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TRAIL and doxorubicin combination enhances anti-glioblastoma effect based on passive tumor targeting of liposomes

Guo, Liangran, Fan, Li, Pang, Zhiqing, Ren, Jinfen, Ren, Yulong, Li, Jingwei, Chen, Jie, Wen, Ziyi, Jiang, Xinguo·2011·Journal of Controlled Release

Abstract

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a novel anticancer agent for glioblastoma multiforme (GBM). Some GBM cell lines, however, are relatively resistant to TRAIL. Doxorubicin (DOX) can sensitize GBM cells to TRAIL-induced apoptosis, indicating that the combination of DOX and TRAIL may be an effective strategy to kill TRAIL-resistant GBM cells. However, the therapeutic effect is limited by the short serum half-life of TRAIL, chronic cardiac toxicity of DOX, multidrug resistance (MDR) property of GBM cells and poor drug delivery across the blood-brain barrier (BBB). To solve such problems, combination treatment of TRAIL liposomes (TRAIL-LP) and DOX liposomes (DOX-LP) were developed for the first time. The in vitro cytotoxicity study indicated that DOX-LP sensitized GBM cell line U87MG but not normal bovine caruncular epithelial cells (BCECs) to TRAIL-LP-induced apoptosis, demonstrating the safety of the combination treatment. This sensitization was accompanied by up-regulation of death receptor 5 (DR5) expression and caspase activation. Furthermore, the combination therapy of TRAIL-LP and DOX-LP displayed stronger anti-GBM effect than free drugs or liposomal drugs alone in vivo. In summary, the combination treatment reported here showed improved therapeutic effect on GBM. Therefore, it has good potential to become a new therapeutic approach for patients with GBM.

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Research works printed but not linked: 45

