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Oncogenesis

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https://www.readbyqxmd.com/read/28414320/inhibition-of-dna2-nuclease-as-a-therapeutic-strategy-targeting-replication-stress-in-cancer-cells
#1
S Kumar, X Peng, J Daley, L Yang, J Shen, N Nguyen, G Bae, H Niu, Y Peng, H-J Hsieh, L Wang, C Rao, C C Stephan, P Sung, G Ira, G Peng
Replication stress is a characteristic feature of cancer cells, which is resulted from sustained proliferative signaling induced by activation of oncogenes or loss of tumor suppressors. In cancer cells, oncogene-induced replication stress manifests as replication-associated lesions, predominantly double-strand DNA breaks (DSBs). An essential mechanism utilized by cells to repair replication-associated DSBs is homologous recombination (HR). In order to overcome replication stress and survive, cancer cells often require enhanced HR repair capacity...
April 17, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28414319/mir-186-inhibited-aerobic-glycolysis-in-gastric-cancer-via-hif-1%C3%AE-regulation
#2
L Liu, Y Wang, R Bai, K Yang, Z Tian
No abstract text is available yet for this article.
April 17, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28414318/initial-sites-of-hepadnavirus-integration-into-host-genome-in-human-hepatocytes-and-in-the-woodchuck-model-of-hepatitis-b-associated-hepatocellular-carcinoma
#3
R Chauhan, N D Churchill, P M Mulrooney-Cousins, T I Michalak
Hepatitis B virus (HBV) and the closely related woodchuck hepatitis virus (WHV) are potent carcinogens that trigger development of primary hepatocellular carcinoma (HCC). The initial sites of hepadnavirus-host genome integration, their diversity and kinetics of formation can be central to virus persistence and the initiation and progression of HCC. To recognize the nature of the very early virus-host interactions, we explored de novo infection of human hepatocyte-like HepaRG cells with authentic HBV and naive woodchucks with WHV...
April 17, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28414317/p16-controls-epithelial-cell-growth-and-suppresses-carcinogenesis-through-mechanisms-that-do-not-require-rb1-function
#4
M Sen, N Akeno, A Reece, A L Miller, D S Simpson, K A Wikenheiser-Brokamp
The p16/RB1 tumor suppressor pathway is inactivated in the vast majority, if not all, human cancers. The current paradigm is that p16 and RB1 function in a linear pathway to suppress tumorigenesis; however p16 is preferentially lost in human cancers suggesting that p16 has critical tumor suppressive functions not mediated through RB1. Carcinomas arise from transformed epithelial cells and account for 80% of adult malignancies highlighting the need to understand p16/RB1 pathway function in organ epithelia. Lung cancer is the leading cause of cancer deaths and is associated with p16/RB1 pathway deregulation...
April 17, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28394358/mage-trim28-complex-promotes-the-warburg-effect-and-hepatocellular-carcinoma-progression-by-targeting-fbp1-for-degradation
#5
X Jin, Y Pan, L Wang, L Zhang, R Ravichandran, P R Potts, J Jiang, H Wu, H Huang
Hepatocellular carcinoma (HCC) is one of the leading cause of cancer death in the world. Fructose-1,6-biphosphatase (FBP1), a rate-limiting enzyme in gluconeogenesis, has been identified recently as a tumor suppressor in HCC and other cancer types. In this study, we demonstrated that the tripartite motif-containing protein 28 (TRIM28) binds directly to and promotes FBP1 for ubiquitination and degradation. MAGE-A3 and MAGE-C2, which are known to be overexpressed in HCC, can enhance TRIM28-dependent degradation of FBP1 by forming ubiquitin ligase complexes with TRIM28...
