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Oncogene

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https://www.readbyqxmd.com/read/28714964/inhibition-of-wnt-signaling-attenuates-self-renewal-of-shh-subgroup-medulloblastoma
#1
J Rodriguez-Blanco, L Pednekar, C Penas, B Li, V Martin, J Long, E Lee, W A Weiss, C Rodriguez, N Mehrdad, D M Nguyen, N G Ayad, P Rai, A J Capobianco, D J Robbins
The SMOOTHENED inhibitor vismodegib is FDA approved for advanced basal cell carcinoma (BCC), and shows promise in clinical trials for SONIC HEDGEHOG (SHH)-subgroup medulloblastoma (MB) patients. Clinical experience with BCC patients shows that continuous exposure to vismodegib is necessary to prevent tumor recurrence, suggesting the existence of a vismodegib-resistant reservoir of tumor-propagating cells. We isolated such tumor-propagating cells from a mouse model of SHH-subgroup MB and grew them as sphere cultures...
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714963/fhit-loss-confers-cisplatin-resistance-in-lung-cancer-via-the-akt-nf-%C3%AE%C2%BAb-slug-mediated-puma-reduction
#2
D-W Wu, M-C Lee, N-Y Hsu, T-C Wu, J-Y Wu, Y-C Wang, Y-W Cheng, C-Y Chen, H Lee
This corrects the article DOI: 10.1038/onc.2014.184.
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714962/shp-1-is-a-negative-regulator-of-epithelial-mesenchymal-transition-in-hepatocellular-carcinoma
#3
L-C Fan, C-W Shiau, W-T Tai, M-H Hung, P-Y Chu, F-S Hsieh, H Lin, H-C Yu, K-F Chen
This corrects the article DOI: 10.1038/onc.2014.445.
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714961/b-cell-lymphoma-leukemia-10-promotes-oral-cancer-progression-through-stat1-atf4-s100p-signaling-pathway
#4
T-S Wu, C-T Tan, C-C Chang, B-R Lin, W-T Lai, S-T Chen, M Yen-Ping Kuo, C-L Rau, F-S Jaw, H-H Chang
This corrects the article DOI: 10.1038/onc.2014.43.
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714960/bin1-reverses-pd-l1-mediated-immune-escape-by-inactivating-the-c-myc-and-egfr-mapk-signaling-pathways-in-non-small-cell-lung-cancer
#5
J Wang, Y Jia, S Zhao, X Zhang, X Wang, X Han, Y Wang, M Ma, J Shi, L Liu
Non-small cell lung cancer (NSCLC) is one of the most common and malignant carcinoma worldwide, and the incidence and mortality are increasing rapidly. Immunotherapy targeting programmed death 1/programmed death ligand 1 (PD-L1) signaling has shown prominent clinical effects in treating NSCLC; however, a poor understanding of the associated regulating molecular mechanisms of PD-L1 has become one of the biggest obstacles for further improving efficacy. Bridging integrator-1 (BIN1) can regulate numerous cancer-related molecules to exert multiple tumor-suppressing effects by either interacting or not interacting with c-MYC...
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714959/o-glcnacylation-modulates-bmi-1-protein-stability-and-potential-oncogenic-function-in-prostate-cancer
#6
Y Li, L Wang, J Liu, P Zhang, M An, C Han, Y Li, X Guan, K Zhang
The Polycomb group transcriptional repressor Bmi-1 often overexpressed and participated in stem cells self-renewal and tumorigenesis initiating of prostate cancer. In this progression, Bmi-1 protein was regulated by transcription and post-translational modifications (PTMs). Nobly, the underlying PTMs regulation of Bmi-1 is poorly known. Here we use co-immunoprecipitation show that in C4-2 cell line, Bmi-1 directly interacted with OGT which is the only known enzyme catalyzed the O-GlcNAcylation in human. Furthermore, we identified that Ser255 is the site for Bmi-1 O-GlcNAcylation, and O-GlcNAcylation promoted Bmi-1 protein stability and its oncogenic activity...
