Inhibition of tissue transglutaminase sensitizes TRAIL-resistant lung cancer cells through upregulation of death receptor 5

被引：28

作者：

Frese-Schaper, Manuela ^{[1
]}

Schardt, Julian A. ^{[3
]}

Sakai, Toshiyuki ^{[4
]}

Carboni, Giovanni L. ^{[2
]}

Schmid, Ralph A. ^{[2
]}

Frese, Steffen ^{[1
,2
]}

机构：

[1] Univ Bern, Dept Clin Res, CH-3010 Bern, Switzerland

[2] Univ Hosp Bern, Div Gen Thorac Surg, CH-3010 Bern, Switzerland

[3] Univ Hosp Bern, Dept Med Oncol & Haematol, CH-3010 Bern, Switzerland

[4] Kyoto Prefectural Univ Med, Grad Sch Med Sci, Dept Mol Targeting Canc Prevent, Kamigyo Ku, Kyoto 6028566, Japan

来源：

FEBS LETTERS | 2010年 / 584卷 / 13期

关键词：

Resistance to apoptosis; Tumor necrosis factor-related apoptosis-inducing ligand; Tissue transglutaminase; Death receptor 5; Lung cancer; INDUCED APOPTOSIS; LIGAND; EXPRESSION; SURVIVAL;

D O I：

10.1016/j.febslet.2010.04.072

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Tissue transglutaminase (TG2) is implicated in cellular processes such as apoptosis and cell migration. Its acyl transferase activity cross-links certain proteins, among them transcription factors were described. We show here that the TG2 inhibitor KCC009 reversed resistance to tumor necrosis factor-related apoptosis-inducing factor (TRAIL) in lung cancer cells. Sensitization required upregulation of death receptor 5 (DR5) but not of death receptor 4. Upregulation of DR5 involved the first intron of the DR5 gene albeit it was independent from p53 and nuclear factor kappa B. In conclusion, inhibition of tissue transglutaminase provides an interesting strategy for sensitization to TRAIL-induced apoptosis in p53-deficient lung cancer cells. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：2867 / 2871

页数：5

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