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c-Myc, neuroblastoma

Zhenze Zhao, Xiuye Ma, Spencer D Shelton, Derek C Sung, Monica Li, Daniel Hernandez, Maggie Zhang, Michael D Losiewiz, Yidong Chen, Alexander Pertsemlidis, Xiaojie Yu, Yuanhang Liu, Liqin Du
MYCN amplification is the most common genetic alteration in neuroblastoma and plays a critical role in neuroblastoma tumorigenesis. MYCN regulates neuroblastoma cell differentiation, which is one of the mechanisms underlying its oncogenic function. We recently identified a group of differentiation-inducing microRNAs. Given the demonstrated inter-regulation between MYCN and microRNAs, we speculated that MYCN and the differentiation-inducing microRNAs might form an interaction network to control the differentiation of neuroblastoma cells...
October 15, 2016: Oncotarget
Juan C Corredor, Nicole Redding, Karen Bloté, Stephen M Robbins, Donna L Senger, John C Bell, Paul Beaudry
N-myc oncogene amplification is associated but not present in all cases of high-risk neuroblastoma (NB). Since oncogene expression could often modulate sensitivity to oncolytic viruses, we wanted to examine if N-myc expression status would determine virotherapy efficacy to high-risk NB. We showed that induction of exogenous N-myc in a non-N-myc-amplified cell line background (TET-21N) increased susceptibility to oncolytic vesicular stomatitis virus (mutant VSVΔM51) and alleviated the type I IFN-induced antiviral state...
2016: Molecular Therapy Oncolytics
Sonja Textor, Felicitas Bossler, Kai-Oliver Henrich, Moritz Gartlgruber, Julia Pollmann, Nathalie Fiegler, Annette Arnold, Frank Westermann, Nina Waldburger, Kai Breuhahn, Sven Golfier, Mathias Witzens-Harig, Adelheid Cerwenka
Natural Killer (NK) cells are innate effector cells that are able to recognize and eliminate tumor cells through engagement of their surface receptors. NKp30 is a potent activating NK cell receptor that elicits efficient NK cell-mediated target cell killing. Recently, B7-H6 was identified as tumor cell surface expressed ligand for NKp30. Enhanced B7-H6 mRNA levels are frequently detected in tumor compared to healthy tissues. To gain insight in the regulation of expression of B7-H6 in tumors, we investigated transcriptional mechanisms driving B7-H6 expression by promoter analyses...
July 2016: Oncoimmunology
Handan Kayhan, Meric Arda Esmekaya, Atiye Seda Yar Saglam, Mehmed Zahid Tuysuz, Ayşe Gulnihal Canseven, Abdullah Munci Yagci, Nesrin Seyhan
Neuroblastoma (NB) is a cancer that occurs in sympathetic nervous system arising from neuroblasts and nerve tissue of the adrenal gland, neck, chest, or spinal cord. It is an embryonal malignancy and affects infants and children. In this study, we investigated the effects of microwave (MW) radiation on apoptotic activity, cell viability, and cell cycle progression in human SH-SY5Y NB cells which can give information about MW radiation effects on neural cells covering the period from the embryonic stages to infants...
June 2016: Cell Biochemistry and Biophysics
C R Naveen, Sagar Gaikwad, Reena Agrawal-Rajput
BACKGROUND: Berberine, a plant alkaloid, has been used since many years for treatment of gastrointestinal disorders. It also shows promising medicinal use against metabolic disorders, neurodegenerative disorders and cancer; however its efficacy in neuroblastoma (NB) is poorly explored. HYPOTHESIS: EMT is important in cancer stemness and metastasis resulting in failure to differentiate; thus targeting EMT and related pathways can have clinical benefits. STUDY DESIGN: Potential of berberine was investigated for (i) neuronal differentiation and cancer stemness inhibition, (ii) underlying molecular mechanisms regulating cancer-stemness and (iii) EMT reversal...
