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Allele-specific silencing of mutant p53 attenuates dominant-negative and gain-of-function activities

Iyer, Swathi V., Parrales, Alejandro, Begani, Priya, Narkar, Akshay, Adhikari, Amit S., Martinez, Luis A., Iwakuma, Tomoo·2016·Oncotarget

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Research works printed but not linked: 48

  1. McCormick, 2011, Cancer therapy based on oncogene addiction, J Surg Oncol, 103, 464, 10.1002/jso.21749 · DOI
  2. Boyes, 2014, Oncogene dependency and the potential of targeted RNAi-based anti-cancer therapy, Biochem J, 461, 1, 10.1042/BJ20140173 · DOI
  3. Levine, 2000, Surfing the p53 network, Nature, 408, 307, 10.1038/35042675 · DOI · Paper page
  4. Epstein, 1995, The spectrum of mutations at the p53 locus. Evidence for tissue-specific mutagenesis, selection of mutant alleles, and a “gain of function” phenotype, Ann N Y Acad Sci, 768, 111, 10.1111/j.1749-6632.1995.tb12115.x · DOI
  5. Iwakuma, 2009, Mutant p53 gain of oncogenic function:evidence, mechanism of action and its clinical implications, Fukuoka Igaku Zasshi, 100, 217
  6. Xie, 2013, Silencing of mutant p53 by siRNA induces cell cycle arrest and apoptosis in human bladder cancer cells, World J Surg Oncol, 11, 22, 10.1186/1477-7819-11-22 · DOI
  7. Lozano, 2008, The inherent instability of mutant p53 is alleviated by Mdm2 or p16INK4a loss, Genes Dev, 22, 1337, 10.1101/gad.1662908 · DOI · Paper page
  8. Sacchi, 2006, Mutant p53 gain of function: reduction of tumor malignancy of human cancer cell lines through abrogation of mutant p53 expression, Oncogene, 25, 304, 10.1038/sj.onc.1209026 · DOI · Paper page
  9. Leong, 2009, Mutant p53 mediates survival of breast cancer cells, Br J Cancer, 101, 1606, 10.1038/sj.bjc.6605335 · DOI · Paper page
  10. Chen, 2008, Suppression of inhibitor of differentiation 2, a target of mutant p53, is required for gain-of-function mutations, Cancer Res, 68, 6789, 10.1158/0008-5472.CAN-08-0810 · DOI
  11. Kwok, 2007, p53-R273H gains new function in induction of drug resistance through down-regulation of procaspase-3, Mol Cancer Ther, 6, 1054, 10.1158/1535-7163.MCT-06-0336 · DOI · Paper page
  12. Watanabe, 2014, V843I, a lung cancer predisposing EGFR mutation, is responsible for resistance to EGFR tyrosine kinase inhibitors, Journal of thoracic oncology, 9, 1377, 10.1097/JTO.0000000000000241 · DOI
  13. Kaspar, 2008, Single-nucleotide-specific siRNA targeting in a dominant-negative skin model, J Invest Dermatol, 128, 594, 10.1038/sj.jid.5701060 · DOI
  14. Moore, 2014, Development of allele-specific gene-silencing siRNAs for TGFBI Arg124Cys in lattice corneal dystrophy type I, Invest Ophthalmol Vis Sci, 55, 977, 10.1167/iovs.13-13279 · doi:10.1167/iovs.13-13279
  15. Paulson, 2003, Allele-specific silencing of dominant disease genes, Proc Natl Acad Sci U S A, 100, 7195, 10.1073/pnas.1231012100 · DOI · Paper page
  16. Agami, 2002, Stable suppression of tumorigenicity by virus-mediated RNA interference, Cancer Cell, 2, 243, 10.1016/S1535-6108(02)00122-8 · DOI · Paper page
  17. Lozano, 2004, Gain of function of a p53 hot spot mutation in a mouse model of Li-Fraumeni syndrome, Cell, 119, 861, 10.1016/j.cell.2004.11.006 · DOI · Paper page