  1. Jain, 2007, Angiogenesis in brain tumours, Nat. Rev. Neurosci., 8, 610, 10.1038/nrn2175 · DOI
  2. Holoch, 2009, TNF-related apoptosis-inducing ligand (TRAIL): a new path to anti-cancer therapies, Eur. J. Pharmacol., 625, 63, 10.1016/j.ejphar.2009.06.066 · DOI
  3. Kruyt, 2008, TRAIL and cancer therapy, Cancer Lett., 263, 14, 10.1016/j.canlet.2008.02.003 · DOI
  4. Frese, 2006, Cardiac glycosides initiate Apo2L/TRAIL-induced apoptosis in non-small cell lung cancer cells by up-regulation of death receptors 4 and 5, Cancer Res., 66, 5867, 10.1158/0008-5472.CAN-05-3544 · DOI
  5. Kelley, 2001, Preclinical studies to predict the disposition of Apo2L/tumor necrosis factor-related apoptosis-inducing ligand in humans: characterization of in vivo efficacy, pharmacokinetics, and safety, J. Pharmacol. Exp. Ther., 29, 31, 10.1016/S0022-3565(24)29298-3 · DOI
  6. Ashkenazi, 1999, Safety and antitumor activity of recombinant soluble Apo2 ligand, J. Clin. Invest., 104, 155, 10.1172/JCI6926 · DOI · Paper page
  7. Fesik, 2005, Promoting apoptosis as a strategy for cancer drug discovery, Nat. Rev. Cancer, 5, 876, 10.1038/nrc1736 · DOI
  8. Nagane, 2000, Increased death receptor 5 expression by chemotherapeutic agents in human gliomas causes synergistic cytotoxicity with tumor necrosis factor-related apoptosis-inducing ligand in vitro and in vivo, Cancer Res., 60, 847
  9. Jin, 2009, Genistein enhances TRAIL-induced apoptosis through inhibition of p38 MAPK signaling in human hepatocellular carcinoma Hep3B cells, Chem. Biol. Interact., 180, 143, 10.1016/j.cbi.2009.03.020 · DOI
  10. Park, 2002, Regulation of Akt by EGF-R inhibitors, a possiblemechanism of EGF-R inhibitor-enhanced TRAIL-induced apoptosis, Biochem. Biophys. Res. Commun., 295, 515, 10.1016/S0006-291X(02)00719-2 · DOI
  11. Ding, 2010, Synergistic antitumor effect of TRAIL in combination with sunitinib in vitro and in vivo, Cancer Lett., 293, 158, 10.1016/j.canlet.2010.01.005 · DOI
  12. Nozawa, 2004, The combination of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) and genistein is effective in inhibiting pancreatic cancer growth, Pancreas, 29, 45, 10.1097/00006676-200407000-00055 · DOI
  13. Clawson, 2010, Triptolide and TRAIL combination enhances apoptosis in cholangiocarcinoma, J. Surg. Res., 163, 244, 10.1016/j.jss.2010.03.067 · DOI
  14. Singh, 2003, Synergistic interactions of chemotherapeutic drugs and tumor necrosis factor-related apoptosis-inducing ligand/Apo-2 ligand on apoptosis and on regression of breast carcinoma in vivo, Cancer Res., 63, 5390
  15. Wang, 2010, TRAIL and doxorubicin combination induces proapoptotic and antiangiogenic effects in soft tissue sarcoma in vivo, Clin. Cancer Res., 16, 2591, 10.1158/1078-0432.CCR-09-2443 · DOI
  16. Kelley, 2004, Targeting death receptors in cancer with Apo2L/TRAIL, Curr. Opin. Pharmacol., 4, 333, 10.1016/j.coph.2004.02.006 · DOI
  17. Neuwelt, 2004, Mechanisms of disease: the blood-brain barrier, Neurosurgery, 54, 131, 10.1227/01.NEU.0000097715.11966.8E · DOI
  18. Fabel, 2001, Long-term stabilization in patients with malignant glioma after treatment with liposomal doxorubicin, Cancer, 92, 1936, 10.1002/1097-0142(20011001)92:7<1936::AID-CNCR1712>3.0.CO;2-H · DOI
  19. Siegal, 1995, Doxorubicin encapsulated in sterically stabilized liposomes for the treatment of a brain tumor model biodistribution and therapeutic efficacy, J. Neurosurg., 83, 1029, 10.3171/jns.1995.83.6.1029 · DOI · Paper page
  20. Han, 2007, Enhanced circulation time and antitumor activity of doxorubicin by comblike polymer-incorporated liposomes, J. Control. Release, 120, 161, 10.1016/j.jconrel.2007.03.020 · DOI
  21. Kok, 2009, Esculetin enhances TRAIL-induced apoptosis through DR5 upregulation in human oral cancer SAS cells, Oral. Oncol., 45, 1067, 10.1016/j.oraloncology.2009.07.018 · DOI
  22. Lee, 2008, Essential roles of caspases and their upstream regulators in rotenone-induced apoptosis, Biochem. Biophys. Res. Commun., 371, 33, 10.1016/j.bbrc.2008.03.149 · DOI
  23. Zhan, 2010, Cyclic RGD conjugated poly(ethylene glycol)-co-poly(lactic acid) micelle enhances paclitaxel anti-glioblastoma effect, J. Control. Release, 143, 136, 10.1016/j.jconrel.2009.12.020 · DOI
  24. Kim, 2008, Arsenic trioxide sensitizes human glioma cells, but not normal astrocytes, to TRAIL-induced apoptosis via CCAAT/enhancer-binding protein homologous protein-dependent DR5 up-regulation, Cancer Res., 68, 266, 10.1158/0008-5472.CAN-07-2444 · DOI
