Event Abstract

The effect of Z36 on Human T-cell Leukemia

  • 1 Department of Immunology and Parasitology, School of Medicine, Japan

Human T-cell Leukemia is aggressive and malignant blood disease. Above all, Adult T-cell Leukemia (ATL) has a very poor prognosis even with intensive chemotherapy, indicating the need for development for new drugs to treat the disease. Z36 which is BCL-XL inhibitor have been known induces autophagy. But the effect in Human T-cell Leukemia of Z36 is not reported. In this study, we demonstrate that the effect of Z36 on cell viability of Human T-cell Leukemia cell lines such as Hut 78, Hut 102, jurkat, MT-1, MT-2 and MT-4 in vitro. Z36 inhibited proliferation of all Human T-cell Leukemia cell lines with different sensitivity at 24 hr after the treatment. The effect of Z36 on Human T-cell Leukemia was restored by bafilomycin-A but not by 3-MA and choloroqine, which are known to be autophagy inhibitors. Western blot showed that Z36 induced LC3-II, which is known as a marker for autophagy. Proliferation of SiATG5-treated cells did not inhibit by Z36. These results suggest that Z36 induced autophagic cell death through ATG5 in human T-cell leukemia.

Keywords: T-cell leukemia, cell-death, Apoptosis, Autophagy, z36, cucurbitacin D

Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013.

Presentation Type: Abstract

Topic: Translational immunology and immune intervention

Citation: Nakanishi T (2013). The effect of Z36 on Human T-cell Leukemia. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00870

Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters.

The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated.

Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed.

For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions.

Received: 21 Jun 2013; Published Online: 22 Aug 2013.

* Correspondence: Dr. Tsukasa Nakanishi, Department of Immunology and Parasitology, School of Medicine, Kitakyushu, Japan, naka-t1@med.uoeh-u.ac.jp