Inhibition of PAI-1 limits chemotherapy resistance of lung cancer through suppressing myofibroblasts characteristic of cancer-associated fibroblasts.
| Project/Area Number |
15K19419
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Hiroshima University |
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Principal Investigator |
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| Research Collaborator |
Namba Masashi
Nakashima Taku
Hattori Noboru
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 肺癌 / 癌関連線維芽細胞 / PAI-1 / 筋線維芽細胞 / 化学療法 |
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| Outline of Final Research Achievements |
Plasminogen activator inhibitor-1 (PAI-1) is associated with the differentiation of fibroblast into myofibroblasts (MF). Fibroblasts in the tumor stroma are called cancer-associated fibroblasts (CAFs). CAFs with MF phenotype promote chemotherapy resistance. Here, we investigated whether inhibition of PAI-1 suppresses the MF phenotype of CAFs and results in increased chemosensitivity in lung cancer. We found that PAI-1 inhibition in CAFs co-cultured with lung cancer cells increased the effects of chemotherapy. Our data suggest that inhibition of PAI-1 increases the chemosensitivity of lung cancer cells by suppressing the MF phenotype of CAFs. Hence, PAI-1 might be a promising therapeutic target for patients with chemoresistant lung cancer with CAFs.
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Report
(4 results)
Research Products
(22 results)
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[Journal Article] Comparative Study of Circulating MMP-7, CCL18, KL-6, SP-A, and SP-D as Disease Markers of Idiopathic Pulmonary Fibrosis.2016
Author(s)
Hamai K, Iwamoto H, Ishikawa N, Horimasu Y, Masuda T, Miyamoto S, Nakashima T, Ohshimo S, Fujitaka K, Hamada H, Hattori N, Kohno N
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Journal Title
Dis Markers
Volume: なし
Pages: 4759040-4759040
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] MT95-4, a fully humanized antibody raised against aminopeptidase N, reduces tumor progression in a mouse model.2015
Author(s)
Akita S, Hattori N, Masuda T, Horimasu Y, Nakashima T, Iwamoto H, Fujitaka K, Miyake M, Kohno N.
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Journal Title
Cancer Sci
Volume: 106
Pages: 921-928
Related Report
Peer Reviewed
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