2017 Fiscal Year Final Research Report
A novel tricellular tight junction molecule LSR in diagnosis and therapy for cancer
| Project/Area Number |
15K08350
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
幸野 貴之 札幌医科大学, 医学部, 講師 (10374563)
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| Co-Investigator(Renkei-kenkyūsha) |
KONDOH MASAO 大阪大学, 薬学部, 准教授 (50309697)
SAWADA NORIMASA 札幌医科大学, 医学部, 教授 (30154149)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 子宮内膜癌 / 膵臓癌 / LSR / 悪性化 / Hippo pathway / TEAD1/AREG / claudin-1 |
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| Outline of Final Research Achievements |
In the present study, to apply a novel tricellular tight junction molecule LSR to diagnosis and therapy for cancer, we investigated the roles and the regulated mechanisms of LSR during malignancy of endometrial cancer and pancreatic cancer by using cancer cell lines and normal human epithelial cells. Knockdown of LSR by the siRNA in cancer cell lines promoted the migration and the invasion of cancer cells via transcriptional factor TEAD1/growth factor AREG. The mechanisms in migration and invasion of cancer cells by loss of LSR, are 1) the Hippo pathway (YAP/AMOT/merin) and 2) the pathway of the increase of MMP1 via induction of tight junction molecule claudin-1. In normal human epithelial cells, knockdown of LSR induced claudin-1 expression. Taken together, loss of LSR may contribute to the malignancy of cancer via the complex mechanisms.
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| Free Research Field |
細胞生物学、病理学
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