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Meng-Li Gu, Ya-Mei Wang, Xin-Xin Zhou, Hang-Ping Yao, Song Zheng, Zun Xiang, Feng Ji
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasm featured by activated mutations of KIT and PDGFRA. Although overall survival rates have greatly improved by the development of receptor tyrosine kinase inhibitors, most patients ultimately acquire resistance due to secondary mutations of KIT or PDGFRA. Inhibition of the histone acetyltransferases (HATs) CREB‑binding protein (CBP) and p300 results in antineoplastic effects in various cancers. To determine whether CBP/p300 can serve as an antineoplastic target for GISTs, specific short interfering RNA sequences and the selective HAT inhibitor C646 were administered to GIST882 cells...
September 12, 2016: Oncology Reports
João Vinagre, Joana Nabais, Jorge Pinheiro, Rui Batista, Rui Caetano Oliveira, António Pedro Gonçalves, Ana Pestana, Marta Reis, Bárbara Mesquita, Vasco Pinto, Joana Lyra, Maria Augusta Cipriano, Miguel Godinho Ferreira, José Manuel Lopes, Manuel Sobrinho-Simões, Paula Soares
One of the hallmarks of cancer is its unlimited replicative potential that needs a compensatory mechanism for the consequential telomere erosion. Telomerase promoter (TERTp) mutations were recently reported as a novel mechanism for telomerase re-activation/expression in order to maintain telomere length. Pancreatic endocrine tumors (PETs) were so far recognized to rely mainly on the alternative lengthening of telomeres (ALT) mechanism. It was our objective to study if TERTp mutations were present in pancreatic endocrine tumors (PET) and could represent an alternative mechanism to ALT...
2016: Scientific Reports
Steffen Heeg, Koushik K Das, Maximilian Reichert, Basil Bakir, Shigetsugu Takano, Julia Caspers, Nicole M Aiello, Katherine Wu, Albrecht Neesse, Anirban Maitra, Christine A Iacobuzio-Donahue, Philip Hicks, Anil K Rustgi
BACKGROUND & AIMS: The ETS-transcription factor ETV1 is involved in epithelial-mesenchymal transition during pancreatic development and is induced in mouse pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC). We investigated the function of ETV1 in stromal expansion of PDAC and metastasis, as well as its effects on a novel downstream target Sparc, which encodes a matricellular protein found in PDAC stroma that has been associated with invasiveness, metastasis and poor patient outcomes...
September 2016: Gastroenterology
La Ta, Chengrui Xuan, Nianzeng Xing, Xiaojun Zhu
Constitutive photomorphogenic 1 (COP1) belongs to the COP‑de-etiolated (DET)‑fusca (FUS) protein family and has been demonstrated to suppress prostate adenocarcinomas and other types of tumor, such as liver and gastric cancer. The present study investigated the expression of COP1 and its downstream factor, ets variant 1 (ETV1) in renal cell carcinoma (RCC) tissue samples, and evaluated the correlation of COP1 expression levels with the clinicopathological characteristics of RCC. In addition, the role of COP1 in the proliferation and migration of RCC ACHN cells was investigated...
August 2016: Molecular Medicine Reports
Emilio J Sanchez-Barcelo, Maria D Mediavilla, Jerry Vriend, Russel J Reiter
The ubiquitin proteasome system has been proposed as a possible mechanism involved in the multiple actions of melatonin. COP1 (constitutive photomorphogenesis protein 1), a RING finger-type ubiquitin E3 ligase formerly identified in Arabidopsis, is a central switch for the transition from plant growth underground in darkness (etiolation) to growth under light exposure (photomorphogenesis). In darkness, COP1 binds to photomorphogenic transcription factors driving its degradation via the 26S proteasome; blue light, detected by cryptochromes, and red and far-red light detected by phytochromes, negatively regulate COP1...
August 2016: Journal of Pineal Research
Makoto Okazawa, Haruka Abe, Shigetada Nakanishi
In the early postnatal period, cerebellar granule cells exhibit an activity-dependent downregulation of a set of immaturation genes involved in cell growth and migration and are shifted to establishment of a mature network formation. Through the use of a granule cell culture and both pharmacological and RNA interference (siRNA) analyses, the present investigation revealed that the downregulation of these immaturation genes is controlled by strikingly unified signaling mechanisms that operate sequentially through the stimulation of AMPA and NMDA receptors, tetrodotoxin-sensitive Na(+) channels and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII)...
May 13, 2016: Biochemical and Biophysical Research Communications
Baojin Ding, John W Cave, Paul R Dobner, Debra Mullikin-Kilpatrick, Marina Bartzokis, Hong Zhu, Chi-Wing Chow, Richard M Gronostajski, Daniel L Kilpatrick
Nuclear Factor One (NFI) transcription factors regulate temporal gene expression required for dendritogenesis and synaptogenesis via delayed occupancy of target promoters in developing cerebellar granule neurons (CGNs). Mechanisms that promote NFI temporal occupancy have not been previously defined. We show here that the transcription factor ETV1 directly binds to and is required for expression and NFI occupancy of a cohort of NFI-dependent genes in CGNs maturing in vivo. Expression of ETV1 is low in early postnatal cerebellum and increases with maturation, mirroring NFI temporal occupancy of coregulated target genes...
