Protumoral roles of melanoma inhibitory activity 2 in oral squamous cell carcinoma

• Material Type: 博士論文
• Title: Protumoral roles of melanoma inhibitory activity 2 in oral squamous cell carcinoma
• Author/Editor: Kurihara, Miyako; Kirita, Tadaaki; Sasahira, Tomonori; Ohmori, Hitoshi; Matsushima, Sayako; Yamamoto, Kazuhiko; Bosserhoff, Anja Katrin; Kuniyasu, Hiroki
• Author Heading: Kurihara, Miyako; Kirita, Tadaaki; Sasahira, Tomonori; Ohmori, Hitoshi; Matsushima, Sayako; Yamamoto, Kazuhiko; Bosserhoff, Anja Katrin; Kuniyasu, Hiroki
• Publication, Distribution, etc.: Nature Publishing
• Publication Date: 2013-04-16
• Publication Date (W3CDTF): 2013-04-16
• Alternative Title: 口腔扁平上皮癌におけるmelanoma inhibitory activity 2 (MIA2)の腫瘍促進性
• Periodical title: British journal of cancer
• No. or year of volume/issue: 108 7
• Volume: 108
• Issue: 7
• Pages: 1460-1469
• ISSN (Periodical Title): ISSN : 0007-0920
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2013-11-27
• Dissertation Number: 甲第605号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: apoptosis; VEGF; integrin; MAPK
• Target Audience: 一般
• Note (General): type:Thesis; The role of melanoma inhibitory activity 2 (MIA2) was examined in human oral squamous cell carcinoma (OSCC). MIA2 expression was observed in 62 (66.7%) of 93 OSCCs and was associated with tumor expansion and nodal metastasis. MIA2 expression was inversely correlated with intratumoral infiltration of lymphocytes. MIA2 expression was found in 3 human OSCC lines. Invasion and anti-apoptotic survival were reduced by MIA2 knockdown in HSC3 cells. The number of MOLT-3 lymphocytes infiltrating the HSC3 cell layer was increased by MIA2 knockdown or MIA2 depletion by MIA2 knockdown and absorption with the antibody. In HSC3 cells, MIA2 knockdown decreased the expressions of vascular endothelial growth factor (VEGF), VEGF-C, VEGF-D. The downregulation of VEGF-C and -D was caused by inhibition of p38 and extracellular signal-regulated kinase (ERK)1/2, respectively. MIA2 was coprecipitated with integrin α4 andα5 in HSC3 cells. Integrin α4 knockdown decreased p38 phosphorylation and increased apoptosis, whereas integrin α5 knockdown decreased c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis. Inhibition of JNK decreased apoptosis in the HSC3 cells. These findings suggest that the roles of MIA2 might be based on the variety of the integrins and the subtypes of mitogen-activated protein kinase.; 博士（医学）・甲第605号・平成25年11月27日; identifier:British journal of cancer Vol.108 No.7 p.1460-1469; identifier:00070920; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/2670; identifier:British journal of cancer, 108(7): 1460-1469
• Source: fulltext; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2670/1/01%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2670/2/02%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2670/3/03%e6%9c%ac%e6%96%87.pdf
• Access Restrictions: インターネット公開
• Periodical Title (NCID): AA00574355; https://ci.nii.ac.jp/ncid/AA00574355
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU