| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2018-10-31 |
| タイトル |
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|
タイトル |
Toll-Like Receptor 4 Signaling Promotes the Migration of Human Melanoma Cells |
| 言語 |
|
|
言語 |
eng |
| DOI |
|
|
|
関連識別子 |
https://doi.org/10.1620/tjem.234.57 |
|
|
関連名称 |
10.1620/tjem.234.57 |
| キーワード |
|
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主題 |
nnate immunity, melanoma, migration, proliferation, Toll-like receptor 4 |
| 資源タイプ |
|
|
資源 |
http://purl.org/coar/resource_type/c_6501 |
|
タイプ |
journal article |
| 著者 |
Takazawa, Yuko
Kiniwa, Yukiko
Ogawa, Eisaku
Uchiyama, Aya
Ashida, Atsuko
Uhara, Hisashi
Goto, Yasufumi
Okuyama, Ryuhei
|
| 信州大学研究者総覧へのリンク |
|
|
氏名 |
Okuyama, Ryuhei |
|
URL |
http://soar-rd.shinshu-u.ac.jp/profile/ja.ZpfNHFSF.html |
| 出版者 |
|
|
出版者 |
TOHOKU UNIV MEDICAL PRESS |
| 引用 |
|
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内容記述 |
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE.234(1):57-65(2014) |
| 書誌情報 |
TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE
巻 234,
号 1,
p. 57-65,
発行日 2014-08-30
|
| 抄録 |
|
|
内容記述 |
Immune cell Toll-like receptors (TLRs) recognize conserved microbial components, leading to immune and inflammatory responses. However, TLRs are also expressed in cancer cells, including melanoma cells, which express TLR2-4. TLR4 ligands have received attention as immunotherapies; therefore, we assessed the expression of TLR4 in human melanoma specimens (29 primary lesions and 28 metastatic lesions) representing different types of melanoma. A high percentage (≥ 90%) of melanoma lesions expressed TLR4, as judged by immunohistochemistry. Next, the role of TLR4 in cell proliferation and migration was assessed using the TLR4-positive (TLR4+) melanoma cell lines 501mel and 888mel, and TLR4-negative (TLR4‒) 928mel melanoma cells. Lipopolysaccharide (LPS), a TLR4 agonist, increased the proliferation of TLR4+ melanoma cells but not of TLR4‒ 928mel cells. The proliferation-inducing effect of LPS in 888mel cells was abolished by blockade of TLR4 signaling via treatment with short interfering RNA (siRNA) targeting TLR4 or myeloid differentiation primary response gene 88 (MyD88), a molecule downstream of TLR4. However, knockdown of TLR4 or MyD88 expression did not affect the LPS-induced proliferation of 501mel cells, suggesting that residual TLR4 signaling is sufficient to maintain cell proliferation. By contrast, LPS increased the migration of TLR4+ melanoma cells, and this effect was substantially inhibited by TLR4 or MyD88 knockdown. Furthermore, TLR4 knockdown decreased cell migration even in the absence of LPS, suggesting the presence of an endogenous TLR4 ligand(s) in melanoma cells. TLR4 signaling may contribute to melanoma progression, and caution should be exercised when using TLR4 ligands as adjuvant therapy for cancer. |
| 資源タイプ（コンテンツの種類） |
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| ISSN |
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収録物識別子タイプ |
PISSN |
|
収録物識別子 |
0040-8727 |
| 書誌レコードID |
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|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA00863920 |
| PubMed |
|
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|
識別子タイプ |
PMID |
|
|
関連識別子 |
https://www.ncbi.nlm.nih.gov/pubmed/25175033 |
|
|
関連名称 |
25175033 |
| 権利 |
|
|
権利情報 |
© 2014 Tohoku University Medical Press |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| WoS |
|
|
URL |
http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000341616000007 |
234_57.pdf (793.6 kB)
