Promotion of TRAIL/Apo2L-induced apoptosis by low-dose interferon-β in human malignant melanoma cells

Akira Kazaana, Emiko Sano, Sodai Yoshimura, Kotaro Makita, Hiroyuki Hara, Atsuo Yoshino, Takuya Ueda

研究成果: Article

1 引用 (Scopus)

抄録

Interferon β (IFN-β) is considered a signaling molecule with important therapeutic potential in cancer since IFN-β-induced gene transcription mediates antiproliferation and cell death induction. Whereas, TNF-related apoptosis inducing ligand/Apo2 ligand (TRAIL/Apo2L) has emerged as a promising anticancer agent because it induces apoptosis specifically in cancer cells. In this study, we elucidated that IFN-β augments TRAIL-induced apoptosis synergistically using five human malignant melanoma cells. All of these cells were induced apoptosis by TRAIL. Whereas, the response against IFN-β was different in amelanotic cells (A375 and CRL1579) and melanotic cells (G361, SK-MEL-28, and MeWo). The responsibility of amelanotic cells against IFN-β was higher than those of melanotic cells. The synergism of IFN-β and TRAIL were correlated with the responsibilities of the cells against IFN-β. The synergistic interaction was confirmed by a combination index based on the Chou-Talalay method. The upregulation of apoptosis in amelanotic cells was caused by very low doses of IFN-β (over 0.1 IU/ml). Both of p53-mediated intrinsic pathway and Fas-related extrinsic pathway were activated by IFN-β alone and combination with TRAIL. Further, TRAIL death receptors (DR4 and DR5) were upregulated by a low-dose IFN-β (over 0.1 IU/ml) and the expression was more promoted by the combination with TRAIL. It was clarified that the upregulation of DR5 is associated with the declination of viability.

元の言語English
ジャーナルJournal of Cellular Physiology
DOI
出版物ステータスAccepted/In press - 2019 1 1
外部発表Yes

Fingerprint

TNF-Related Apoptosis-Inducing Ligand
Interferons
Melanoma
Apoptosis
Ligands
Death Domain Receptors
Cell death
Transcription
Antineoplastic Agents
Genes
Cells
Up-Regulation
TNF-Related Apoptosis-Inducing Ligand Receptors
Molecules
Neoplasms
Cell Death

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

これを引用

Kazaana, A., Sano, E., Yoshimura, S., Makita, K., Hara, H., Yoshino, A., & Ueda, T. (受理済み/印刷中). Promotion of TRAIL/Apo2L-induced apoptosis by low-dose interferon-β in human malignant melanoma cells. Journal of Cellular Physiology. https://doi.org/10.1002/jcp.28029

Promotion of TRAIL/Apo2L-induced apoptosis by low-dose interferon-β in human malignant melanoma cells. / Kazaana, Akira; Sano, Emiko; Yoshimura, Sodai; Makita, Kotaro; Hara, Hiroyuki; Yoshino, Atsuo; Ueda, Takuya.

:: Journal of Cellular Physiology, 01.01.2019.

研究成果: Article

Kazaana, Akira ; Sano, Emiko ; Yoshimura, Sodai ; Makita, Kotaro ; Hara, Hiroyuki ; Yoshino, Atsuo ; Ueda, Takuya. / Promotion of TRAIL/Apo2L-induced apoptosis by low-dose interferon-β in human malignant melanoma cells. :: Journal of Cellular Physiology. 2019.
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AU - Hara, Hiroyuki

AU - Yoshino, Atsuo

AU - Ueda, Takuya

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AB - Interferon β (IFN-β) is considered a signaling molecule with important therapeutic potential in cancer since IFN-β-induced gene transcription mediates antiproliferation and cell death induction. Whereas, TNF-related apoptosis inducing ligand/Apo2 ligand (TRAIL/Apo2L) has emerged as a promising anticancer agent because it induces apoptosis specifically in cancer cells. In this study, we elucidated that IFN-β augments TRAIL-induced apoptosis synergistically using five human malignant melanoma cells. All of these cells were induced apoptosis by TRAIL. Whereas, the response against IFN-β was different in amelanotic cells (A375 and CRL1579) and melanotic cells (G361, SK-MEL-28, and MeWo). The responsibility of amelanotic cells against IFN-β was higher than those of melanotic cells. The synergism of IFN-β and TRAIL were correlated with the responsibilities of the cells against IFN-β. The synergistic interaction was confirmed by a combination index based on the Chou-Talalay method. The upregulation of apoptosis in amelanotic cells was caused by very low doses of IFN-β (over 0.1 IU/ml). Both of p53-mediated intrinsic pathway and Fas-related extrinsic pathway were activated by IFN-β alone and combination with TRAIL. Further, TRAIL death receptors (DR4 and DR5) were upregulated by a low-dose IFN-β (over 0.1 IU/ml) and the expression was more promoted by the combination with TRAIL. It was clarified that the upregulation of DR5 is associated with the declination of viability.

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