2017 Fiscal Year Final Research Report
The regulation for laminin receptor expression of prostate cancer during EMT-MET process
Project/Area Number |
15K20067
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Urology
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Research Institution | Hirosaki University |
Principal Investigator |
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Project Period (FY) |
2015-04-01 – 2018-03-31
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Keywords | 神経周囲浸潤 / ラミニン受容体 / 上皮間葉移行 |
Outline of Final Research Achievements |
Although tumor microenvironment of highly innervated prostate considered to be laminin-rich and up-regulation of metastasis promoting laminin-binding integrin α6β1 contributed to perineural invasion (PNI) and following metastasis of prostate cancer, many papers did not consider an anti-metastatic effect of laminin-binding glycan (LNBG) on α-dystroglycan in prostate cancer (PC). Here we identified that the SDF-1-CXCR4 axis and metastasis promoting integrin α6β1 upregulation occurred during EMT responsible for enhancement of migration capacity to perineural cells and perineural invasion capacity in metastatic PC cells. We also showed that translational repression of β4GAT1 by hsa-let-7i-5p miRNA was responsible for anti-metastatic LNBG depletion occurred during EMT process. These findings suggest that the SDF-1-CXCR4 axis and regulation of laminin receptor expression occurred during EMT especially, let-7i-5p regulated LNBG synthesis might be important for PNI and PC metastasis.
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Free Research Field |
糖鎖生物学
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