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Oncogene

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https://www.readbyqxmd.com/read/28892050/carcinoembryonic-antigen-related-cell-adhesion-molecule-6-ceacam6-promotes-egf-receptor-signaling-of-oral-squamous-cell-carcinoma-metastasis-via-the-complex-n-glycosylation
#1
W-F Chiang, T-M Cheng, C-C Chang, S-H Pan, C A Changou, T-H Chang, K-H Lee, S-Y Wu, Y-F Chen, K-H Chuang, D-B Shieh, Y-L Chen, C-C Tu, W-L Tsui, M-H Wu
Aberrant protein glycosylation could be a distinct surface-marker of cancer cells that influences cancer progression and metastasis because glycosylation can regulate membrane protein folding which alters receptor activation and changes epitope exposure for antibody (Ab) recognition. Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6), a glycophosphoinositol-anchored protein, is a heavily glycosylated tumor antigen. However, the clinical significance and biological effect of CEACAM6 glycosylation has not been addressed in cancers...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892049/membrane-mucin-muc4-promotes-blood-cell-association-with-tumor-cells-and-mediates-efficient-metastasis-in-a-mouse-model-of-breast-cancer
#2
A R Rowson-Hodel, J H Wald, J Hatakeyama, W K O'Neal, J R Stonebraker, K VanderVorst, M J Saldana, A D Borowsky, C Sweeney, K L Carraway
Mucin-4 (Muc4) is a large cell surface glycoprotein implicated in the protection and lubrication of epithelial structures. Previous studies suggest that aberrantly expressed Muc4 can influence the adhesiveness, proliferation, viability and invasiveness of cultured tumor cells, as well as the growth rate and metastatic efficiency of xenografted tumors. Although it has been suggested that one of the major mechanisms by which Muc4 potentiates tumor progression is via its engagement of the ErbB2/HER2 receptor tyrosine kinase, other mechanisms exist and remain to be delineated...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892048/cdkn2b-deletion-is-essential-for-pancreatic-cancer-development-instead-of-unmeaningful-co-deletion-due-to-juxtaposition-to-cdkn2a
#3
Q Tu, J Hao, X Zhou, L Yan, H Dai, B Sun, D Yang, S An, L Lv, B Jiao, C Chen, R Lai, P Shi, X Zhao
Pancreatic cancer is among the deadliest malignancies; however, the genetic events that lead to pancreatic carcinogenesis in adults remain unclear. In vivo models in which these genetic alterations occur in adult animals may more accurately reflect the features of human cancer. In this study, we demonstrate that inactivation of Cdkn2b (p15ink4b) is necessary for induction of pancreatic cancer by oncogenic KRAS(G12D) expression and inactivation of Tp53 and Cdkn2a in adult mouse pancreatic ductal cells (P60 or older)...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892047/a-system-for-detecting-high-impact-low-frequency-mutations-in-primary-tumors-and-metastases
#4
M Anjanappa, Y Hao, E R Simpson, P Bhat-Nakshatri, J B Nelson, S A Tersey, R G Mirmira, A A Cohen-Gadol, M R Saadatzadeh, L Li, F Fang, K P Nephew, K D Miller, Y Liu, H Nakshatri
Tumor complexity and intratumor heterogeneity contribute to subclonal diversity. Despite advances in next-generation sequencing (NGS) and bioinformatics, detecting rare mutations in primary tumors and metastases contributing to subclonal diversity is a challenge for precision genomics. Here, in order to identify rare mutations, we adapted a recently described epithelial reprograming assay for short-term propagation of epithelial cells from primary and metastatic tumors. Using this approach, we expanded minor clones and obtained epithelial cell-specific DNA/RNA for quantitative NGS analysis...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892046/targeting-nuclear-receptors-in-cancer-associated-fibroblasts-as-concurrent-therapy-to-inhibit-development-of-chemoresistant-tumors
#5
J S K Chan, M K Sng, Z Q Teo, H C Chong, J S Twang, N S Tan
Most anticancer therapies to date focus on druggable features of tumor epithelia. Despite the increasing repertoire of treatment options, patient responses remain varied. Moreover, tumor resistance and relapse remain persistent clinical challenges. These observations imply an incomplete understanding of tumor heterogeneity. The tumor microenvironment is a major determinant of disease progression and therapy outcome. Cancer-associated fibroblasts (CAFs) are the dominant cell type within the reactive stroma of tumors...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892045/mn1-overexpression-is-driven-by-loss-of-dnmt3b-methylation-activity-in-inv-16-pediatric-aml