  18. Rangarajan, 2014, Identification of a novel AMPK-PEA15 axis in the anoikis-resistant growth of mammary cells, Breast Cancer Res, 16, 420, 10.1186/s13058-014-0420-z · DOI
  19. Ayuso-Sacido, 2012, Genomic instability of surgical sample and cancer-initiating cell lines from human glioblastoma, Front Biosci (Landmark Ed), 17, 1469, 10.2741/3998 · DOI
  20. Birch, 1997, A detailed study of loss of heterozygosity on chromosome 17 in tumours from Li-Fraumeni patients carrying a mutation to the TP53 gene, Oncogene, 14, 865, 10.1038/sj.onc.1201041 · DOI
  21. Donehower, 2014, Effects of TP53 mutational status on gene expression patterns across 10 human cancer types, J Pathol, 232, 522, 10.1002/path.4321 · DOI
  22. Donehower, 1998, Retention of wild-type p53 in tumors from p53 heterozygous mice: reduction of p53 dosage can promote cancer formation, EMBO J, 17, 4657, 10.1093/emboj/17.16.4657 · DOI · Paper page
  23. Vogelstein, 1990, p53 gene mutations occur in combination with 17p allelic deletions as late events in colorectal tumorigenesis, Cancer Res, 50, 7717
  24. Marks, 1991, Maintenance of p53 alterations throughout breast cancer progression, Cancer Res, 51, 2605
  25. Iglehart, 1991, p53 alterations in all stages of breast cancer, J Surg Oncol, 48, 260, 10.1002/jso.2930480409 · DOI
  26. El-Deiry, 2014, Targeting tumor suppressor p53 for cancer therapy: strategies, challenges and opportunities, Current drug targets, 15, 80, 10.2174/1389450114666140106101412 · DOI · Paper page
  27. Jung, 2010, p53 inhibits tumor cell invasionthe degradation of snail protein in hepatocellular carcinoma, FEBS letters, 584, 2231, 10.1016/j.febslet.2010.04.006 · DOI
  28. Elledge, 2009, Principles of cancer therapy: oncogene and non-oncogene addiction, Cell, 136, 823, 10.1016/j.cell.2009.02.024 · DOI · Paper page
  29. Batra, 2011, Activated KrasG(1)(2)D is associated with invasion and metastasis of pancreatic cancer cells through inhibition of E-cadherin, Br J Cancer, 104, 1038, 10.1038/bjc.2011.31 · DOI
  30. Liu, 2003, Silencing of H-ras gene expression by retrovirus-mediated siRNA decreases transformation efficiency and tumorgrowth in a model of human ovarian cancer, Oncogene, 22, 5694, 10.1038/sj.onc.1206858 · DOI
  31. Xiefu, 2014, Knockdown of EGFR inhibits growth and invasion of gastric cancer cells, Cancer Gene Ther, 21, 491, 10.1038/cgt.2014.55 · DOI
  32. Strebhardt, 2004, Silencing of the HER2/neu gene by siRNA inhibits proliferation and induces apoptosis in HER2/neu-overexpressing breast cancer cells, Neoplasia, 6, 786, 10.1593/neo.04313 · DOI
  33. Kiessling, 2004, Small interfering RNA (siRNA) inhibits the expression of the Her2/neu gene, upregulates HLA class I and induces apoptosis of Her2/neu positive tumor cell lines, Int J Cancer, 108, 71, 10.1002/ijc.11497 · DOI
  34. Rotter, 2007, Transcription regulation by mutant p53, Oncogene, 26, 2202, 10.1038/sj.onc.1210294 · DOI · Paper page
  35. Lozano, 2012, p53-mediated senescence impairs the apoptotic response to chemotherapy and clinical outcome in breast cancer, Cancer Cell, 21, 793, 10.1016/j.ccr.2012.04.027 · DOI · Paper page
  36. Poon, 2004, How many mutant p53 molecules are needed to inactivate a tetramer?, Mol Cell Biol, 24, 3536, 10.1128/MCB.24.8.3536-3551.2004 · DOI · Paper page
  37. Carpizo, 2014, Small molecule compounds targeting the p53 pathway: are we finally making progress?, Apoptosis, 19, 1055, 10.1007/s10495-014-0990-3 · DOI · Paper page