May 1, 2016: Molecular Biology of the Cell
Hao-Chen Wang, Tzu-Ying Li, Ying-Jui Chao, Ya-Chin Hou, Yuan-Shuo Hsueh, Kai-Hsi Hsu, Yan-Shen Shan
PURPOSE: KIT mutations, the most prevalent genetic event in gastrointestinal stromal tumors (GIST), are associated with malignant features and poor prognosis. Aggressive GISTs possess a high propensity to spread to the liver. This study aimed to explore the role of KIT mutations in GIST liver metastasis. EXPERIMENTAL DESIGN: A total of 170 GISTs were used to determine the association between KIT mutations and liver metastasis. Immunohistochemistry was performed to assess the correlation of KIT mutations with CXCR4 and ETV1 expression...
July 15, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
Dhruba Pathak, Dongxu Guan, Robert C Foehring
The action potential (AP) is a fundamental feature of excitable cells that serves as the basis for long-distance signaling in the nervous system. There is considerable diversity in the appearance of APs and the underlying repolarization mechanisms in different neuronal types (reviewed in Bean BP. Nat Rev Neurosci 8: 451-465, 2007), including among pyramidal cell subtypes. In the present work, we used specific pharmacological blockers to test for contributions of Kv1, Kv2, or Kv4 channels to repolarization of single APs in two genetically defined subpopulations of pyramidal cells in layer 5 of mouse somatosensory cortex (etv1 and glt) as well as pyramidal cells from layer 2/3...
May 1, 2016: Journal of Neurophysiology
Chandan Kumar-Sinha, Shanker Kalyana-Sundaram, Arul M Chinnaiyan
Enabled by high-throughput sequencing approaches, epithelial cancers across a range of tissue types are seen to harbor gene fusions as integral to their landscape of somatic aberrations. Although many gene fusions are found at high frequency in several rare solid cancers, apart from fusions involving the ETS family of transcription factors which have been seen in approximately 50% of prostate cancers, several other common solid cancers have been shown to harbor recurrent gene fusions at low frequencies. On the other hand, many gene fusions involving oncogenes, such as those encoding ALK, RAF or FGFR kinase families, have been detected across multiple different epithelial carcinomas...
2015: Genome Medicine
Grigory A Raskin, Kazimir M Pozharisski, Aglaya G Iyevleva, Ivan V Rikov, Rashida V Orlova, Evgeny N Imyanitov
BACKGROUND: Use of molecular assays is gradually becoming a mandatory part of the clinical management of soft tissue tumors, however the choice and the interpretation of these tests may present a challenge. SUMMARY: This report demonstrates an unusual presentation of sarcoma, which was initially diagnosed as a tumor of unknown primary site. Given the presence of vimentin, Fli-1, CD99 and S100 markers, lack of immunostaining for melan A, HMB45, MITF, synaptophysin, CD56, myf4, CKAE1/3 and WT-1, as well as the presence of EWSR1 translocation determined by a break-apart FISH assay, Ewing's sarcoma (ES) diagnosis seemed to be well justified...
September 2015: Gastrointestinal Tumors
Megan Cionni, Chelsea Menke, Rolf W Stottmann
Key facets of mammalian forebrain cortical development include the radial migration of projection neurons and subsequent cellular differentiation into layer-specific subtypes. Inappropriate regulation of these processes can lead to a number of congenital brain defects in both mouse and human, including lissencephaly and intellectual disability. The genes regulating these processes are still not all identified, suggesting genetic analyses will continue to be a powerful tool in mechanistically studying the development of the cerebral cortex...
February 2016: Mammalian Genome: Official Journal of the International Mammalian Genome Society
Rowena Suriben, Kelly A Kaihara, Magdalena Paolino, Mike Reichelt, Sarah K Kummerfeld, Zora Modrusan, Debra L Dugger, Kim Newton, Meredith Sagolla, Joshua D Webster, Jinfeng Liu, Matthias Hebrok, Vishva M Dixit
A variety of signals finely tune insulin secretion by pancreatic β cells to prevent both hyper-and hypoglycemic states. Here, we show that post-translational regulation of the transcription factors ETV1, ETV4, and ETV5 by the ubiquitin ligase COP1 (also called RFWD2) in β cells is critical for insulin secretion. Mice lacking COP1 in β cells developed diabetes due to insulin granule docking defects that were fully rescued by genetic deletion of Etv1, Etv4, and Etv5. Genes regulated by ETV1, ETV4, or ETV5 in the absence of mouse COP1 were enriched in human diabetes-associated genes, suggesting that they also influence human β-cell pathophysiology...