June 15, 2016: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
Orli Yogev, Karen Barker, Arti Sikka, Gilberto S Almeida, Albert Hallsworth, Laura M Smith, Yann Jamin, Ruth Ruddle, Alexander Koers, Hannah T Webber, Florence I Raynaud, Sergey Popov, Chris Jones, Kevin Petrie, Simon P Robinson, Hector C Keun, Louis Chesler
Neuroblastoma is the most common childhood extracranial solid tumor. In high-risk cases, many of which are characterized by amplification of MYCN, outcome remains poor. Mutations in the p53 (TP53) tumor suppressor are rare at diagnosis, but evidence suggests that p53 function is often impaired in relapsed, treatment-resistant disease. To address the role of p53 loss of function in the development and pathogenesis of high-risk neuroblastoma, we generated a MYCN-driven genetically engineered mouse model in which the tamoxifen-inducible p53ER(TAM) fusion protein was expressed from a knock-in allele (Th-MYCN/Trp53(KI))...
May 15, 2016: Cancer Research
Rosemary O'Brien, Sieu L Tran, Michelle F Maritz, Bing Liu, Cheng Fei Kong, Stefania Purgato, Chen Yang, Jayne Murray, Amanda J Russell, Claudia L Flemming, Georg von Jonquieres, Hilda A Pickett, Wendy B London, Michelle Haber, Preethi H Gunaratne, Murray D Norris, Giovanni Perini, Jamie I Fletcher, Karen L MacKenzie
The RNA-binding protein dyskerin, encoded by the DKC1 gene, functions as a core component of the telomerase holoenzyme as well as ribonuclear protein complexes involved in RNA processing and ribosome biogenesis. The diverse roles of dyskerin across many facets of RNA biology implicate its potential contribution to malignancy. In this study, we examined the expression and function of dyskerin in neuroblastoma. We show that DKC1 mRNA levels were elevated relative to normal cells across a panel of 15 neuroblastoma cell lines, where both N-Myc and c-Myc directly targeted the DKC1 promoter...
June 15, 2016: Cancer Research
Li-Ling Lin, Chao-Cheng Huang, Chia-Ling Wu, Min-Tsui Wu, Wen-Ming Hsu, Jiin-Haur Chuang
Neuroblastoma (NB) is the deadliest pediatric solid tumor due to its pleomorphic molecular characteristics. In the innate immune system, toll-like receptor 3 (TLR3) recognizes viral double-stranded RNAs to initiate immune signaling. Positive TLR3 expression indicates a favorable prognosis in NB patients, and is associated with MYCN-non-amplified. However, TLR3-mediated innate immune responses remain elusive in NB. In this study, we attempted to dissect the molecular mechanism underlying TLR3-agonist polyinosinic-polycytidylic acid [poly(I:C)] treatment in NB in vivo...
July 2016: Laboratory Investigation; a Journal of Technical Methods and Pathology
Kelly Waldeck, Carleen Cullinane, Kerry Ardley, Jake Shortt, Ben Martin, Richard W Tothill, Jason Li, Ricky W Johnstone, Grant A McArthur, Rodney J Hicks, Paul J Wood
Neuroblastoma is the most common extra-cranial malignancy in childhood and accounts for ∼15% of childhood cancer deaths. Amplification of MYCN in neuroblastoma is associated with aggressive disease and predicts for poor prognosis. Novel therapeutic approaches are therefore essential to improving patient outcomes in this setting. The histone deacetylases are known to interact with N-Myc and regulate numerous cellular processes via epigenetic modulation, including differentiation. In this study, we used the TH-MYCN mouse model of neuroblastoma to investigate the antitumor activity of the pan-HDAC inhibitor, panobinostat...
July 1, 2016: International Journal of Cancer. Journal International du Cancer
Jun Li, Yue Liu, Jing-Hong Xu, Zheng-Ping Xu, Shu Zheng, Ke-Feng Ding
α-fetoprotein (AFP)-producing colorectal adenocarcinoma is rare and typically not well recognized. In the present study, 3 cases of AFP-producing colorectal cancer are described. All 3 of these cases demonstrated increased levels of blood AFP associated with disease progression. Only case 2 exhibited classical histological hepatoid features. Following immunohistochemical tissue staining, all 3 cases were observed to be positive for AFP expression. In addition, the expression of hepatocyte growth factor (HGF), c-Met receptor and the transcription factor c-Myc were identified to be associated with the expression of AFP...
