2016 Fiscal Year Final Research Report
Development of early diagnostic method and order-made immunotherapy for oral cancer by using anti-tumor T cells
| Project/Area Number |
24249091
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
豊嶋 健史 九州大学, 歯学研究科(研究院), 研究員 (20546569)
吉田 裕樹 佐賀大学, 医学部, 教授 (40260715)
山田 亮 久留米大学, 付置研究所, 教授 (50158177)
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| Project Period (FY) |
2012-04-01 – 2017-03-31
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| Keywords | オーダーメイド免疫療法 / 口腔扁平上皮癌 / RCAS1 / PD-L1 / 腫瘍会合性マクロファージ |
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| Outline of Final Research Achievements |
Receptor-binding cancer antigen expressed on SiSo cell (RCAS1) is derived from uterine adenocarcinoma and can induce apoptosis in lymphocytes. In this study, we investigated expression patterns of RCAS1 and the effect on apoptosis in oral squamous cell carcinoma (OSCC). RCAS1 mRNA and proteins were expressed in all of OSCC cell lines. Membranous pattern were expressed in all cell lines, while soluble pattern was detected in all supernatants. RCAS1 mRNA, membranous and soluble RCAS1 were significantly seen in SQUU-B more than the other 3 cell lines. K562 apoptosis was induced in co-culture with each of all cell lines, particularly with SQUU-B. Apoptosis was markedly reduced in co-culture with RCAS1 knockdown cells, but was induced in co-culture without cell contract of SQUU-B. Our study suggests that RCAS1 has an apoptotic function via membranous/soluble expression pattern in OSCC cells. RCAS1 may thus affect tumor escape from immune surveillance in OSCC by inducing apoptosis.
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| Free Research Field |
口腔外科学
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