  25. Shankar, 2005, Effects of sequential treatments with chemotherapeutic drugs followed by TRAIL on prostate cancer in vitro and in vivo, Prostate, 62, 165, 10.1002/pros.20126 · DOI
  26. Zhang, 2000, Differential localization and regulation of death and decoy receptors for TNF-related apoptosis-inducing ligand (TRAIL) in human melanoma cells, J. Immunol., 164, 3961, 10.4049/jimmunol.164.8.3961 · DOI
  27. Song, 2008, ABT-737 induces expression of the death receptor 5 and sensitizes human cancer cells to TRAIL-induced apoptosis, J. Biol. Chem., 283, 25003, 10.1074/jbc.M802511200 · DOI
  28. Guan, 2001, Evidence that the death receptor DR4 is a DNA damage-inducible, p53-regulated gene, J. Cell Physiol., 188, 98, 10.1002/jcp.1101 · DOI
  29. Voelkel-Johnson, 2002, Resistance of prostate cancer cells to soluble TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) can be overcome by doxorubicin or adenoviral delivery of full-length TRAIL, Cancer Gene. Ther., 9, 164, 10.1038/sj.cgt.7700420 · DOI
  30. Batist, 2001, Reduced cardiotoxicity and preserved antitumor efficacy of liposome-encapsulated doxorubicin and cyclophosphamide compared with conventional doxorubicin and cyclophosphamide in a randomized, multicenter trial of metastatic breast cancer, J. Clin. Oncol., 19, 1444, 10.1200/JCO.2001.19.5.1444 · DOI
  31. Rahman, 1990, A phase I clinical trial and pharmacokinetic evaluation of liposome-encapsulated doxorubicin, J. Clin. Oncol. S, 1093, 10.1200/JCO.1990.8.6.1093 · DOI
  32. Cowens, 1990, Phase I study of doxorubicin encapsulated in liposomes, Proc. Am. Soc. Clin. Oncol., 9, 87
  33. Gabizon, 1989, Systemic administration of doxorubicin-containing liposomes in cancer patients: a phase I study, Eur. J. Cancer Clin. Oncol., 25, 1795, 10.1016/0277-5379(89)90350-7 · DOI
  34. Singal, 1998, Doxorubicin-induced cardiomyopathy, N. Engl. J. Med., 339, 900, 10.1056/NEJM199809243391307 · DOI
  35. Secchiero, 2004, Evidence for a proangiogenic activity of TNF-related apoptosis-inducing ligand, Neoplasia, 6, 364, 10.1593/neo.03421 · DOI
  36. Zauli, 2003, Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sequentially upregulates nitric oxide and prostanoid production in primary human endothelial cells, Circ. Res., 92, 732, 10.1161/01.RES.0000067928.83455.9C · DOI
  37. Liu, 2004, Death receptor regulation and celecoxib-induced apoptosis in human lung cancer cells, J. Natl. Cancer Inst., 96, 1769, 10.1093/jnci/djh322 · DOI
  38. Nakata, 2004, Histone deacetylase inhibitors upregulate death receptor 5/TRAIL-R2 and sensitize apoptosis induced by TRAIL/APO2-L in human malignant tumor cells, Oncogene, 23, 6261, 10.1038/sj.onc.1207830 · DOI
  39. Horak, 2005, Contribution of epigenetic silencing of tumor necrosis factor-related apoptosis inducing ligand receptor 1 (DR4) to TRAIL resistance and ovarian cancer, Mol. Cancer Res., 3, 335, 10.1158/1541-7786.MCR-04-0136 · DOI
  40. Zhang, 2008, TRAIL resistance of breast cancer cells is associated with constitutive endocytosis of death receptors 4 and 5, Mol. Cancer Res., 6, 1861, 10.1158/1541-7786.MCR-08-0313 · DOI
  41. Bai, 2005, Predominant Bcl-XL knockdown disables antiapoptotic mechanisms: tumor necrosis factor-related apoptosis-inducing ligand-based triple chemotherapy overcomes chemoresistance in pancreatic cancer cells in vitro, Cancer Res., 65, 2344, 10.1158/0008-5472.CAN-04-3502 · DOI
  42. Chawla-Sarker, 2004, Downregulation of Bcl-2, FLIP or IAPs (XIAP and survivin) by siRNAs sensitizes resistant melanoma cells to Apo2L/TRAIL-induced apoptosis, Cell Death Differ., 11, 915, 10.1038/sj.cdd.4401416 · DOI
  43. Monsky, 1999, Augmentation of transvascular transport of macromolecules and nanoparticles in tumors using vascular endothelial growth factor, Cancer Res., 59, 4129
  44. Yuan, 1994, Vascular permeability and microcirculation of gliomas and mammary carcinomas transplanted in rat and mouse cranial windows, Cancer Res., 54, 4564
  45. Juillerat-Jeanneret, 2008, The targeted delivery of cancer drugs across the blood–brain barrier: chemical modifications of drugs or drug-nanoparticles?, Drug Discov. Today, 13, 1099, 10.1016/j.drudis.2008.09.005 · DOI

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Metadata

Authors
Guo, L., Fan, L., Pang, Z., Ren, J., Ren, Y., Li, J., Chen, J., Wen, Z., & Jiang, X.
Venue
Journal of Controlled Release
Publisher
Elsevier BV
Published
2011-08
Volume
154
Issue
1
Pages
93-102
ISSN
0168-3659
Cited by
75
References
2
Language
en

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