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Tumor necrosis factor-α-induced apoptosis of gastric cancer MKN28 cells: accelerated degradation of the inhibitor of apoptosis family members.
Arch Biochem Biophys. 2015 Jan 15; 566:43-8.AB

Abstract

The role of the inhibitor of apoptosis (IAP) family members in tumor necrosis factor-α (TNF-α)-induced apoptosis of human gastric cancer MKN28 cells was explored. TNF-α induced up-regulation of cIAP2, whereas cycloheximide (CHX) induced down-regulation of XIAP and survivin. Degradation of cIAP1 and XIAP, but not survivin, was accelerated by co-treatment of cells with TNF-α and CHX, and TNF-α-induced up-regulation of cIAP2 was inhibited by BMS-345541 (NF-κB inhibitor). Treatment of MKN28 cells with TNF-α plus CHX induced degradation of survivin and activation of caspase-8 and -3, followed by degradation of cIAP1 and XIAP and apoptosis. Proteasome inhibitors (MG132 and epoxomicin) suppressed TNF-α plus CHX-induced degradation of survivin, cIAP1, and XIAP as well as apoptosis. A caspase inhibitor (z-VAD-fmk) suppressed TNF-α plus CHX-induced apoptosis, but allowed degradation of survivin, cIAP1 and XIAP. TNF-α receptor 1 and 2 were expressed on MKN28 cells. The magnitude of apoptosis induced by TNF-α plus BMS-345541 was much less than that induced by TNF-α plus CHX. These findings suggest that TNF-α plus CHX-induced apoptosis of gastric cancer MKN28 cells may be caused by accelerated degradation of the IAP family members (survivin, cIAP1, and XIAP), in addition to inhibition of NF-κB-dependent synthesis of anti-apoptotic molecules.

Authors+Show Affiliations

Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan. Electronic address: icam-s@koto.kpu-m.ac.jp.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan. Electronic address: shiozaki@koto.kpu-m.ac.jp.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kajii-cho, Kamigyo-ku, Kyoto 602-8566, Japan.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25513960

Citation

Kitagawa, Maki, et al. "Tumor Necrosis Factor-α-induced Apoptosis of Gastric Cancer MKN28 Cells: Accelerated Degradation of the Inhibitor of Apoptosis Family Members." Archives of Biochemistry and Biophysics, vol. 566, 2015, pp. 43-8.
Kitagawa M, Shiozaki A, Ichikawa D, et al. Tumor necrosis factor-α-induced apoptosis of gastric cancer MKN28 cells: accelerated degradation of the inhibitor of apoptosis family members. Arch Biochem Biophys. 2015;566:43-8.
Kitagawa, M., Shiozaki, A., Ichikawa, D., Nakashima, S., Kosuga, T., Konishi, H., Komatsu, S., Fujiwara, H., Okamoto, K., & Otsuji, E. (2015). Tumor necrosis factor-α-induced apoptosis of gastric cancer MKN28 cells: accelerated degradation of the inhibitor of apoptosis family members. Archives of Biochemistry and Biophysics, 566, 43-8. https://doi.org/10.1016/j.abb.2014.12.003
Kitagawa M, et al. Tumor Necrosis Factor-α-induced Apoptosis of Gastric Cancer MKN28 Cells: Accelerated Degradation of the Inhibitor of Apoptosis Family Members. Arch Biochem Biophys. 2015 Jan 15;566:43-8. PubMed PMID: 25513960.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Tumor necrosis factor-α-induced apoptosis of gastric cancer MKN28 cells: accelerated degradation of the inhibitor of apoptosis family members. AU - Kitagawa,Maki, AU - Shiozaki,Atsushi, AU - Ichikawa,Daisuke, AU - Nakashima,Shingo, AU - Kosuga,Toshiyuki, AU - Konishi,Hirotaka, AU - Komatsu,Shuhei, AU - Fujiwara,Hitoshi, AU - Okamoto,Kazuma, AU - Otsuji,Eigo, Y1 - 2014/12/13/ PY - 2014/09/23/received PY - 2014/11/09/revised PY - 2014/12/04/accepted PY - 2014/12/17/entrez PY - 2014/12/17/pubmed PY - 2015/3/20/medline KW - Apoptosis KW - Gastric cancer KW - Inhibitor of apoptosis KW - Tumor necrosis factor-α SP - 43 EP - 8 JF - Archives of biochemistry and biophysics JO - Arch Biochem Biophys VL - 566 N2 - The role of the inhibitor of apoptosis (IAP) family members in tumor necrosis factor-α (TNF-α)-induced apoptosis of human gastric cancer MKN28 cells was explored. TNF-α induced up-regulation of cIAP2, whereas cycloheximide (CHX) induced down-regulation of XIAP and survivin. Degradation of cIAP1 and XIAP, but not survivin, was accelerated by co-treatment of cells with TNF-α and CHX, and TNF-α-induced up-regulation of cIAP2 was inhibited by BMS-345541 (NF-κB inhibitor). Treatment of MKN28 cells with TNF-α plus CHX induced degradation of survivin and activation of caspase-8 and -3, followed by degradation of cIAP1 and XIAP and apoptosis. Proteasome inhibitors (MG132 and epoxomicin) suppressed TNF-α plus CHX-induced degradation of survivin, cIAP1, and XIAP as well as apoptosis. A caspase inhibitor (z-VAD-fmk) suppressed TNF-α plus CHX-induced apoptosis, but allowed degradation of survivin, cIAP1 and XIAP. TNF-α receptor 1 and 2 were expressed on MKN28 cells. The magnitude of apoptosis induced by TNF-α plus BMS-345541 was much less than that induced by TNF-α plus CHX. These findings suggest that TNF-α plus CHX-induced apoptosis of gastric cancer MKN28 cells may be caused by accelerated degradation of the IAP family members (survivin, cIAP1, and XIAP), in addition to inhibition of NF-κB-dependent synthesis of anti-apoptotic molecules. SN - 1096-0384 UR - https://www.unboundmedicine.com/medline/citation/25513960/Tumor_necrosis_factor_α_induced_apoptosis_of_gastric_cancer_MKN28_cells:_accelerated_degradation_of_the_inhibitor_of_apoptosis_family_members_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0003-9861(14)00405-6 DB - PRIME DP - Unbound Medicine ER -