January 2016: Oncology Letters
Huabo Wang, Peter Teriete, Angela Hu, Dhanya Raveendra-Panickar, Kelsey Pendelton, John S Lazo, Julie Eiseman, Toril Holien, Kristine Misund, Ganna Oliynyk, Marie Arsenian-Henriksson, Nicholas D P Cosford, Anders Sundan, Edward V Prochownik
Many oncogenic signals originate from abnormal protein-protein interactions that are potential targets for small molecule inhibitors. However, the therapeutic disruption of these interactions has proved elusive. We report here that the naturally-occurring triterpenoid celastrol is an inhibitor of the c-Myc (Myc) oncoprotein, which is over-expressed in many human cancers. Most Myc inhibitors prevent the association between Myc and its obligate heterodimerization partner Max via their respective bHLH-ZIP domains...
October 20, 2015: Oncotarget
Blake R Wilde, Donald E Ayer
Metabolic reprogramming towards aerobic glycolysis is a common feature of transformed cells and can be driven by a network of transcription factors. It is well established that c-Myc and hypoxia-inducible factor-1α (HIF-1α) contribute to metabolic reprogramming by driving the expression of glycolytic target genes. More recently, the c-Myc-related transcription factor MondoA has been shown to restrict glucose uptake and aerobic glycolysis via its induction of thioredoxin-interacting protein (TXNIP). Three recent studies demonstrate that complex and cancer type-specific interactions between c-Myc, MondoA and HIF-1α underlie metabolism, tumourigenesis and drug response...
December 1, 2015: British Journal of Cancer
L Gan, R Xiu, P Ren, M Yue, H Su, G Guo, D Xiao, J Yu, H Jiang, H Liu, G Hu, G Qing
Deregulation of the MYC oncogene produces Myc protein that regulates multiple aspects of cancer cell metabolism, contributing to the acquisition of building blocks essential for cancer cell growth and proliferation. Therefore, disabling Myc function represents an attractive therapeutic option for cancer treatment. However, pharmacological strategies capable of directly targeting Myc remain elusive. Here, we identified that 3-bromopyruvate (3-BrPA), a drug candidate that primarily inhibits glycolysis, preferentially induced massive cell death in human cancer cells overexpressing the MYC oncogene, in vitro and in vivo, without appreciable effects on those exhibiting low MYC levels...
June 9, 2016: Oncogene
Julia V Cockle, Karishma Rajani, Shane Zaidi, Timothy Kottke, Jill Thompson, Rosa Maria Diaz, Kevin Shim, Tim Peterson, Ian F Parney, Susan Short, Peter Selby, Elizabeth Ilett, Alan Melcher, Richard Vile
BACKGROUND: Systemic delivery of a complementary cDNA library expressed from the vesicular stomatitis virus (VSV) treats tumors by vaccinating against a wide range of tumor associated antigens (TAAs). For subcutaneous B16 melanomas, therapy was achieved using a specific combination of self-TAAs (neuroblastoma-Ras, cytochrome c, and tyrosinase-related protein 1) expressed from VSV. However, for intracranial B16 tumors, a different combination was therapeutic (consisting of VSV-expressed hypoxia-inducible factor [HIF]-2α, Sox-10, c-Myc, and tyrosinase-related protein 1)...
April 2016: Neuro-oncology
Brian J Altman, Annie L Hsieh, Arjun Sengupta, Saikumari Y Krishnanaiah, Zachary E Stine, Zandra E Walton, Arvin M Gouw, Anand Venkataraman, Bo Li, Pankuri Goraksha-Hicks, Sharon J Diskin, David I Bellovin, M Celeste Simon, Jeffrey C Rathmell, Mitchell A Lazar, John M Maris, Dean W Felsher, John B Hogenesch, Aalim M Weljie, Chi V Dang
The MYC oncogene encodes MYC, a transcription factor that binds the genome through sites termed E-boxes (5'-CACGTG-3'), which are identical to the binding sites of the heterodimeric CLOCK-BMAL1 master circadian transcription factor. Hence, we hypothesized that ectopic MYC expression perturbs the clock by deregulating E-box-driven components of the circadian network in cancer cells. We report here that deregulated expression of MYC or N-MYC disrupts the molecular clock in vitro by directly inducing REV-ERBα to dampen expression and oscillation of BMAL1, and this could be rescued by knockdown of REV-ERB...
