2021 Fiscal Year Final Research Report
Functional analysis of AIP using AIP-deficient cell lines
Project/Area Number |
19K17994
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 54040:Metabolism and endocrinology-related
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Research Institution | Fukuoka University |
Principal Investigator |
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Project Period (FY) |
2019-04-01 – 2022-03-31
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Keywords | 成長ホルモン / 下垂体腺腫 |
Outline of Final Research Achievements |
arylhydrocarbon receptor-interacting protein (AIP) is the causative gene for familial pituitary adenomas. Familial pituitary adenomas are known to have large tumors and resistance to drug therapy. We generated AIP KO GH3, a genome-edited deletion of AIP in GH3, a rat growth hormone (GH)-producing pituitary tumor cell. AIP KO GH3 was screened for drugs as a model of drug resistance. The drug screening revealed that Cucurbitacin I can inhibit cell proliferation and GH secretion by suppressing Stat3 phosphorylation.
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Free Research Field |
下垂体
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Academic Significance and Societal Importance of the Research Achievements |
下垂体腺腫は頭蓋内腫瘍の中で頻度が高い腫瘍である。GHを産生する下垂体腺腫であるGH産生下垂体腺腫は手術療法に加えて薬剤治療も用いられるが薬剤治療に反応しない症例も多い。我々はStat3のリン酸化が薬剤抵抗性下垂体腺腫の機序の一つとなることを示した。Stat3のリン酸化に作用する薬剤を検討することが薬剤抵抗性下垂体腺腫の症例における新たな薬剤治療につながる可能性を示した。
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