| Project/Area Number |
18K16333
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 55020:Digestive surgery-related
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| Research Institution | Nippon Medical School |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2021: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | PDIA3 / 肝細胞癌 / mTOR / HCC / ｍTOR / 16F16 / アポトーシス / 細胞増殖 / mTOR経路 |
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| Outline of Final Research Achievements |
Previous studies have shown that high expression of protein disulfideisomerase A3 (PDIA3) is associated with poor prognosis in hepatocellular carcinoma (HCC). In the present study, using human hepatocellular carcinoma culture lines, we showed that suppression of PDIA3 expression decreased cell growth and increased apoptosis. The results of this study suggest that PDIA3 is involved in HCC cell proliferation and suppression of apoptosis. In this study, we focused on the mTOR pathway, which plays an important role in tumor cell proliferation, and suppressed the expression of PDIA3 and investigated changes in downstream molecules. However, the results are cell line dependent and its role is still unclear.
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| Academic Significance and Societal Importance of the Research Achievements |
ヒト肝細胞癌培養株を用いた今回の研究で、PDIA3の発現がHCCの細胞増殖やアポトーシス抑制に関与していることが明らかとなった。PDIA3制御によって腫瘍の増殖抑制やアポトーシス促進が得られれば、予後改善につながる新規肝細胞癌治療薬に結び付く可能性
がある。PDIA3のmTOR経路への関与については一定の見解は得られなかったが、mTOR経路への関与を示唆する結果であり、今後のHCCにおけるPDIA3の役割のさらなる解明の一助になると考える。
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