  38. Wiman, 2014, Mutant p53 reactivation by small molecules makes its way to the clinic, FEBS letters, 588, 2622, 10.1016/j.febslet.2014.04.017 · DOI · Paper page
  39. Fang, 2014, Development of synthetic lethality anticancer therapeutics, J Med Chem, 57, 7859, 10.1021/jm500415t · DOI
  40. Saini, 2012, RNA interference therapeutics for cancer: challenges and opportunities (review), Mol Med Rep, 6, 9
  41. Fogal, 2012, Targeted tumor-penetrating siRNA nanocomplexes for credentialing the ovarian cancer oncogene ID4, Sci Transl Med, 4, 147ra112
  42. He, 2014, Enhanced gene delivery efficiency of cationic liposomes coated with PEGylated hyaluronic acid for anti P-glycoprotein siRNA: A potential candidate for overcoming multi-drug resistance, International journal of pharmaceutics, 477, 590, 10.1016/j.ijpharm.2014.11.012 · DOI
  43. Harashima, 2014, “Programmed packaging” for gene delivery, J Control Release, 193, 316, 10.1016/j.jconrel.2014.04.023 · DOI
  44. Wang, 2008, Targeting the MDM2-p53 interaction for cancer therapy, Clin Cancer Res, 14, 5318, 10.1158/1078-0432.CCR-07-5136 · DOI · Paper page
  45. Rusin, 2013, Nutlin-3a, an MDM2 antagonist and p53 activator, helps to preserve the replicative potential of cancer cells treated with a genotoxic dose of resveratrol, Molecular biology reports, 40, 5013, 10.1007/s11033-013-2602-7 · DOI
  46. Iwakuma, 2010, CD117 and Stro-1 Identify Osteosarcoma Tumor-Initiating Cells Associated with Metastasis and Drug Resistance, Cancer Res, 70, 4602, 10.1158/0008-5472.CAN-09-3463 · DOI · Paper page
  47. Lee, 2009, Combined integrin phosphoproteomic analyses and small interfering RNA--based functional screening identify key regulators for cancer cell adhesion and migration, Cancer Res, 69, 3713, 10.1158/0008-5472.CAN-08-2515 · DOI
  48. Wagner, 2004, Cell cycle arrest and cell death are controlled by p53-dependent and p53-independent mechanisms in Tsg101-deficient cells, J Biol Chem, 279, 35984, 10.1074/jbc.M400408200 · DOI

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Metadata

Authors
Iyer, S. V., Parrales, A., Begani, P., Narkar, A., Adhikari, A. S., Martinez, L. A., & Iwakuma, T.
Affiliations
  • Department of Cancer Biology, The University of Kansas Cancer Center, University of Kansas Medical Center, Kansas City, KS, USA
  • Center for Advanced Preclinical Research, Center for Cancer Research, National Cancer Institute, Frederick, MD, USA
  • Department of Pathology, Stony Brook School of Medicine, Stony Brook, NY, USA
Venue
Oncotarget
Published
2015-12-16
Volume
7
Issue
5
Pages
5401-5415
ISSN
1949-2553
Cited by
28
References
8
Language
en

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CoChat. (2026). Citation check: Allele-specific silencing of mutant p53 attenuates dominant-negative and gain-of-function activities. https://app.cochat.ai/papers/10.18632/oncotarget.6634
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Iyer, S. V., Parrales, A., Begani, P., Narkar, A., Adhikari, A. S., Martinez, L. A., & Iwakuma, T. (2016). Allele-specific silencing of mutant p53 attenuates dominant-negative and gain-of-function activities. Oncotarget. https://doi.org/10.18632/oncotarget.6634

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