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714958/roles-of-grainyhead-like-transcription-factors-in-cancer
#7
REVIEW
S M Frisch, J C Farris, P M Pifer
The mammalian homologs of the D. melanogaster Grainyhead gene, Grainyhead-like 1-3 (GRHL1, GRHL2 and GRHL3), are transcription factors implicated in wound healing, tubulogenesis and cancer. Their induced target genes encode diverse epithelial cell adhesion molecules, while mesenchymal genes involved in cell migration and invasion are repressed. Moreover, GRHL2 suppresses the oncogenic epithelial-mesencyhmal transition, thereby acting as a tumor suppressor. Mechanisms, some involving established cancer-related signaling/transcription factor pathways (for example, Wnt, TGF-β, mir200, ZEB1, OVOL2, p63 and p300) and translational implications of the Grainyhead proteins in cancer are discussed in this review article...
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28714957/il-11-contribution-to-tumorigenesis-in-an-nrf2-addiction-cancer-model
#8
H Kitamura, Y Onodera, S Murakami, T Suzuki, H Motohashi
The interaction between cancer cells and their microenvironment is an important determinant of the pathological nature of cancers, particularly their tumorigenic abilities. The KEAP1-NRF2 system, originally identified as a critical defense mechanism against oxidative stress, is often dysregulated in various human cancers forming solid tumors, resulting in the aberrant activation of NRF2. Increased accumulation of NRF2 in cancers is strongly associated with the poor prognoses of cancer patients, including those with lung and breast cancers...
July 17, 2017: Oncogene
https://www.readbyqxmd.com/read/28692058/tumor-suppressor-pdcd4-attenuates-sin1-translation-to-inhibit-invasion-in-colon-carcinoma
#9
Q Wang, J Zhu, Y-W Wang, Y Dai, Y-L Wang, C Wang, J Liu, A Baker, N H Colburn, H-S Yang
Programmed cell death 4 (Pdcd4), a tumor invasion suppressor, is frequently downregulated in colorectal cancer and other cancers. In this study, we find that loss of Pdcd4 increases the activity of mammalian target of rapamycin complex 2 (mTORC2) and thereby upregulates Snail expression. Examining the components of mTORC2 showed that Pdcd4 knockdown increased the protein but not mRNA level of stress-activated-protein kinase interacting protein 1 (Sin1), which resulted from enhanced Sin1 translation. To understand how Pdcd4 regulates Sin1 translation, the SIN1 5' untranslated region (5'UTR) was fused with luciferase reporter and named as 5'Sin1-Luc...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692057/the-interactome-of-metabolic-enzyme-carbonic-anhydrase-ix-reveals-novel-roles-in-tumor-cell-migration-and-invadopodia-mmp14-mediated-invasion
#10
M Swayampakula, P C McDonald, M Vallejo, E Coyaud, S C Chafe, A Westerback, G Venkateswaran, J Shankar, G Gao, E M N Laurent, Y Lou, K L Bennewith, C T Supuran, I R Nabi, B Raught, S Dedhar
Carbonic anhydrase IX (CAIX) is a hypoxia inducible factor 1-induced, cell surface pH regulating enzyme with an established role in tumor progression and clinical outcome. However, the molecular basis of CAIX-mediated tumor progression remains unclear. Here, we have utilized proximity dependent biotinylation (BioID) to map the CAIX 'interactome' in breast cancer cells in order to identify physiologically relevant CAIX-associating proteins with potential roles in tumor progression. High confidence proteins identified include metabolic transporters, β1 integrins, integrin-associated protein CD98hc and matrix metalloprotease 14 (MMP14)...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692056/pdzk1-inhibits-the-development-and-progression-of-renal-cell-carcinoma-by-suppression-of-shp-1-phosphorylation
#11
T Tao, X Yang, J Zheng, D Feng, Q Qin, X Shi, Q Wang, C Zhao, Z Peng, H Liu, W G Jiang, J He
