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Nakanishi T, Song Y, He C, et al. Relationship between triterpenoid anticancer drug resistance, autophagy, and caspase-1 in adult T-cell leukemia. PeerJ. 2016;4:e2026doi: 10.7717/peerj.2026.
Nakanishi, T., Song, Y., He, C., Wang, D., Morita, K., Tsukada, J., Kanazawa, T., & Yoshida, Y. (2016). Relationship between triterpenoid anticancer drug resistance, autophagy, and caspase-1 in adult T-cell leukemia. PeerJ, 4e2026. https://doi.org/10.7717/peerj.2026
Nakanishi, Tsukasa, et al. "Relationship between triterpenoid anticancer drug resistance, autophagy, and caspase-1 in adult T-cell leukemia." PeerJ vol. 4 (2016): e2026. doi: https://doi.org/10.7717/peerj.2026
Nakanishi T, Song Y, He C, Wang D, Morita K, Tsukada J, Kanazawa T, Yoshida Y. Relationship between triterpenoid anticancer drug resistance, autophagy, and caspase-1 in adult T-cell leukemia. PeerJ. 2016 May 12;4:e2026. doi: 10.7717/peerj.2026. eCollection 2016. PMID: 27190722; PMCID: PMC4868592.
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PeerJ. 2016 May 12;4:e2026. doi: 10.7717/peerj.2026. eCollection 2016.

Relationship between triterpenoid anticancer drug resistance, autophagy, and caspase-1 in adult T-cell leukemia.

PeerJ

Tsukasa Nakanishi, Yuan Song, Cuiying He, Duo Wang, Kentaro Morita, Junichi Tsukada, Tamotsu Kanazawa, Yasuhiro Yoshida

Affiliations

  1. Department of Immunology and Parasitology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
  2. Department of Hematology, University of Occupational and Environmental Health, Kitakyushu, Japan.
  3. Department of Clinical Laboratory, Fourth Hospital of Hebei Medical University, Shijiazhuang, China.

PMID: 27190722 PMCID: PMC4868592 DOI: 10.7717/peerj.2026

Abstract

We previously reported that the inflammasome inhibitor cucurbitacin D (CuD) induces apoptosis in human leukemia cell lines. Here, we investigated the effects of CuD and a B-cell lymphoma extra-large (Bcl-xL) inhibitor on autophagy in peripheral blood lymphocytes (PBL) isolated from adult T-cell leukemia (ATL) patients. CuD induced PBL cell death in patients but not in healthy donors. This effect was not significantly inhibited by treatment with rapamycin or 3-methyladenine (3-MA). The Bcl-xL inhibitor Z36 induced death in primary cells from ATL patients including that induced by CuD treatment, effects that were partly inhibited by 3-MA. Similarly, cell death induced by the steroid prednisolone was enhanced in the presence of Z36. A western blot analysis revealed that Z36 also promoted CuD-induced poly(ADP ribose) polymerase cleavage. Interestingly, the effects of CuD and Z36 were attenuated in primary ATL patient cells obtained upon recurrence after umbilical cord blood transplantation, as compared to those obtained before chemotherapy. Furthermore, cells from this patient expressed a high level of caspase-1, and treatment with caspase-1 inhibitor-enhanced CuD-induced cell death. Taken together, these results suggest that rescue from resistance to steroid drugs can enhance chemotherapy, and that caspase-1 is a good marker for drug resistance in ATL patients.

Keywords: ATL; Apoptosis; Autophagy; Caspase-1; Cucurbitacin D

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