Ionizing radiation enhances the therapeutic potential of TRAIL in prostate cancer in vitro and in vivo: Intracellular mechanisms.
作者： Sharmila Shankar , Thiyam Ramsing Singh , Rakesh K. Srivastava
DOI: 10.1002/PROS.20069
关键词: Cancer research 、 Propidium iodide 、 Pathology 、 FADD 、 LNCaP 、 Tumor necrosis factor alpha 、 Cancer cell 、 Bcl-2 Homologous Antagonist-Killer Protein 、 Annexin 、 Medicine 、 Apoptosis
摘要: Background We assessed the influence of sequential treatment ionizing radiation followed by tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) on intracellular mechanisms apoptosis prostate cells in vitro and vivo. Methods Prostate normal cancer were exposed to irradiation TRAIL. Four- 6-week-old athymic nude mice injected s.c. with PC-3 cells. Tumor bearing TRAIL, either alone or combination (TRAIL after 24 hr irradiation), growth, apoptosis, survival examined. Expressions death receptors, Bcl-2 family members, caspase measured Western blotting, ELISA, ribonuclease protection assay; cellularity was HE inhibition p53 performed RNA interference (RNAi) technology, annexin V/propidium iodide staining, terminal deoxynucleotidyltransferase-mediated nick end labeling assay. Results Irradiation significantly augmented TRAIL-induced through upregulation DR5, Bax, Bak, induction activation. Dominant negative FADD siRNA inhibited synergistic interaction between The pretreatment TRAIL enhanced more than single agent concurrent treatment. Furthermore, sensitized TRAIL-resistant LNCaP undergo apoptosis. xenografted activation caspase-3, Bax Bcl-2, completely eradicated established tumors mice. Conclusion The can be used as a viable option enhance therapeutic potential cancer. © 2004 Wiley-Liss, Inc.
sci-hub.se 参考文章(63)
Clemens A. Schmitt, Christine T. Rosenthal, Scott W. Lowe, Genetic analysis of chemoresistance in primary murine lymphomas Nature Medicine. ,vol. 6, pp. 1029- 1035 ,(2000) , 10.1038/79542
Gary J. Kelloff, Perspectives on Cancer Chemoprevention Research and Drug Development Advances in Cancer Research. ,vol. 78, pp. 199- 334 ,(1999) , 10.1016/S0065-230X(08)61026-X
Pascal Schneider, Jean-Luc Bodmer, Margot Thome, Kay Hofmann, Nils Holler, Jürg Tschopp, CHARACTERIZATION OF TWO RECEPTORS FOR TRAIL FEBS Letters. ,vol. 416, pp. 329- 334 ,(1997) , 10.1016/S0014-5793(97)01231-3
Heiko Stahl, Peter H. Krammer, Axel Bouchon, Henning Walczak, Tumor necrosis factor-related apoptosis-inducing ligand retains its apoptosis-inducing capacity on Bcl-2- or Bcl-xL-overexpressing chemotherapy-resistant tumor cells. Cancer Research. ,vol. 60, pp. 3051- 3057 ,(2000)
Sandhya Mandlekar, Steve Ruben, A-N. Tony Kong, Rong Yu, Jian Ni, Tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in androgen-independent prostate cancer cells. Cancer Research. ,vol. 60, pp. 2384- 2389 ,(2000)
Tatsushi Yoshida, Ayaka Maeda, Naoki Tani, Toshiyuki Sakai, Promoter structure and transcription initiation sites of the human death receptor 5/TRAIL‐R2 gene1 FEBS Letters. ,vol. 507, pp. 381- 385 ,(2001) , 10.1016/S0014-5793(01)02947-7
Dharam P. Chopra, Dean G. Tang, Arthur T. Porter, Li Li, Extended Survivability of Prostate Cancer Cells in the Absence of Trophic Factors: Increased Proliferation, Evasion of Apoptosis, and the Role of Apoptosis Proteins Cancer Research. ,vol. 58, pp. 3466- 3479 ,(1998)
Sayda M. Elbashir, Jens Harborth, Winfried Lendeckel, Abdullah Yalcin, Klaus Weber, Thomas Tuschl, Duplexes of 21-nucleotide RNAs mediate RNA interference in cultured mammalian cells Nature. ,vol. 411, pp. 494- 498 ,(2001) , 10.1038/35078107
Wafik S. El-Deiry, Albert J. Fornace, Timothy F. Burns, Gen Sheng Wu, Sally Amundson, Ying Huang, M. Saeed Sheikh, Kia S. Brooks, p53-dependent and -independent Regulation of the Death Receptor KILLER/DR5 Gene Expression in Response to Genotoxic Stress and Tumor Necrosis Factor α Cancer Research. ,vol. 58, pp. 1593- 1598 ,(1998)
Donald W. Nicholson, From bench to clinic with apoptosis-based therapeutic agents Nature. ,vol. 407, pp. 810- 816 ,(2000) , 10.1038/35037747