#6
N S D Larmonie, T C J M Arentsen-Peters, A Obulkasim, D Valerio, E Sonneveld, A A Danen-van Oorschot, V de Haas, D Reinhardt, M Zimmermann, J Trka, A Baruchel, R Pieters, M M van den Heuvel-Eibrink, C M Zwaan, M Fornerod
In acute myeloid leukemia (AML), specific genomic aberrations induce aberrant methylation, thus directly influencing the transcriptional programing of leukemic cells. Therefore, therapies targeting epigenetic processes are advocated as a promising therapeutic tool for AML treatment. However, to develop new therapies, a comprehensive understanding of the mechanism(s) driving the epigenetic changes as a result of acquired genetic abnormalities is necessary. This understanding is still lacking. In this study, we performed genome-wide CpG-island methylation profiling on pediatric AML samples...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892044/a-novel-mouse-model-of-rhabdomyosarcoma-underscores-the-dichotomy-of-mdm2-alt1-function-in-vivo
#7
D F Comiskey, A G Jacob, B L Sanford, M Montes, A K Goodwin, H Steiner, E Matsa, A S Tapia-Santos, T W Bebee, J Grieves, K La Perle, P Boyaka, D S Chandler
Alternative splicing of the oncogene murine double minute 2 (MDM2) is induced in response to genotoxic stress. MDM2-ALT1, the major splice variant generated, is known to activate the p53 pathway and impede full-length MDM2's negative regulation of p53. Despite this perceptible tumor-suppressive role, MDM2-ALT1 is also associated with several cancers. Furthermore, expression of MDM2-ALT1 has been observed in aggressive metastatic disease in pediatric rhabdomyosarcoma (RMS), irrespective of histological subtype...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28892043/loss-of-prp4k-drives-anoikis-resistance-in-part-by-dysregulation-of-epidermal-growth-factor-receptor-endosomal-trafficking
#8
D P Corkery, L E Clarke, S Gebremeskel, J Salsman, J Pinder, C Le Page, L Meunier, Z Xu, A-M Mes-Masson, J N Berman, B Johnston, G Dellaire
Anoikis acts as a critical barrier to metastasis by inducing cell death upon cancer cell detachment from the extracellular matrix (ECM), thereby preventing tumor cell dissemination to secondary sites. The induction of anoikis requires the lysosomal-mediated downregulation of epidermal growth factor receptors (EGFRs) leading to termination of pro-survival signaling. In this study, we demonstrate that depletion of pre-mRNA splicing factor 4 kinase (PRP4K; also known as PRPF4B) causes dysregulation of EGFR trafficking and anoikis resistance...
September 11, 2017: Oncogene
https://www.readbyqxmd.com/read/28869607/mrpl33-and-its-splicing-regulator-hnrnpk-are-required-for-mitochondria-function-and-implicated-in-tumor-progression
#9
L Liu, C Luo, Y Luo, L Chen, Y Liu, Y Wang, J Han, Y Zhang, N Wei, Z Xie, W Wu, G Wu, Y Feng
MRPL33 gene encodes a large mitoribosomal subunit protein, which may be involved in mitochondrial translation. Although two splice variants of MRPL33 have been described, its splicing regulation remains elusive. Here we observed that inclusion of alternative exon 3 was greatly promoted in a panel of human cancer cells. Depletion of the exon 3-containing long isoform of MRPL33 (MRPL33-L) led to impaired proliferation and increased apoptosis in cancer cell lines and in a xenograft model. MRPL33-L knockdown could also induce mitochondrial dysfunction including increased accumulation of reactive oxygen species, decreased ATP production and 16 S rRNA levels...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869606/kctd12-promotes-tumorigenesis-by-facilitating-cdc25b-cdk1-aurora-a-dependent-g2-m-transition
#10
Y Zhong, J Yang, W W Xu, Y Wang, C-C Zheng, B Li, Q-Y He
