| Project/Area Number |
16K14610
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Tumor biology
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| Research Institution | Kagawa University |
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Principal Investigator |
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| Research Collaborator |
NISHIYAMA Akira
YASUDA Jun
YACHIDA Shinichi
KIYOMOTO Hideyasu
MASAKI Tsutomu
YUZAWA Yukio
TAKAI Shinji
TAKAHASHI Kazuo
YAMAGUCHI Hisateru
FUJISAWA Yoshihide
YAMAZAKI Daisuke
RAHMAN Asadur
FUJIMORI Takayuki
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | (プロ)レニン受容体 / 膵臓がん / ゲノム不安定性 / 発がん / クロマチンリモデリング / （P)RR / 癌 / ゲノム |
|---|
| Outline of Final Research Achievements |
The aim of this study is to elucidate whether (pro)renin receptor [(P)RR] is involved in the genesis of pancreatic ductal adenocarcinoma (PDAC). Human whole-genome analysis revealed that aberrant (P)RR expression induced massive chromosomal rearrangements and enhanced the total number of somatic mutations at the global level in human pancreatic ductal epithelial (HPDE) cells, which are capable of transforming into PDAC. (P)RR-expressing HPDE cell population engrafted into the renal subcapsules of immunodeficient mice showed the biological characters of malignant tumour such as atypical cells including abnormal nuclear shapes. (P)RR overexpression also resulted in the failure of genomic stability pathways such as DNA replication, DNA repair and telomere maintenance. In conclusion, our findings demonstrate that aberrant (P)RR expression induces genomic instability by the disorder of genomic stability pathways.
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