Database : MEDLINE
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[PMID]: 29511172
[Au] Autor:Zhou Y; Wei R; Zhang L; Chen Y; Lu S; Liang C; Wang Y; Xiao L; Zhang J; Bremner R; Chen D
[Ad] Address:Research Laboratory of Ophthalmology and Vision Sciences, Torsten-Wiesel Research Institute of World Eye Organization, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
[Ti] Title:Rb is required for retinal angiogenesis and lamination.
[So] Source:Cell Death Dis;9(3):370, 2018 Mar 06.
[Is] ISSN:2041-4889
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Retinoblastoma tumor suppressor (Rb) promotes cell cycle exit, survival, differentiation, and tumor suppression in the retina. Here, we show it is also essential for vascularization and lamination. Despite minimal effects on Hif1a target expression, intraretinal vascular plexi did not form in the Rb murine retina. Deleting adenovirus E2 promoter binding factor 3 (E2f3), which rescues starburst amacrine cell differentiation, or E2f2, had no effect, but deleting E2f1, which promotes neuronal cell cycle exit and survival, restored retinal vasculature. We specifically linked cell loss to the defect because removing Bax rescued rod and bipolar neurons and the vasculature, but not cell cycle exit. Despite rescuing Rb neurons, Bax deletion exacerbated a delay in outer retina lamination, and exposed a requirement for Rb in inner retina lamination. The latter resembled Sem5 or FAT atypical cadherin 3 (Fat3) mutants, but expression of Sem5/Fat3 pathway components, or that of Neogenin, which perturbs migration in the Rb cortex, was unchanged. Instead, lamination defects correlated with ectopic division, and were E2f1-dependent, implicating the cell cycle machinery. These in vivo studies expose new developmental roles for Rb, pinpoint aberrant E2f1 and Bax activity in neuronal death and vascular loss, and further implicate E2f1 in defective lamination. Links between Rb, angiogenesis and lamination have implications for the treatment of neovascularization, neurodegeneration and cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1038/s41419-018-0411-6

  2 / 21766 MEDLINE  
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[PMID]: 29369481
[Au] Autor:Xiao C; Wang Y; Zheng M; Chen J; Song G; Zhou Z; Zhou C; Sun X; Zhong L; Ding E; Zhang Y; Yang L; Wu G; Xu S; Zhang H; Wang X
[Ad] Address:Department of General Surgery, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
[Ti] Title:RBBP6 increases radioresistance and serves as a therapeutic target for preoperative radiotherapy in colorectal cancer.
[So] Source:Cancer Sci;, 2018 Jan 25.
[Is] ISSN:1349-7006
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Radiotherapy (RT) can be used as preoperative treatment to downstage initially unresectable locally rectal carcinoma, but radioresistance and recurrence remain significant problems. Retinoblastoma binding protein 6 (RBBP6) has been implicated in the regulation of cell cycle, apoptosis and chemoresistance both in vitro and in vivo. The present study investigated whether the inhibition of RBBP6 expression would improve radiosensitivity in human colorectal cancer cells. After SW620 and HT29 cells were exposed to radiation, the levels of RBBP6 mRNA and protein increased over time in both cells. Moreover, a significant reduction in clonogenic survival and a decrease in cell viability in parallel with an obvious increase in cell apoptosis were demonstrated in irradiated RBBP6-knockdown cells. Transfection with RBBP6 shRNA improved the levels of G2-M phase arrest, which blocked the cells in a more radiosensitive period of the cell cycle. These observations indicated that cell cycle and apoptosis mechanisms may be connected with tumor cell survival following radiotherapy. In vivo, the tumor growth rate of nude mice in the RBBP6-knockdown group was significantly slower than that in other groups. These results indicated that RBBP6 overexpression could resist colorectal cancer cells against radiation by regulating cell cycle and apoptosis pathways, and inhibition of RBBP6 could enhance radiosensitivity of human colorectal cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/cas.13516