Renal cell carcinoma (RCC) is one of the most aggressive urologic cancers, however, the mechanism on supporting RCC carcinogenesis is still not clear. By using gene expression profile analysis and functional clustering, PDZ domain-containing 1 (PDZK1) was revealed to be downregulated in human clear cell renal cell carcinoma (ccRCC) samples, which was also verified in several independent public ccRCC data sets. Using PDZK1 overexpression and knockdown models in ccRCC cell lines, we demonstrated that PDZK1 inhibited cell proliferation, cell cycle G1/S phase transition, cell migration and invasion, indicating a tumor-suppressor role in the development and progression of ccRCC...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692055/cellular-prion-protein-prp-c-in-the-development-of-merlin-deficient-tumours
#12
L Provenzano, Y Ryan, D A Hilton, J Lyons-Rimmer, F Dave, E A Maze, C L Adams, R Rigby-Jones, S Ammoun, C O Hanemann
Loss of function mutations in the neurofibromatosis Type 2 (NF2) gene, coding for a tumour suppressor, Merlin, cause multiple tumours of the nervous system such as schwannomas, meningiomas and ependymomas. These tumours may occur sporadically or as part of the hereditary condition neurofibromatosis Type 2 (NF2). Current treatment is confined to (radio) surgery and no targeted drug therapies exist. NF2 mutations and/or Merlin inactivation are also seen in other cancers including some mesothelioma, breast cancer, colorectal carcinoma, melanoma and glioblastoma...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692054/modeling-cancer-driver-events-in-vitro-using-barrier-bypass-clonal-expansion-assays-and-massively-parallel-sequencing
#13
H Huskova, M Ardin, A Weninger, K Vargova, S Barrin, S Villar, M Olivier, T Stopka, Z Herceg, M Hollstein, J Zavadil, M Korenjak
The information on candidate cancer driver alterations available from public databases is often descriptive and of limited mechanistic insight, which poses difficulties for reliable distinction between true driver and passenger events. To address this challenge, we performed in-depth analysis of whole-exome sequencing data from cell lines generated by a barrier bypass-clonal expansion (BBCE) protocol. The employed strategy is based on carcinogen-driven immortalization of primary mouse embryonic fibroblasts and recapitulates early steps of cell transformation...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692053/pre-45s-rrna-promotes-colon-cancer-and-is-associated-with-poor-survival-of-crc-patients
#14
H Tsoi, K C Lam, Y Dong, X Zhang, C K Lee, J Zhang, S C Ng, S S M Ng, S Zheng, Y Chen, J Fang, J Yu
One characteristic of cancer cells is the abnormally high rate of cell metabolism to sustain their enhanced proliferation. However, the behind mechanism of this phenomenon is still elusive. Here we find that enhanced precursor 45s ribosomal RNA (pre-45s rRNA) is one of the core mechanisms in promoting the pathogenesis of colorectal cancer (CRC). Pre-45s rRNA expression is significantly higher in primary CRC tumor tissues samples and cancer cell lines compared with the non-tumorous colon tissues, and is associated with tumor sizes...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692052/disrupting-g6pd-mediated-redox-homeostasis-enhances-chemosensitivity-in-colorectal-cancer
#15
H-Q Ju, Y-X Lu, Q-N Wu, J Liu, Z-L Zeng, H-Y Mo, Y Chen, T Tian, Y Wang, T-B Kang, D Xie, M-S Zeng, P Huang, R-H Xu
Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme that generates NADPH to maintain reduced glutathione (GSH), which scavenges reactive oxygen species (ROS) to protect cancer cell from oxidative damage. In this study, we mainly investigate the potential roles of G6PD in colorectal cancer (CRC) development and chemoresistance. We discover that G6PD is overexpressed in CRC cells and patient specimens. High expression of G6PD predicts poor prognosis and correlated with poor outcome of oxaliplatin-based first-line chemotherapy in patients with CRC...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692051/transcriptional-regulation-of-ataxia-telangiectasia-and-rad3-related-protein-by-activated-p21-activated-kinase-1-protects-keratinocytes-in-uv-b-induced-premalignant-skin-lesions
#16
S Beesetti, J Mavuluri, R P Surabhi, T M Oberyszyn, K Tober, R S Pitani, L D Joseph, G Venkatraman, S K Rayala
