| Budget Amount *help |
¥16,900,000 (Direct Cost: ¥13,000,000、Indirect Cost: ¥3,900,000)
Fiscal Year 2018: ¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥5,850,000 (Direct Cost: ¥4,500,000、Indirect Cost: ¥1,350,000)
Fiscal Year 2016: ¥6,240,000 (Direct Cost: ¥4,800,000、Indirect Cost: ¥1,440,000)
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| Outline of Final Research Achievements |
Cellular senescence is the state of essentially irreversible cell cycle arrest that can be induced by a variety of potentially oncogenic stimuli and is therefore considered to act as an important tumor suppression mechanism in vivo. On the other hand, cellular senescence also causes secretion of various inflammatory factors, which seems to contribute age-associated diseases. We have investigated that epigenetic de-regulation of genomic DNA induces the aberrant expression of non-coding RNA in senescent cells. Surprisingly, ectopic expression of non-coding RNA provokes chromosomal instability, which resulted in tumorigenesis in mice. It is therefore possible that the overexpression of non-coding RNA in old mice may eventually promotes tumorigenesis, especially in case of accidental re-initiation of cell proliferation in senescent cells. These results indicate that senescence-associated epigenetic dysregulation may contribute to transformation from benign tumor to cancer.
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