| Records |
| Author |
Kim, M.Y.; Park, S.-J.; Shim, J.W.; Song, Y.J.; Yang, K.; Park, S.-J.; Heo, K. |
| Title |
Accumulation of low-dose BIX01294 promotes metastatic potential of U251 glioblastoma cells |
Type |
Journal Article |
| Year |
2017 |
Publication |
Oncology Letters |
Abbreviated Journal  |
Oncol Lett |
| Volume |
13 |
Issue |
3 |
Pages |
1767-1774 |
| Keywords |
Bix01294; epithelial-mesenchymal transition; glioblastoma stem cells; metastasis |
| Abstract |
BIX01294 (Bix) is known to be a euchromatic histone-lysine N-methyltransferase 2 inhibitor and treatment with Bix suppresses cancer cell survival and proliferation. In the present study, it was observed that sequential treatment with low-dose Bix notably increases glioblastoma cell migration and metastasis. It was demonstrated that U251 cells sequentially treated with low-dose Bix exhibited induced characteristic changes in critical epithelial-mesenchymal transition (EMT) markers, including E-cadherin, N-cadherin, beta-catenin and zinc finger protein SNAI2. Notably, sequential treatment with Bix also increased the expression of cancer stem cell-associated markers, including sex determining region Y-box 2, octamer-binding transcription factor 4 and cluster of differentiation 133. Neurosphere formation was significantly enhanced in cells sequentially treated with Bix, compared with control cells (control: P=0.011; single treatment of Bix, P=0.045). The results of the present study suggest that accumulation of low-dose Bix enhanced the migration and metastatic potential of glioblastoma cells by regulating EMT-associated gene expression, which may be the cause of the altered properties of glioblastoma stem cells. |
| Address |
Research Center, Dongnam Institute of Radiological and Medical Science (DIRAMS), Busan 619-953, Republic of Korea |
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English |
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| ISSN |
1792-1074 |
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| Notes |
PMID:28454322 |
Approved |
no |
| Call Number |
ref @ user @ |
Serial |
96588 |
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| Author |
Phanthaphol, N.; Techasen, A.; Loilome, W.; Thongchot, S.; Thanan, R.; Sungkhamanon, S.; Khuntikeo, N.; Yongvanit, P.; Namwat, N. |
| Title |
Upregulation of TCTP is associated with cholangiocarcinoma progression and metastasis |
Type |
Journal Article |
| Year |
2017 |
Publication |
Oncology Letters |
Abbreviated Journal |
Oncol Lett |
| Volume |
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Issue |
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Pages |
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| Keywords |
64, 65 |
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1792-1074 |
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Approved |
no |
| Call Number |
ref @ user @ |
Serial |
98395 |
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| Author |
Guerrero, P.A.; Tchaicha, J.H.; Chen, Z.; Morales, J.E.; McCarty, N.; Wang, Q.; Sulman, E.P.; Fuller, G.; Lang, F.F.; Rao, G.; McCarty, J.H. |
| Title |
Glioblastoma stem cells exploit the alphavbeta8 integrin-TGFbeta1 signaling axis to drive tumor initiation and progression |
Type |
Journal Article |
| Year |
2017 |
Publication |
Oncogene |
Abbreviated Journal |
Oncogene |
| Volume |
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Issue |
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Pages |
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| Abstract |
Glioblastoma (GBM) is a primary brain cancer that contains populations of stem-like cancer cells (GSCs) that home to specialized perivascular niches. GSC interactions with their niche influence self-renewal, differentiation and drug resistance, although the pathways underlying these events remain largely unknown. Here, we report that the integrin alphavbeta8 and its latent transforming growth factor beta1 (TGFbeta1) protein ligand have central roles in promoting niche co-option and GBM initiation. alphavbeta8 integrin is highly expressed in GSCs and is essential for self-renewal and lineage commitment in vitro. Fractionation of beta8high cells from freshly resected human GBM samples also reveals a requirement for this integrin in tumorigenesis in vivo. Whole-transcriptome sequencing reveals that alphavbeta8 integrin regulates tumor development, in part, by driving TGFbeta1-induced DNA replication and mitotic checkpoint progression. Collectively, these data identify the alphavbeta8 integrin-TGFbeta1 signaling axis as crucial for exploitation of the perivascular niche and identify potential therapeutic targets for inhibiting tumor growth and progression in patients with GBM.Oncogene advance online publication, 7 August 2017; doi:10.1038/onc.2017.248. |
| Address |
Department of Neurosurgery, M. D. Anderson Cancer Center, Houston, TX, USA |
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English |
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Edition |
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| ISSN |
0950-9232 |
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| Notes |
PMID:28783169 |
Approved |
no |
| Call Number |
ref @ user @ |
Serial |
96572 |
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| Author |
Sareddy, G.R.; Viswanadhapalli, S.; Surapaneni, P.; Suzuki, T.; Brenner, A.; Vadlamudi, R.K. |
| Title |