December 1, 2015: Cell Metabolism
Tarek Shalaby, Michael A Grotzer
The MYC family plays essential roles during brain development and their oncogenic deregulation is implicated in the formation of embryonal neural tumors such as medulloblastomas (MB) and neuroblastoma (NB). Amplification of the MYCN is the predominant marker for aggressive NB and correlates with poor prognosis, while c-MYC overexpression is a defining feature of MB subgroups inflected with aggressive biological behavior and increased likelihood of metastasis. Not surprisingly MYC has emerged as an attractive target for pediatric neural cancer therapy...
2016: Current Cancer Drug Targets
Robert A Ross, Jeanette D Walton, Dan Han, Hong-Fen Guo, Nai-Kong V Cheung
Neuroblastoma, a malignancy of multipotent embryonic neural crest cells, is the most common extracranial solid cancer in childhood and most common cancer in infancy. Cellular phenotype has been shown to be an important determinant of the malignant potential in human neuroblastoma cells and tumors. Whereas neuroblastic (N-type) are moderately malignant and nonneuronal (S-type) cells are nonmalignant, I-type stem cells are highly tumorigenic, irrespective of N-myc amplification status. In the present study, we sought to determine which genes were overexpressed in the I-type cells which might characterize and maintain the stem cell state and/or malignancy of human neuroblastoma cancer stem cells...
September 2015: Stem Cell Research
Arnold Junior Tatsinkam, Barbara Mulloy, Christopher C Rider
Gremlin is a member of the CAN (cerberus and DAN) family of secreted BMP (bone morphogenetic protein) antagonists and also an agonist of VEGF (vascular endothelial growth factor) receptor-2. It is critical in limb skeleton and kidney development and is re-expressed during tissue fibrosis. Gremlin binds strongly to heparin and heparan sulfate and, in the present study, we sought to investigate its heparin-binding site. In order to explore a putative non-contiguous binding site predicted by computational molecular modelling, we substituted a total of 11 key arginines and lysines located in three basic residue sequence clusters with homologous sequences from cerberus and DAN (differential screening selected gene abberative in neuroblastoma), CAN proteins which lack basic residues in these positions...
August 15, 2015: Biochemical Journal
L L Wang, R Teshiba, N Ikegaki, X X Tang, A Naranjo, W B London, M D Hogarty, J M Gastier-Foster, A T Look, J R Park, J M Maris, S L Cohn, R C Seeger, S Asgharzadeh, H Shimada
BACKGROUND: MYCN amplification with subsequent MYCN protein overexpression is a powerful indicator of poor prognosis of neuroblastoma patients. Little is known regarding the prognostic significance of the homologous MYC protein expression in neuroblastoma. METHODS: Immunostaining for MYCN and MYC protein was performed on 357 undifferentiated/poorly differentiated neuroblastomas. Results were analysed with other prognostic markers. RESULTS: Sixty-seven (19%) tumours were MYCN(+), 38 (11%) were MYC(+), and one(0...
June 30, 2015: British Journal of Cancer
De-Wang Shao, Chun-Yan Yang, Bing Liu, Wei Chen, Hua Wang, Hai-Xia Ru, Min Zhang, Ying Wang
AIMS: The aim of this study was to identify potential candidates and explore the possible mechanism in congenital cataract induced by tudor domain-containing 7 (TDRD7) deficiency. METHODS: The gene expression profile GSE25812 generated from 18 samples was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between disease and normal groups were identified. Then, gene ontology and pathway enrichment analysis of DEGs were performed...
2015: Ophthalmic Research
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