Prolyl oligopeptidase participates in the cytosine arabinoside-induced nuclear translocation of glyceraldehyde 3-phosphate dehydrogenase in a human neuroblastoma cell line
| Autor: | Satoshi Tanaka, Ai Shiokawa, Miyuki Kanazawa, Fumi Kikyo, Minoru Sakaguchi, Shiori Ikeguchi, Rie Kondo, Mika Mitsumori, Yui Yamada, Mika Bando, Ryota Nishiuchi |
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| Rok vydání: | 2021 |
| Předmět: |
Programmed cell death
genetic structures Proline Cell Survival Biophysics Oligopeptidase Dehydrogenase behavioral disciplines and activities Biochemistry chemistry.chemical_compound stomatognathic system Glyceraldehyde Neuroblastoma medicine Tumor Cells Cultured Humans Enzyme Inhibitors Cytotoxicity Molecular Biology Glyceraldehyde 3-phosphate dehydrogenase Cell Nucleus biology Cell Death Chemistry Cytarabine food and beverages Glyceraldehyde-3-Phosphate Dehydrogenases Cell Biology medicine.disease Molecular biology carbohydrates (lipids) Blot biology.protein Thiazolidines Prolyl Oligopeptidases |
| Zdroj: | Biochemical and biophysical research communications. 572 |
| ISSN: | 1090-2104 |
| Popis: | Previously, we reported that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) is a binding partner of prolyl oligopeptidase (POP) in neuroblastoma NB-1 cells and that the POP inhibitor, SUAM-14746, inhibits cytosine arabinoside (Ara-C)-induced nuclear translocation of GAPDH and protects against Ara-C cytotoxicity. To carry out a more in-depth analysis of the interaction between POP and GAPDH, we generated POP-KO NB-1 cells and compared the nuclear translocation of GAPDH after Ara-C with or without SUAM-14746 treatment to wild-type NB-1 cells by western blotting and fluorescence immunostaining. Ara-C did not induce the nuclear translocation of GAPDH and SUAM-14746 did not protect against Ara-C cytotoxicity in POP-KO cells. These results indicate that the anticancer effects of Ara-C not only include the commonly known antimetabolic effects, but also the induction of cell death by nuclear transfer of GAPDH through interaction with POP. |
| Databáze: | OpenAIRE |
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