April 10, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28394357/loss-of-lzap-inactivates-p53-and-regulates-sensitivity-of-cells-to-dna-damage-in-a-p53-dependent-manner
#6
J J Wamsley, C Gary, A Biktasova, M Hajek, G Bellinger, R Virk, N Issaeva, W G Yarbrough
Chemotherapy and radiation, the two most common cancer therapies, exert their anticancer effects by causing damage to cellular DNA. However, systemic treatment damages DNA not only in cancer, but also in healthy cells, resulting in the progression of serious side effects and limiting efficacy of the treatment. Interestingly, in response to DNA damage, p53 seems to play an opposite role in normal and in the majority of cancer cells-wild-type p53 mediates apoptosis in healthy tissues, attributing to the side effects, whereas mutant p53 often is responsible for acquired cancer resistance to the treatment...
April 10, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28394356/twist1-dnmt3a-and-mir186-establish-a-regulatory-circuit-that-controls-inflammation-associated-prostate-cancer-progression
#7
X Zhao, R Deng, Y Wang, H Zhang, J Dou, L Li, Y Du, R Chen, J Cheng, J Yu
Increasing evidences suggest that inflammatory microenvironment has a crucial role in prostate cancer (PCa) progression; however, the underlying mechanisms are unclear. Here, we used the inflammation-associated prostate cellular transformation model to screen out a crucial microRNA, miR186, which was significantly downregulated in the transformed cells and effectively rescued the transformed phenotype. On stimulation of inflammatory cytokines, the activated nuclear factor kappa B (NF-κB)/p65 was able to induce miR186 expression through binding to its promoter in non-transformed cells, whereas this pathway was lost in transformed cells...
April 10, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28394355/a-natural-food-sweetener-with-anti-pancreatic-cancer-properties
#8
C Liu, L-H Dai, D-Q Dou, L-Q Ma, Y-X Sun
No abstract text is available yet for this article.
April 10, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28394354/oncogenic-mct-1-activation-promotes-yy1-egfr-mnsod-signaling-and-tumor-progression
#9
H-Y Tseng, Y-A Chen, J Jen, P-C Shen, L-M Chen, T-D Lin, Y-C Wang, H-L Hsu
Tumor cells often produce high levels of reactive oxygen species (ROS) and display an increased ROS scavenging system. However, the molecular mechanism that balances antioxidative and oxidative stress in cancer cells is unclear. Here, we determined that oncogenic multiple copies in T-cell malignancy 1 (MCT-1) activity promotes the generation of intracellular ROS and mitochondrial superoxide. Overexpression of MCT-1 suppresses p53 accumulation but elevates the manganese-dependent superoxide dismutase (MnSOD) level via the YY1-EGFR signaling cascade, which protects cells against oxidative damage...
April 10, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28368392/met-amplification-and-epithelial-to-mesenchymal-transition-exist-as-parallel-resistance-mechanisms-in-erlotinib-resistant-egfr-mutated-nsclc-hcc827-cells
#10
K R Jakobsen, C Demuth, A T Madsen, D Hussmann, J Vad-Nielsen, A L Nielsen, B S Sorensen
Although many epidermal growth factor receptor (EGFR)-mutated lung cancer patients initially benefit from the EGFR-inhibitor erlotinib, all acquire resistance. So far, several mechanisms implicated in resistance have been identified, but the existence of multiple resistance mechanisms in parallel have only been sparsely investigated. In this study, we investigated parallel resistance mechanisms acquired by HCC827, an EGFR-mutated adenocarcinoma cell line dependent on EGFR activity and sensitive to erlotinib...
April 3, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28368391/p53-targets-tspan8-to-prevent-invasion-in-melanoma-cells
#11
G Agaësse, L Barbollat-Boutrand, M El Kharbili, O Berthier-Vergnes, I Masse
Cutaneous melanoma is a very deadly cancer because of its proclivity to metastasize. Despite the recent development of targeted and immune therapies, patient survival remains low. It is therefore crucial to enhance understanding of the molecular mechanisms underlying invasion. We previously identified tetraspanin 8 (TSPAN8) as an important modulator of melanoma invasiveness, and several of its transcriptional regulators, which affect TSPAN8 expression during melanoma progression toward an invasive stage. This study found that TSPAN8 promoter contains consensus-binding sites for p53 transcription factor...
