2023 Fiscal Year Final Research Report
Function of SETD5 in pancreatic cancer
| Project/Area Number |
21H02458
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 43050:Genome biology-related
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| Research Institution | Tohoku University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
舟山 亮 東北大学, 医学系研究科, 准教授 (20452295)
細金 正樹 東北大学, 医学系研究科, 助教 (30734347)
中川 直 山陽小野田市立山口東京理科大学, 薬学部, 講師 (30707013)
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| Project Period (FY) |
2021-04-01 – 2024-03-31
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| Keywords | SETD5 / 抗癌剤 / 細胞増殖 / エピゲノム / 膵臓癌 |
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| Outline of Final Research Achievements |
The objective of this research plan was to elucidate the mechanism of acquiring resistance to MEK inhibitors by increasing the expression level of SETD5. However, the study plan had to be drastically changed from the original plan because SETD5 was not increased by MEK inhibitors. However, we generated SETD5-deficient cells and examined their response to drugs in vitro and their proliferative ability in vivo, and found significant differences in both. We plan to elucidate the molecular mechanism by which SETD5 affects tumor growth in the future by exploring MEK inhibitor-treated cells and tumors that have formed.
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| Free Research Field |
分子生物学
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| Academic Significance and Societal Importance of the Research Achievements |
MEK阻害薬によるSETD5の増加を認めなかったが、SETD5の欠失細胞を作製し、in vitroで薬剤に対する応答性、in vivoでの増殖能を検討した結果、いずれも有意な差を認めることができた。しかしながら、In vitro培養条件下でのTranscriptome 解析では、これらの現象を説明できる遺伝子を見出すことはできず、この増殖抑制のメカニズムの理解には、さらなる条件検討が必要であると考える。今後、MEK阻害薬処理をした細胞や、形成された腫瘍を探索することで、SETD5が腫瘍増殖に与える分子機構を明らかにすることで腫瘍増殖の新たな分子機構の理解につながると期待できる。
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