Sensitization of Gastric Cancer Cells to Irinotecan by p53 Activation
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- Zhang Shun
- Department of Gastroenterology and Minimally Invasive Surgery, Juntendo University Hospital Department of Gastroenterology Surgery, Shanghai East Hospital (East Hospital Affiliated to Tongji University)
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- Kohira Yoshinori
- Department of Gastroenterology and Minimally Invasive Surgery, Juntendo University Hospital
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- Orita Hajime
- Department of Gastroenterology and Minimally Invasive Surgery, Juntendo University Hospital
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- Ishimine Momoko
- Department of Biochemistry, Juntendo University Graduate School of Medicine
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- Kobayashi Toshiyuki
- Department of Molecular Pathogenesis, Juntendo University Graduate School of Medicine
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- Mae Buendia Chua Sharlyn
- Human Genetics Laboratory, National Institute of Genetics
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- Nakaoka Hirofumi
- Human Genetics Laboratory, National Institute of Genetics
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- Inoue Ituro
- Human Genetics Laboratory, National Institute of Genetics
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- Hino Okio
- Department of Molecular Pathogenesis, Juntendo University Graduate School of Medicine
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- Yokomizo Takehiko
- Department of Biochemistry, Juntendo University Graduate School of Medicine
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- Fukunaga Tetsu
- Department of Gastroenterology and Minimally Invasive Surgery, Juntendo University Hospital
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- Lee-Okada Hyeon-Cheol
- Department of Biochemistry, Juntendo University Graduate School of Medicine
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<p>Irinotecan (camptothecin-11 [CPT-11]) is a topoisomerase I inhibitor that has been used in the treatment of a wide spectrum of cancers including gastric cancer. Recent reports suggest that the expression of CES2, a serine hydrolase that converts irinotecan to its active compound SN-38, is regulated by the tumor-suppressor p53. In this study, we investigated whether irinotecan acted synergistically with a p53 activator nutlin-3a in human gastric cancer cells. Nutlin-3a treatment enhanced the expression of CES2 in gastric cancer cell lines with wild-type p53. However, this effect was not observed in cells with non-functional p53. Irinotecan showed synergistic antitumor effects in combination with nutlin-3a in gastric cancer cells with wild-type p53, whereas the survival of cells with non-functional p53 was not significantly affected by the presence of nutlin-3a. These results provide evidence that p53 activation can enhance the antitumor effect of irinotecan or other anticancer prodrugs activated by CES2 in gastric cancer cells through upregulation of CES2 expression.</p>
収録刊行物
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- BPB Reports
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BPB Reports 2 (6), 130-133, 2019
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390849376476855936
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- NII論文ID
- 130007940492
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- ISSN
- 2434432X
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- 本文言語コード
- en
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- データソース種別
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- JaLC
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