April 3, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28368390/the-pleiotropic-regulation-of-cyclin-d1-by-newly-identified-sesaminol-binding-protein-ant2
#12
M Watanabe, Y Iizumi, M Sukeno, M Iizuka-Ohashi, Y Sowa, T Sakai
The expression of cyclin D1 is upregulated in various cancer cells by diverse mechanisms, such as increases in mRNA levels, the promotion of the translation by mammalian target of rapamycin complex 1 (mTORC1) signaling and the protein stabilization. We here show that sesaminol, a sesame lignan, reduces the expression of cyclin D1 with decreasing mRNA expression levels, inhibiting mTORC1 signaling and promoting proteasomal degradation. We subsequently generated sesaminol-immobilized FG beads to newly identify sesaminol-binding proteins...
April 3, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28368389/wnt-signaling-in-triple-negative-breast-cancer
#13
REVIEW
Sö-G Pohl, N Brook, M Agostino, F Arfuso, A P Kumar, A Dharmarajan
Wnt signaling regulates a variety of cellular processes, including cell fate, differentiation, proliferation and stem cell pluripotency. Aberrant Wnt signaling is a hallmark of many cancers. An aggressive subtype of breast cancer, known as triple-negative breast cancer (TNBC), demonstrates dysregulation in canonical and non-canonical Wnt signaling. In this review, we summarize regulators of canonical and non-canonical Wnt signaling, as well as Wnt signaling dysfunction that mediates the progression of TNBC...
April 3, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28368388/methylation-of-wnt-target-genes-axin2-and-dkk1-as-robust-biomarkers-for-recurrence-prediction-in-stage-ii-colon-cancer
#14
R Kandimalla, J F Linnekamp, S van Hooff, A Castells, X Llor, M Andreu, R Jover, A Goel, J P Medema
Stage II colon cancer (CC) still remains a clinical challenge with patient stratification for adjuvant therapy (AT) largely relying on clinical parameters. Prognostic biomarkers are urgently needed for better stratification. Previously, we have shown that WNT target genes AXIN2, DKK1, APCDD1, ASCL2 and LGR5 are silenced by DNA methylation and could serve as prognostic markers in stage II CC patients using methylation-specific PCR. Here, we have extended our discovery cohort AMC90-AJCC-II (N=65) and methylation was analyzed by quantitative pyrosequencing...
April 3, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28319096/hyperglycemia-exacerbates-colon-cancer-malignancy-through-hexosamine-biosynthetic-pathway
#15
A Vasconcelos-Dos-Santos, H F B R Loponte, N R Mantuano, I A Oliveira, I F de Paula, L K Teixeira, J C M de-Freitas-Junior, K C Gondim, N Heise, R Mohana-Borges, J A Morgado-Díaz, W B Dias, A R Todeschini
Hyperglycemia is a common feature of diabetes mellitus, considered as a risk factor for cancer. However, its direct effects in cancer cell behavior are relatively unexplored. Herein we show that high glucose concentration induces aberrant glycosylation, increased cell proliferation, invasion and tumor progression of colon cancer. By modulating the activity of the rate-limiting enzyme, glutamine-fructose-6-phosphate amidotransferase (GFAT), we demonstrate that hexosamine biosynthetic pathway (HBP) is involved in those processes...