  3 / 21766 MEDLINE  
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[PMID]: 29522490
[Au] Autor:Wu CH; Liu FC; Pan CH; Lai MT; Lan SJ; Wu CH; Sheu MJ
[Ad] Address:School of Pharmacy, China Medical University, Taichung 40402, Taiwan. u101055003@cmu.edu.tw.
[Ti] Title:Suppression of Cell Growth, Migration and Drug Resistance by Ethanolic Extract of Antrodia cinnamomea in Human Lung Cancer A549 Cells and C57BL/6J Allograft Tumor Model.
[So] Source:Int J Mol Sci;19(3), 2018 Mar 09.
[Is] ISSN:1422-0067
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:The purpose of this study was to investigate the inhibitory activities of ethanolic extracts from (EEAC) on lung cancer. Cell proliferation and cell cycle distribution were analyzed using (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) (MTT) assay and flow cytometry, respectively. Wound-healing assay, Western blotting, and a murine tumor model were separately used to examine cell migration, protein expression, and tumor repression. Our results showed that EEAC induced cell cycle arrest at the G0/G1 phase resulting decreased cell viability in A549 cells. Moreover, EEAC up-regulated the growth-suppressing proteins, adenosine 5'-monophosphate-activated protein kinase (AMPK), p21 and p27, but down-regulated the growth-promoting proteins, protein kinase B (Akt), mammalian tarfet of rapamycin (mTOR), extracellular signal-regulating kinase 1/2 (ERK1/2), retinoblastoma protein (Rb), cyclin E, and cyclin D1. EEAC also inhibited A549 cell migration and reduced expression of gelatinases. In addition, our data showed that tumor growth was suppressed after treatment with EEAC in a murine allograft tumor model. Some bioactive compounds from EEAC, such as cordycepin and zhankuic acid A, were demonstrated to reduce the protein expressions of matrix metalloproteinase (MMP)-9 and cyclin D1 in A549 cells. Furthermore, EEAC enhanced chemosensitivity of A549 to paclitaxel by reducing the protein levels of caveolin-1. Our data suggests that EEAC has the potential to be an adjuvant medicine for the treatment of lung cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process

  4 / 21766 MEDLINE  
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[PMID]: 29518772
[Au] Autor:Çakmakli S; Çankaya T; Gürsoy S; Koç A; Kirbiyik Ö; Kiliçarslan ÖA; Özer E; Erçal D; Bozkaya ÖG
[Ad] Address:Department of Medical Genetics, Faculty of Medicine, Dokuz Eylul University, Izmir, Turkey.
[Ti] Title:Two Cases with Ring Chromosome 13 at either End of the Phenotypic Spectrum.
[So] Source:Cytogenet Genome Res;, 2018 Mar 09.
[Is] ISSN:1424-859X
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Ring chromosome 13 is a rare genetic condition with an incidence of 1/58,000 in live births. Major clinical features of patients with ring chromosome 13 include growth and developmental retardation, microcephaly, facial dysmorphism, ambiguous genitalia, anal atresia, eye malformations, retinoblastoma, and hand, foot, and toe abnormalities. The severity of the phenotype depends on the amount of genetic material lost during ring chromosome formation. Here, we report 2 cases with ring chromosome 13 at either end of the phenotypic spectrum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1159/000486775

  5 / 21766 MEDLINE  
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[PMID]: 29518612
[Au] Autor:Du X; Qi F; Lu S; Li Y; Han W
[Ad] Address:Department of Pulmonary Medicine, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao 266011, China.
[Ti] Title:Nicotine upregulates FGFR3 and RB1 expression and promotes non-small cell lung cancer cell proliferation and epithelial-to-mesenchymal transition via downregulation of miR-99b and miR-192.
[So] Source:Biomed Pharmacother;101:656-662, 2018 Mar 05.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:BACKGROUND: Tobacco smoke is by far the greatest risk factor for non-small-cell lung cancer (NSCLC). Nicotine, an active alkaloid in tobacco, is unable to initiate tumorigenesis in humans and rodents, but can promote the growth and metastasis of various tumors, including NSCLC, initiated by tobacco carcinogens. Recently, cigarette smoke is reported to downregulate 24 miRNAs more than 3-fold in the lungs of rats, and most of these downregulated miRNAs are associated with NSCLC initiation and development. Nicotine as the major tobacco component might be associated with the expression changes of some miRNAs. METHODS: qRT-PCR was performed to determine the miRNA and mRNA expression, and western blot was conducted to measure protein expression. MTT assay was used to detect cell proliferation. RESULTS: The effects of nicotine on the expression of 24 miRNAs in NSCLC cell lines were determined, and the results showed that nicotine treatment decreased miR-99b and miR-192 expression. Cell proliferation and epithelial-to-mesenchymal transition (EMT) detection showed that nicotine promoted NSCLC cell proliferation and EMT, and restoration of miR-99b or miR-192 expression relieved the effects of nicotine on NSCLC cell proliferation and EMT. Subsequently, fibroblast growth factor receptor 3 (FGFR3) and retinoblastoma 1 (RB1) were confirmed to be the targets of miR-99b and miR-192, respectively, and were upregulated by nicotine in NSCLC cells. In addition, FGFR3 or RB1 knockdown inhibited NSCLC cell proliferation and EMT. CONCLUSION: This study, for the first time, elucidates nicotine-miR-99b/miR-192-FGFR3/RB1 regulatory network that nicotine promotes NSCLC cell proliferation and EMT by downregulating miR-99b and miR-192, and upregulating their targets FGFR3 and RB1. These findings offer novel insights into the understanding of underlying molecular mechanisms of NSCLC related with the nicotine effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher

  6 / 21766 MEDLINE  
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[PMID]: 29468545
[Au] Autor:Pérez-Morales J; Núñez-Marrero A; Santiago-Cardona PG
[Ad] Address:Biochemistry and Cancer Biology Divisions, Basic Science Department, Ponce Health Sciences University, Ponce, Puerto Rico. jaileene.perez@gmail.com.
[Ti] Title:Immunohistochemical Detection of Retinoblastoma Protein Phosphorylation in Human Tumor Samples.
[So] Source:Methods Mol Biol;1726:77-84, 2018.
[Is] ISSN:1940-6029
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The retinoblastoma protein (pRb) is an important tumor suppressor and cell cycle repressor. pRb is a phosphoprotein whose function is regulated primarily at the level of phosphorylation, and therefore, detecting pRb's phosphorylation status in human tissue samples can be clinically informative. Unfortunately, detection of phosphorylated pRb residues can be technically challenging, as these residues can often be weak antigens. In this chapter, we describe an enhanced sensitivity immunohistochemistry protocol for the staining of phosphorylated serine 249 in pRb, in human lung tumor samples.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/978-1-4939-7565-5_8

  7 / 21766 MEDLINE  
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[PMID]: 29468543
[Au] Autor:Santiago-Cardona PG; Pérez-Morales J; González-Flores J
[Ad] Address:Biochemistry and Cancer Biology Divisions, Basic Science Department, Ponce Health Sciences University, Ponce, Puerto Rico. psantiago@psm.edu.
[Ti] Title:Detection of Retinoblastoma Protein Phosphorylation by Immunoblot Analysis.
[So] Source:Methods Mol Biol;1726:49-64, 2018.
[Is] ISSN:1940-6029
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The retinoblastoma tumor suppressor protein (pRb) is a preeminent tumor suppressor that acts as a cell cycle repressor, specifically as an inhibitor of the G1-S transition of the cell cycle . pRb is a phosphoprotein whose function is repressed by extensive phosphorylation in several key residues, and therefore, pRb's phosphorylation status has become a surrogate for pRb activity. In particular, hyperphosphorylation of pRb has been associated with pathological states such as cancer, and therefore, assessing pRb's phosphorylation status is increasingly gaining diagnostic and prognostic value, may be used to inform therapeutic decisions, and is also an important tool for the cancer biologists seeking an understanding of the molecular etiology of cancer. In this chapter, we discuss an immunoblot protocol to detect pRb phosphorylation in two residues, serine 612 and threonine 821, in protein extracts from cancer cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/978-1-4939-7565-5_6

  8 / 21766 MEDLINE  
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[PMID]: 29400026
[Au] Autor:El Bakkouri W; Blanc R; Benzakin S; Abdellaoui A; Boyeldieu L; Ayache D
[Ti] Title:[Innovations in interventional radiology applied to the field of otolaryngology: A pictorial essay].
[So] Source:Rev Laryngol Otol Rhinol (Bord);136(3):91-5, 2015.
[Is] ISSN:0035-1334
[Cp] Country of publication:France
[La] Language:fre
[Ab] Abstract:The management of hypervascular ENT tumors is usually complex and requires a multidisciplinary approach because of the risk of serious intra-operative bleeding and of potential injuries to cranial nerves and/or large cervical vessels. Over the last four decades, advances in neuro-interventional radio­logical procedures have produced a range of adjunctive endo­vascular techniques in addition to conventional surgery. A pictorial essay in ENT specialty is presented in this article highlighting the most relevant innovations in interventional radiology.
[Mh] MeSH terms primary: Otolaryngology
Radiology, Interventional
[Mh] MeSH terms secundary: Hemorrhage/therapy
Humans
Ophthalmic Artery
Retinal Neoplasms/drug therapy
Retinoblastoma/drug therapy
Tinnitus/therapy
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:180206
[St] Status:MEDLINE