December 3, 2015: Cell
Gülşen Sürmeli, Daniel Cosmin Marcu, Christina McClure, Derek L F Garden, Hugh Pastoll, Matthew F Nolan
Deep layers of the medial entorhinal cortex are considered to relay signals from the hippocampus to other brain structures, but pathways for routing of signals to and from the deep layers are not well established. Delineating these pathways is important for a circuit level understanding of spatial cognition and memory. We find that neurons in layers 5a and 5b have distinct molecular identities, defined by the transcription factors Etv1 and Ctip2, and divergent targets, with extensive intratelencephalic projections originating in layer 5a, but not 5b...
December 2, 2015: Neuron
Javier C Angulo, Guillermo Andrés, Nadia Ashour, Manuel Sánchez-Chapado, Jose I López, Santiago Ropero
PURPOSE: Detection of DNA hypermethylation has emerged as a novel molecular biomarker for prostate cancer diagnosis and evaluation of prognosis. We sought to define whether a hypermethylation profile of patients with prostate cancer on androgen deprivation would predict castrate resistant prostate cancer. MATERIALS AND METHODS: Genome-wide methylation analysis was performed using a methylation cancer panel in 10 normal prostates and 45 tumor samples from patients placed on androgen deprivation who were followed until castrate resistant disease developed...
March 2016: Journal of Urology
(no author information available yet)
There is substantial heterogeneity among primary prostate cancers, evident in the spectrum of molecular abnormalities and its variable clinical course. As part of The Cancer Genome Atlas (TCGA), we present a comprehensive molecular analysis of 333 primary prostate carcinomas. Our results revealed a molecular taxonomy in which 74% of these tumors fell into one of seven subtypes defined by specific gene fusions (ERG, ETV1/4, and FLI1) or mutations (SPOP, FOXA1, and IDH1). Epigenetic profiles showed substantial heterogeneity, including an IDH1 mutant subset with a methylator phenotype...
November 5, 2015: Cell
Chengcheng Liu, Yulong Niu, Xuedong Zhou, Xin Xu, Yi Yang, Yan Zhang, Liwei Zheng
BACKGROUND: Ameloblast differentiation is the most critical stepwise process in amelogenesis, and it is controlled by precise molecular events. To better understand the mechanism controlling pre-ameloblasts (PABs) differentiation into secretory ameloblasts (SABs), a more precise identification of molecules and signaling networks will elucidate the mechanisms governing enamel formation and lay a foundation for enamel regeneration. RESULTS: We analyzed transcriptional profiles of human PABs and SABs...
2015: BMC Genomics
Bo Gun Jang, Hee Eun Lee, Woo Ho Kim
Gastrointestinal stromal tumors (GISTs) develop from interstitial cells of Cajal (ICCs) mainly by activating mutations in the KIT or PDGFRA genes. Immunohistochemical analysis for KIT, DOG1, and PKC-θ is used for the diagnosis of GIST. Recently, ETV1 has been shown to be a lineage survival factor for ICCs and required for tumorigenesis of GIST. We investigated the diagnostic value of ETV1expression in GIST. On fresh-frozen tissue samples, RT-PCR analysis showed that ETV1 as well as KIT, DOG1, and PKC-θ are highly expressed in GISTs...
October 2015: Virchows Archiv: An International Journal of Pathology
Zoulika Kherrouche, Didier Monte, Elisabeth Werkmeister, Luc Stoven, Yvan De Launoit, Alexis B Cortot, David Tulasne, Anne Chotteau-Lelievre
Various solid tumors including lung or gastric carcinomas display aberrant activation of the Met receptor which correlates with aggressive phenotypes and poor prognosis. Although downstream signaling of Met is well described, its integration at the transcriptional level is poorly understood. We demonstrate here that in cancer cells harboring met gene amplification, inhibition of Met activity with tyrosine kinase inhibitors or specific siRNA drastically decreased expression of ETV1, ETV4 and ETV5, three transcription factors constituting the PEA3 subgroup of the ETS family, while expression of the other members of the family were less or not affected...
November 2015: Molecular Oncology
Ronit Cohen, Eyal Greenberg, Yael Nemlich, Jacob Schachter, Gal Markel
Melanoma is an aggressive malignancy with a high metastatic potential. microRNA-17 (miR-17) is a member of the oncogenic miR-17/92 cluster. Here we study the effect of miR-17 on melanoma cell motility. Over expression of the mature or pri-microRNA form of miR-17 in WM-266-4 and 624mel melanoma lines enhances cell motility, evident in both wound healing and transwell migration assays. TargetScan algorithm predicts the PEA3-subfamily member ETV1 as a direct target of miR-17. Indeed, a 3-4-fold decrease of ETV1 protein levels are observed following miR-17 transfection into the various melanoma lines, with no significant change in ETV1 mRNA expression...
August 7, 2015: Oncotarget
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