March 20, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28319095/rcn1-suppresses-er-stress-induced-apoptosis-via-calcium-homeostasis-and-perk-chop-signaling
#16
S Xu, Y Xu, L Chen, Q Fang, S Song, J Chen, J Teng
Endoplasmic reticulum (ER) stress is caused by the disturbance of ER homeostasis and leads to the activation of the unfolded protein response (UPR), which alleviates stress at an early stage and triggers apoptosis if homeostasis fails over a prolonged timeframe. Here, we report that reticulocalbin 1 (RCN1), a member of the CREC family, is transactivated by nuclear factor kappa B (NF-κB) during ER stress and inhibits ER stress-induced apoptosis. The depletion of RCN1 increases the UPR during drug-induced ER stress by activating PRKR-like ER kinase-CCAAT/enhancer-binding protein-homologous protein (PERK-CHOP) signaling, thus inducing apoptosis...
March 20, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28287613/knockdown-of-long-non-coding-rna-xist-increases-blood-tumor-barrier-permeability-and-inhibits-glioma-angiogenesis-by-targeting-mir-137
#17
H Yu, Y Xue, P Wang, X Liu, J Ma, J Zheng, Z Li, Z Li, H Cai, Y Liu
Antiangiogenic therapy plays a significant role in combined glioma treatment. However, poor permeability of the blood-tumor barrier (BTB) limits the transport of chemotherapeutic agents, including antiangiogenic drugs, into tumor tissues. Long non-coding RNAs (lncRNAs) have been implicated in various diseases, especially malignant tumors. The present study found that lncRNA X-inactive-specific transcript (XIST) was upregulated in endothelial cells that were obtained in a BTB model in vitro. XIST knockdown increased BTB permeability and inhibited glioma angiogenesis...
March 13, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28287612/overexpression-of-smc4-activates-tgf%C3%AE-smad-signaling-and-promotes-aggressive-phenotype-in-glioma-cells
#18
L Jiang, J Zhou, D Zhong, Y Zhou, W Zhang, W Wu, Z Zhao, W Wang, W Xu, L He, Y Ma, Y Hu, W Zhang, J Li
Overexpression of structural maintenance of chromosomes 4 (SMC4) has been reported to be involved in tumor cell growth, migration and invasion, and to be correlated with poor prognosis of cancer patient. However, its clinical significance and biological role in glioma remain unknown. Herein, we found that SMC4 expression at both mRNA and protein level was markedly increased in glioma cells and clinical tissues and that it correlated with poor prognosis. SMC4 overexpression markedly promoted the glioma cell proliferation rate and migration and invasive capability in vitro and in vivo, whereas SMC4 downregulation reduced it...
March 13, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28287611/fam83a-is-amplified-and-promotes-cancer-stem-cell-like-traits-and-chemoresistance-in-pancreatic-cancer
#19
S Chen, J Huang, Z Liu, Q Liang, N Zhang, Y Jin
Cancer stem cells (CSCs), also known as tumor-initiating cells (TICs), contribute to tumorigenesis, resistance to chemoradiotherapy and recurrence in human cancers, suggesting targeting CSCs may represent a potential therapeutic strategy. In the current study, we found family with sequence similarity 83, member A (FAM83A) is significantly overexpressed and associated with poorer overall survival and disease-free survival in pancreatic cancer. Overexpression of FAM83A markedly promoted, whereas inhibition of FAM83A decreased, CSC-like traits and chemoresistance both in vitro and in an in vivo mouse model of pancreatic cancer...
March 13, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28240737/fatty-acid-synthase-regulates-estrogen-receptor-%C3%AE-signaling-in-breast-cancer-cells
#20
J A Menendez, R Lupu
Fatty acid synthase (FASN), the key enzyme for endogenous synthesis of fatty acids, is overexpressed and hyperactivated in a biologically aggressive subset of sex steroid-related tumors, including breast carcinomas. Using pharmacological and genetic approaches, we assessed the molecular relationship between FASN signaling and estrogen receptor alpha (ERα) signaling in breast cancer. The small compound C75, a synthetic slow-binding inhibitor of FASN activity, induced a dramatic augmentation of estradiol (E2)-stimulated, ERα-driven transcription...
February 27, 2017: Oncogenesis
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