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A Wnt Pathway Activator Induces Apoptosis and Cell Death in Mouse Monocytic Leukemia Cells

Yoshiro Kato*, Yoshikazu Naiki, Takayuki Komatsu, Kazuko Takahashi, Jiro Nakamura*, Naoki Koide

* Division of Diabetes, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan
† Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Oncology Research 2017, 25(4), 479-483. https://doi.org/10.3727/096504016X14721731148893

Abstract

A Wnt agonist, 2-amino-4-[3,4-(methylenedioxy)benzylamino]-6-(3-methoxyphenyl) pyrimidine, is a cellpermeable pyrimidine compound that has been shown to mimic the effect of Wnt. In this study, leukemic mouse cell lines, RAW 264.7 and J774.1, were incubated with the Wnt agonist. The Wnt agonist showed cell death in the concentration of 1–10 mM. The Wnt agonist did not show inhibition of GSK-3β activity but induced β-catenin accumulation in the nucleus. The Wnt agonist showed caspase-independent cell death, but no further involvement in cell death ER stress signaling. Here we discuss the possible mechanism of Wnt agonist-induced apoptotic cell death in RAW 264.7 cells.

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APA Style
Kato, Y., Naiki, Y., Komatsu, T., Takahashi, K., Nakamura, J. et al. (2017). A wnt pathway activator induces apoptosis and cell death in mouse monocytic leukemia cells. Oncology Research, 25(4), 479-483. https://doi.org/10.3727/096504016X14721731148893
Vancouver Style
Kato Y, Naiki Y, Komatsu T, Takahashi K, Nakamura J, Koide N. A wnt pathway activator induces apoptosis and cell death in mouse monocytic leukemia cells. Oncol Res. 2017;25(4):479-483 https://doi.org/10.3727/096504016X14721731148893
IEEE Style
Y. Kato, Y. Naiki, T. Komatsu, K. Takahashi, J. Nakamura, and N. Koide, “A Wnt Pathway Activator Induces Apoptosis and Cell Death in Mouse Monocytic Leukemia Cells,” Oncol. Res., vol. 25, no. 4, pp. 479-483, 2017. https://doi.org/10.3727/096504016X14721731148893



cc Copyright © 2017 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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