Cell cycle dysregulation leads to uncontrolled cell proliferation and tumorigenesis. Understanding the molecular mechanisms underlying cell cycle progression can provide clues leading to the identification of key proteins involved in cancer development. In this study, we performed proteomics analysis to identify novel regulators of the cell cycle. We found that potassium channel tetramerization domain containing 12 (KCTD12) was significantly upregulated in M phase compared with S phase. We also found that KCTD12 overexpression not only facilitated the G2/M transition and induced cancer cell proliferation, but also promoted the growth of subcutaneous tumors and Ki-67 proliferation index in mice...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869605/suppression-of-sirt1-sensitizes-lung-cancer-cells-to-wee1-inhibitor-mk-1775-induced-dna-damage-and-apoptosis
#11
G Chen, B Zhang, H Xu, Y Sun, Y Shi, Y Luo, H Jia, F Wang
Lung cancer treatment remains a challenge for clinical practice and new therapeutic approaches are urgently needed. Loss of functional WEE1 kinase causes DNA replication stress, DNA damage and unscheduled mitotic entry due to elevated CDK activity. The selective WEE1 inhibitor MK-1775 synergize with DNA-damaging agent to inhibit cancer cell growth. Here we report that inhibition of Sirt1 deacetylase through small interfering RNA or selective inhibitor Ex527 greatly enhances MK-1775-induced growth inhibition and apoptosis in human lung cancer cells...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869604/myc-target-gene-long-intergenic-noncoding-rna-linc00176-in-hepatocellular-carcinoma-regulates-cell-cycle-and-cell-survival-by-titrating-tumor-suppressor-micrornas
#12
D D H Tran, C Kessler, S E Niehus, M Mahnkopf, A Koch, T Tamura
Hepatocellular carcinoma (HCC) is a frequent form of cancer with a poor prognosis and with limited possibilities for medical intervention. Recent evidence has accumulated that long noncoding RNAs (lncRNAs) are important regulators of disease processes including cancer. Chromatin remodeling in cancer cells may result in an unusual expression of lncRNAs and indeed it has been shown that more than 7000 unannotated lncRNAs are expressed in HCCs. We identified a novel long intergenic noncoding RNA, Linc00176, that plays a role in proliferation and survival of HCC...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869603/a-regulatory-circuit-composed-of-dna-methyltransferases-and-receptor-tyrosine-kinases-controls-lung-cancer-cell-aggressiveness
#13
F Yan, N Shen, J Pang, N Zhao, B Deng, B Li, Y Yang, P Yang, J R Molina, S Liu
Overexpression of DNMT1 and KIT is prevalent in lung cancer, yet the underlying molecular mechanisms are poorly understood. While the deregulated activation of DNMT1 or KIT has been implicated in lung cancer pathogenesis, whether and how DNMT1 and KIT orchestrate lung tumorigenesis are unclear. Here, using human lung cancer tissue microarrays and fresh frozen tissues, we found that the overexpression of DNMT1 is positively correlated with the upregulation of KIT in tumor tissues. We demonstrated that DNMT1 and KIT form a positive regulatory loop, in which ectopic DNMT1 expression increases, whereas targeted DNMT1 depletion abrogates KIT signaling cascade through Sp1/miR-29b network...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869602/targeting-mitochondrial-translation-by-inhibiting-ddx3-a-novel-radiosensitization-strategy-for-cancer-treatment
#14
M R Heerma van Voss, F Vesuna, G M Bol, J Afzal, S Tantravedi, Y Bergman, K Kammers, M Lehar, R Malek, M Ballew, N Ter Hoeve, D Abou, D Thorek, C Berlinicke, M Yazdankhah, D Sinha, A Le, R Abrahams, P T Tran, P J van Diest, V Raman
DDX3 is a DEAD box RNA helicase with oncogenic properties. RK-33 is developed as a small-molecule inhibitor of DDX3 and showed potent radiosensitizing activity in preclinical tumor models. This study aimed to assess DDX3 as a target in breast cancer and to elucidate how RK-33 exerts its anti-neoplastic effects. High DDX3 expression was present in 35% of breast cancer patient samples and correlated with markers of aggressiveness and shorter survival. With a quantitative proteomics approach, we identified proteins involved in the mitochondrial translation and respiratory electron transport pathways to be significantly downregulated after RK-33 or DDX3 knockdown...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869601/role-of-smad-proteins-in-colitis-associated-cancer-from-known-to-the-unknown
#15
REVIEW
P Chandrasinghe, B Cereser, M Moorghen, I Al Bakir, N Tabassum, A Hart, J Stebbing, J Warusavitarne