Sun-induced skin lesions, in particular actinic keratosis, are generally considered as premalignant skin lesions that can progress into squamous cell carcinoma (SCC) and invasive SCC if left untreated. Therefore, understanding the molecular mechanisms by which the ultraviolet-B (UV-B)-exposed cells are being protected and the signaling pathways that promote the progression of certain premalignant skin lesions to malignant lesions will permit us to prevent or cure skin cancers. In the current study, we found that phospho-p21-activated kinase-1 (Pak1) and Pak1 expression was high in clinical samples of sunlight-induced premalignant skin lesions assessed by immunohistochemistry...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692050/crosstalk-between-nrf2-and-hipk2-shapes-cytoprotective-responses
#17
L Torrente, C Sanchez, R Moreno, S Chowdhry, P Cabello, K Isono, H Koseki, T Honda, J D Hayes, A T Dinkova-Kostova, L de la Vega
Homeodomain interacting protein kinase-2 (HIPK2) is a member of the HIPK family of stress-responsive kinases that modulates cell growth, apoptosis, proliferation and development. HIPK2 has several well-characterised tumour suppressor roles, but recent studies suggest it can also contribute to tumour progression, although the underlying mechanisms are unknown. Herein, we have identified novel crosstalk between HIPK2 and the cytoprotective transcription factor NRF2. We show that HIPK2 is a direct transcriptional target of NRF2, identifying a functional NRF2 binding site in the HIPK2 gene locus and demonstrating for the first time a transcriptional mode of regulation for this kinase...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692049/mdm2-selectively-suppresses-dna-damage-arising-from-inhibition-of-topoisomerase-ii-independent-of-p53
#18
J C Senturk, S Bohlman, J J Manfredi
Mdm2 is often overexpressed in tumors that retain wild-type TP53 but may affect therapeutic response independently of p53. Herein is shown that tumor cells with MDM2 amplification are selectively resistant to treatment with topoisomerase II poisons but not other DNA damaging agents. Tumor cells that overexpress Mdm2 have reduced DNA double-strand breaks in response to doxorubicin or etoposide. This latter result is not due to altered drug uptake. The selective attenuation of DNA damage in response to these agents is dependent on both Mdm2 levels and an intact ubiquitin ligase function...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692048/increased-expression-of-programmed-cell-death-protein-1-on-nk-cells-inhibits-nk-cell-mediated-anti-tumor-function-and-indicates-poor-prognosis-in-digestive-cancers
#19
Y Liu, Y Cheng, Y Xu, Z Wang, X Du, C Li, J Peng, L Gao, X Liang, C Ma
Abnormal expression of activating/inhibitory receptors leads to natural killer (NK) cells dysfunction in tumor. Here we show that programmed cell death protein 1 (PD-1), a well-known immune checkpoint of T cells, is highly expressed on peripheral and tumor-infiltrating NK cells from patients with digestive cancers including esophageal, liver, colorectal, gastric and biliary cancer. The increased PD-1 expression on NK cells indicates poorer survival in esophageal and liver cancers. Blocking PD-1/PD-L1 signaling markedly enhances cytokines production and degranulation and suppresses apoptosis of NK cells in vitro...
July 10, 2017: Oncogene
https://www.readbyqxmd.com/read/28692047/androgen-induces-g3bp2-and-sumo-mediated-p53-nuclear-export-in-prostate-cancer
#20
D Ashikari, K Takayama, T Tanaka, Y Suzuki, D Obinata, T Fujimura, T Urano, S Takahashi, S Inoue
The androgen receptor (AR) has a central role in prostate cancer progression, particularly treatment-resistance disease including castration-resistant prostate cancer. Loss of the p53 tumor suppressor, a nuclear transcription factor, is also known to contribute to prostate malignancy. Here we report that p53 is translocated to the cytoplasm by androgen-mediated induction of G3BP2, a newly described direct target gene of AR. G3BP2 induces both cell cycle progression and blocks apoptosis. Translocation of p53 is regulated by androgen-dependent sumoylation mediated by the G3BP2-interacting SUMO-E3 ligase, RanBP2...
July 10, 2017: Oncogene
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