  9 / 21766 MEDLINE  
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[PMID]: 29372378
[Au] Autor:Chen X; Kunda PE; Lin J; Zhou M; Huang J; Zhang H; Liu T
[Ad] Address:The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, 710049, China.
[Ti] Title:SYK-targeted dendritic cell-mediated cytotoxic T lymphocytes enhance the effect of immunotherapy on retinoblastoma.
[So] Source:J Cancer Res Clin Oncol;144(4):675-684, 2018 Apr.
[Is] ISSN:1432-1335
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: Retinoblastoma (RB) is the most common primary intraocular tumor in children. Chemotherapy is currently the main method of RB treatment. Unfortunately, RB often becomes chemoresistant and turns lethal. Here, we used in vitro cell immunotherapy to explore whether adoptive immunotherapy could be used as a potential treatment for RB. We focused on spleen tyrosine kinase (SYK), which is significantly upregulated in RB cells and serves as a marker for RB cells. METHODS: Using lentiviruses, we genetically modified dendritic cells (DCs) to express and present the SYK peptide antigen to cytotoxic T lymphocytes (CTLs) in vitro. We used SYK-negative cell lines (MDA-MB-231, MCF-10A, and hTERT-RPE1) and SYK-positive cell lines (MCF-7 and RB-Y79) to evaluate the specificity and cytotoxicity of DC presented CTLs using FACS, live-cell imaging, and RNA interference. RESULTS: The cytotoxicity of CTLs induced by SYK-overexpressing DCs (SYK-DC-CTLs) was enhanced more than three times in SYK-positive cell lines compared with SYK-negative cell lines. DCs primed with SYK could drive CTL cytotoxicity against SYK-positive cell lines but not against SYK-negative cell lines. Moreover, SYK-silenced RB-Y79 cells successfully evaded the cytotoxic attack from SYK-DC-CTLs. However, SYK-DC-CTLs could target SYK overexpressed hTERT-RPE1 cells, suggesting that SYK is a specific antigen for RB. Furthermore, SYK-DC-CTL exhibited specific cytotoxicity against carboplatin-resistant RB-Y79 cells in vitro. CONCLUSIONS: Our data showed that SYK could be a potential immunotherapy target mediated by DCs. We propose SYK as a candidate target for treatment of chemoresistant RB.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1007/s00432-018-2584-x

  10 / 21766 MEDLINE  
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[PMID]: 29330306
[Au] Autor:Liao Y; Du W
[Ad] Address:From the Ben May Department for Cancer Research, University of Chicago, Chicago, Illinois 60637.
[Ti] Title:An Rb family-independent E2F3 transcription factor variant impairs STAT5 signaling and mammary gland remodeling during pregnancy in mice.
[So] Source:J Biol Chem;293(9):3156-3167, 2018 Mar 02.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:E2F transcription factors are regulated by binding to the retinoblastoma (Rb) tumor suppressor family of proteins. Previously, we reported an mutation that disrupts the binding with Rb proteins without affecting the transcriptional activity of E2F. We also showed that mouse embryonic fibroblasts with an mutation exhibit increased E2F activity and more rapid cell proliferation. In this report, we analyzed mice to further characterize the consequences of Rb family-independent E2F3 activity. We found that homozygous mice were viable and had no obvious developmental defects or tumor growth. Our results also indicated that cells largely retain normal control of cell proliferation However, female mice had partial nursing defects. Examination of the mammary glands revealed increased caveolin-1 (CAV1) expression, reduced prolactin receptor/Stat5 signaling, and impaired pregnancy-induced cell proliferation and differentiation. Of note, ChIP experiments disclosed that E2F3 binds the CAV1 promoter. Furthermore, E2F3 overexpression induced CAV1 expression, and CRISPR/CAS9-mediated E2F3 knockout reduced CAV1 levels and also increased prolactin receptor-induced Stat5 signaling in mammary epithelial cells. Our results suggest that the Rb family-independent E2F3 variant inhibits pregnancy-induced mammary gland cell proliferation and differentiation by up-regulating CAV1 expression and inhibiting Stat5 signaling.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1074/jbc.RA117.000583


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