Analysis and regulation of parasitic metabolism by cancer cells harboring pathogenic mitochondrial DNA mutation
| Project/Area Number |
25430110
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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 |
Tumor biology
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| Research Institution | Shimane University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | ミトコンドリアDNA / 病因性変異 / 肺がん / 転移 / 寄生性がん代謝 / ATP / 乳酸トランスポーター / エネルギー代謝 / グルコース代謝 / 低酸素 / 変異 / 活性酸素種 / 寄生性代謝 / 腫瘍 |
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| Outline of Final Research Achievements |
We investigated the characteristics of mouse lung carcinoma P29mtB82M cells from the aspect of energy metabolism that produce a low level of ATP in vitro due to a frame-shift mutation in the mitochondrial ND6 gene and a missense mutation in the COI gene while show high tumor growth and metastatic potential. The results indicated that P29mtB82M cells produced a higher level of ATP in vivo through higher levels of glycolysis, lactate production via lactate transporter MCT4, parasitic metabolism, glucose uptake under hypoxic conditions, and glucose uptake via stimulation of angiogenesis. In addition, we found that knockdown of MCT4 resulted in cell death of P29mtB82M cells, implying the strategy to suppress mtDNA-regulated metastasis.
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Report
(4 results)
Research Products
(21 results)