Novel KDM1A inhibitors induce differentiation and apoptosis of glioma stem cells via unfolded protein response pathway |
Type |
Journal Article |
| Year |
2017 |
Publication |
Oncogene |
Abbreviated Journal |
Oncogene |
| Volume |
36 |
Issue |
17 |
Pages |
2423-2434 |
| Keywords |
Animals; Apoptosis/*drug effects; Cell Differentiation/*drug effects; Cell Line, Tumor; Cell Survival/drug effects; Cell Transformation, Neoplastic; Disease Progression; Enzyme Inhibitors/*pharmacology; Gene Expression Regulation, Neoplastic/drug effects; Glioma/*pathology; Histone Demethylases/*antagonists & inhibitors; Mice; Neoplastic Stem Cells/*drug effects/metabolism/pathology; Signal Transduction/drug effects; Survival Analysis; Transcription, Genetic/drug effects; Unfolded Protein Response/*drug effects |
| Abstract |
Glioma stem cells (GSCs) have a central role in glioblastoma (GBM) development and chemo/radiation resistance, and their elimination is critical for the development of efficient therapeutic strategies. Recently, we showed that lysine demethylase KDM1A is overexpressed in GBM. In the present study, we determined whether KDM1A modulates GSCs stemness and differentiation and tested the utility of two novel KDM1A-specific inhibitors (NCL-1 and NCD-38) to promote differentiation and apoptosis of GSCs. The efficacy of KDM1A targeting drugs was tested on purified GSCs isolated from established and patient-derived GBMs using both in vitro assays and in vivo orthotopic preclinical models. Our results suggested that KDM1A is highly expressed in GSCs and knockdown of KDM1A using shRNA-reduced GSCs stemness and induced the differentiation. Pharmacological inhibition of KDM1A using NCL-1 and NCD-38 significantly reduced the cell viability, neurosphere formation and induced apoptosis of GSCs with little effect on differentiated cells. In preclinical studies using orthotopic models, NCL-1 and NCD-38 significantly reduced GSCs-driven tumor progression and improved mice survival. RNA-sequencing analysis showed that KDM1A inhibitors modulate several pathways related to stemness, differentiation and apoptosis. Mechanistic studies showed that KDM1A inhibitors induce activation of the unfolded protein response (UPR) pathway. These results strongly suggest that selective targeting of KDM1A using NCL-1 and NCD-38 is a promising therapeutic strategy for elimination of GSCs. |
| Address |
Cancer Therapy and Research Center, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA |
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English |
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0950-9232 |
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| Notes |
PMID:27893719 |
Approved |
no |
| Call Number |
ref @ user @ |
Serial |
96621 |
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| Author |
Corvalan, C.; Garmendia, M.L.; Jones-Smith, J.; Lutter, C.K.; Miranda, J.J.; Pedraza, L.S.; Popkin, B.M.; Ramirez-Zea, M.; Salvo, D.; Stein, A.D. |
| Title |
Nutrition status of children in Latin America |
Type |
Journal Article |
| Year |
2017 |
Publication |
Obesity Reviews : an Official Journal of the International Association for the Study of Obesity |
Abbreviated Journal |
Obes Rev |
| Volume |
18 Suppl 2 |
Issue |
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Pages |
7-18 |
| Keywords |
Latin America; childhood obesity; children; nutrition and physical activity situation |
| Abstract |
The prevalence of overweight and obesity is rapidly increasing among Latin American children, posing challenges for current healthcare systems and increasing the risk for a wide range of diseases. To understand the factors contributing to childhood obesity in Latin America, this paper reviews the current nutrition status and physical activity situation, the disparities between and within countries and the potential challenges for ensuring adequate nutrition and physical activity. Across the region, children face a dual burden of undernutrition and excess weight. While efforts to address undernutrition have made marked improvements, childhood obesity is on the rise as a result of diets that favour energy-dense, nutrient-poor foods and the adoption of a sedentary lifestyle. Over the last decade, changes in socioeconomic conditions, urbanization, retail foods and public transportation have all contributed to childhood obesity in the region. Additional research and research capacity are needed to address this growing epidemic, particularly with respect to designing, implementing and evaluating the impact of evidence-based obesity prevention interventions. |
| Address |
Hubert Department of Global Health of the Rollins School of Public Health, Emory University, Atlanta, GA, USA |
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English |
Summary Language |
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Original Title |
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Series Title |
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Abbreviated Series Title |
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Series Issue |
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Edition |
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| ISSN |
1467-7881 |
ISBN |
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| Notes |
PMID:28741907 |
Approved |
no |
| Call Number |
ref @ user @ |
Serial |
97160 |
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