Small mothers against decapentaplegic (SMAD) proteins are a family of signal transduction molecules in transforming growth factor β (TGFβ) ligand pathways that have been found to have a key role in the pathogenesis of inflammatory bowel disease (IBD). Long standing IBD predisposes individuals to colitis-associated colorectal cancer (CAC), an entity that possess unique characteristics compared to hereditary and sporadic cancer. The ligands of the TGFβ super family along with SMADs have also been implicated in several aspects of colorectal cancer formation...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869600/foxo3-mediated-chemo-protection-in-high-stage-neuroblastoma-depends-on-wild-type-tp53-and-sesn3
#16
M Rupp, J Hagenbuchner, B Rass, H Fiegl, U Kiechl-Kohlendorfer, P Obexer, M J Ausserlechner
Forkhead box O class transcription factors are homeostasis regulators that control cell death, longevity and therapy-resistance. In neuroblastoma (NB), nuclear FOXO3 correlates with stage M disease and poor prognosis. To analyze whether FOXO3 contributes to drug-resistance in this childhood cancer, we investigated how different high-stage-derived NB cells respond to the activation of an ectopic FOXO3 allele. We found endogenous FOXO3 mostly localized to the nucleus-upon activation of an ectopic, 4OHT-activated FOXO3(A3)ER fusion protein two of the cell lines underwent apoptosis, whereas in the others FOXO3-activation even increased survival during drug-treatment...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869599/taxane-mediated-radiosensitization-derives-from-chromosomal-missegregation-on-tripolar-mitotic-spindles-orchestrated-by-aurka-and-tpx2
#17
M Orth, K Unger, U Schoetz, C Belka, K Lauber
Taxane-based radiochemotherapy is a central treatment option for various cancer entities in locally advanced stages. The therapeutic synergism of this combined modality approach due to taxane-mediated radiosensitization of cancer cells is well-known. However, the underlying molecular mechanisms remain largely elusive, and mechanism-derived predictive markers of taxane-based radiochemotherapy are currently not available. Here, we show that clinically relevant doses of Paclitaxel, the prototype taxane, stimulate a tripolar mode of mitosis leading to chromosomal missegregation and aneuploidization rather than interfering with cell cycle progression...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869598/rcc2-is-a-novel-p53-target-in-suppressing-metastasis
#18
C Song, L Liang, Y Jin, Y Li, Y Liu, L Guo, C Wu, C-H Yun, Y Yin
RCC2 (also known as TD60) is a highly conserved protein involved in prognosis in colorectal cancer. However, its relationship with tumor development is less understood. Here we demonstrate a signaling pathway defining regulation of RCC2 and its functions in tumor progression. We report that p53 is a transcriptional regulator of RCC2 that acts through its binding to a palindromic motif in the RCC2 promoter. RCC2 physically interacts and deactivates a small GTPase Rac1 that is known to be involved in metastasis...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869597/atf3-deficiency-promotes-genome-instability-and-spontaneous-tumorigenesis-in-mice
#19
Z Wang, Y He, W Deng, L Lang, H Yang, B Jin, R Kolhe, H-F Ding, J Zhang, T Hai, C Yan
Mice lacking genes involving in the DNA-damage response (DDR) are often tumor prone owing to genome instability caused by oncogenic challenges. Previous studies demonstrate that activating transcription factor 3 (ATF3), a common stress sensor, can activate the tumor suppressor p53 and regulate expression of p53 target genes upon DNA damage. However, whether ATF3 contributes to the maintenance of genome stability and tumor suppression remains unknown. Here we report that Atf3-deficient (Atf3(-/-)) mice developed spontaneous tumors, and died significantly earlier than wild-type (Atf3(+/+)) mice...
September 4, 2017: Oncogene
https://www.readbyqxmd.com/read/28869596/gsk3%C3%AE-controls-epithelial-mesenchymal-transition-and-tumor-metastasis-by-chip-mediated-degradation-of-slug
#20
S-H Kao, W-L Wang, C-Y Chen, Y-L Chang, Y-Y Wu, Y-T Wang, S-P Wang, A I Nesvizhskii, Y-J Chen, T-M Hong, P-C Yang
This corrects the article DOI: 10.1038/onc.2013.279.
September 4, 2017: Oncogene
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