by its receptor RANK. Recent reports demonstrate that RANKL has important roles in organogenesis stimulating proliferation and differentiation of epithelial and stroma cells. RANKL is induced not only by cytokines and hormones but also by UV-irradiation, inflammation and carcinogens. Expression of RANK and RANKL is found in several human cancer cell lines, and RANK signaling stimulates proliferation, migration and epithelial-mesenchymal transition of cancer cells, which may be involved in metastasis via an autocrine/paracrine mechanism. RANKL regulates the number of Tregs that produce RANKL, which may affect cancer metastasis. In this review we discuss the multifunctional roles of RANKL/RANK in osteoclastogenesis, organogenesis, and the metastasis and tumorigenesis of cancer cells.
AB - It is known that there are close relationships between bone destruction and tumor growth in bone metastasis. RANKL is a central factor in bone metastasis, inducing osteoclastogenesis mediated by its receptor RANK. Recent reports demonstrate that RANKL has important roles in organogenesis stimulating proliferation and differentiation of epithelial and stroma cells. RANKL is induced not only by cytokines and hormones but also by UV-irradiation, inflammation and carcinogens. Expression of RANK and RANKL is found in several human cancer cell lines, and RANK signaling stimulates proliferation, migration and epithelial-mesenchymal transition of cancer cells, which may be involved in metastasis via an autocrine/paracrine mechanism. RANKL regulates the number of Tregs that produce RANKL, which may affect cancer metastasis. In this review we discuss the multifunctional roles of RANKL/RANK in osteoclastogenesis, organogenesis, and the metastasis and tumorigenesis of cancer cells.
UR - http://www.scopus.com/inward/record.url?scp=84887294582&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84887294582&partnerID=8YFLogxK
U2 - 10.2217/fon.13.115
DO - 10.2217/fon.13.115
M3 - Review article
VL - 9
SP - 1609
EP - 1622
JO - Future Oncology
JF - Future Oncology
SN - 1479-6694
IS - 11
ER -