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https://www.readbyqxmd.com/read/29157111/hmga2-cooperates-with-either-p27-kip1-deficiency-or-cdk4-r24c-mutation-in-pituitary-tumorigenesis
#1
Monica Fedele, Orlando Paciello, Davide De Biase, Mario Monaco, Gennaro Chiappetta, Michela Vitiello, Antonio Barbieri, Domenica Rea, Antonio Luciano, Serenella Papparella, Claudio Arra, Alfredo Fusco
We have previously reported a critical role of HMGA proteins in pituitary tumorigenesis since either the Hmga1 or Hmga2 gene overexpression/activation induces the development of mixed growth hormone/prolactin cell pituitary adenomas by activating the E2F transcription factor 1, and then enhancing the G1/S transition of the cell cycle. Consistently, amplification and overexpression of the HMGA2 gene was found in human pituitary prolactinomas. Since impairment of the cell cycle control represents a feature of experimental and human pituitary adenomas, we have investigated the possible synergism between the alterations of other cell cycle regulators, such as p27 deficiency or Cdk4(R24C) mutation, with Hmga2 overexpression in pituitary tumorigenesis...
November 20, 2017: Cell Cycle
https://www.readbyqxmd.com/read/29151585/defining-the-molecular-basis-of-oncogenic-cooperation-between-tal1-expression-and-pten-deletion-in-t-all-using-a-novel-pro-t-cell-model-system
#2
S Bornschein, S Demeyer, R Stirparo, O Gielen, C Vicente, E Geerdens, B Ghesquière, S Aerts, J Cools, C E de Bock
T-cell acute lymphoblastic leukemia (T-ALL) is caused by the accumulation of multiple mutations combined with the ectopic expression of transcription factors in developing T cells. However, the molecular basis underlying cooperation between transcription factor expression and additional oncogenic mutations in driving T-ALL has been difficult to assess due to limited robust T cell model systems. Here we utilize a new ex vivo pro-T cell model to study oncogenic cooperation. Using a systems biological approach we first dissect the pro-T cell signaling network driven by interleukin-7 (Il7), stem cell factor (Scf) and Notch1 and identify key downstream Akt, Stat, E2f and Myc genetic signaling networks...
November 20, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/29138545/activation-of-notch1-signaling-alleviates-dysfunction-of-bone-marrow-derived-mesenchymal-stem-cells-induced-by-cigarette-smoke-extract
#3
Yi Cheng, Wen Gu, Guorui Zhang, Xiaoming Li, Xuejun Guo
Bone marrow-derived mesenchymal stem cells (BM-MSCs) are considered attractive therapeutic agents for the treatment of COPD. However, little is known about the impact of Notch on the proliferation, migration, and survival of MSCs in a cigarette smoke (CS) microenvironment. Here, we used CS extract to mimic the CS microenvironment in vitro, with the intention to investigate the effect of Notch in regulating proliferation, migration, and survival of BM-MSCs. Rat bone marrow mesenchymal stem cells were infected with lentivirus vector containing the intracellular domain of Notch1 (N1ICD) and challenged with CS extract...
2017: International Journal of Chronic Obstructive Pulmonary Disease
https://www.readbyqxmd.com/read/29137393/synergistic-effect-of-eribulin-and-cdk-inhibition-for-the-treatment-of-triple-negative-breast-cancer
#4
Shreyas S Rao, Jenna Stoehr, Danijela Dokic, Lei Wan, Joseph T Decker, Kristine Konopka, Alexandra L Thomas, Jia Wu, Virginia G Kaklamani, Lonnie D Shea, Jacqueline S Jeruss
Activation of CDK2 in triple negative breast cancer (TNBC) can contribute to non-canonical phosphorylation of a TGFβ signaling component, Smad3, promoting cell proliferation and migration. Inhibition of CDK2 was shown to decrease breast cancer oncogenesis. Eribulin chemotherapy was used effectively in the treatment of TNBC. To this end, we tested therapeutic efficacy of a novel CDK2/9 inhibitor, CYC065, eribulin, and the combination of CYC065 and eribulin in 3 different TNBC cell lines, and an in vivo xenograft model...
October 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/29136005/a-17-molecule-set-as-a-predictor-of-complete-response-to-neoadjuvant-chemotherapy-with-docetaxel-cisplatin-and-5-fluorouracil-in-esophageal-cancer
#5
Hajime Fujishima, Shoichi Fumoto, Tomotaka Shibata, Kohei Nishiki, Yoshiyuki Tsukamoto, Tsuyoshi Etoh, Masatsugu Moriyama, Norio Shiraishi, Masafumi Inomata
BACKGROUND: Recently, neoadjuvant chemotherapy with docetaxel/cisplatin/5-fluorouracil (NAC-DCF) was identified as a novel strong regimen with a high rate of pathological complete response (pCR) in advanced esophageal cancer in Japan. Predicting pCR will contribute to the therapeutic strategy and the prevention of surgical invasion. However, a predictor of pCR after NAC-DCF has not yet been developed. The aim of this study was to identify a novel predictor of pCR in locally advanced esophageal cancer treated with NAC-DCF...
2017: PloS One
https://www.readbyqxmd.com/read/29125603/cell-cycle-arrest-through-indirect-transcriptional-repression-by-p53-i-have-a-dream
#6
REVIEW
Kurt Engeland
Activation of the p53 tumor suppressor can lead to cell cycle arrest. The key mechanism of p53-mediated arrest is transcriptional downregulation of many cell cycle genes. In recent years it has become evident that p53-dependent repression is controlled by the p53-p21-DREAM-E2F/CHR pathway (p53-DREAM pathway). DREAM is a transcriptional repressor that binds to E2F or CHR promoter sites. Gene regulation and deregulation by DREAM shares many mechanistic characteristics with the retinoblastoma pRB tumor suppressor that acts through E2F elements...
November 10, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29115436/sirt5-promotes-cell-proliferation-and-invasion-in-hepatocellular-carcinoma-by-targeting-e2f1
#7
Liang Chang, Liang Xi, Yubin Liu, Rui Liu, Zhongshi Wu, Zhixiang Jian
Sirtuin 5 (SIRT5) is a member of the NAD+‑dependent class III protein deacetylases. Although it is known that SIRT5 deacetylates and activates urate oxidase in the liver mitochondria of mice, the mechanism of SIRT5 in the proliferation of hepatocellular carcinoma (HCC) remains to be fully elucidated. The present study investigated the expression and functional significance of SIRT5 in HCC, and examined the relevant mechanism. SIRT5 was found to be upregulated in HCC tissues and cell lines, and the higher expression of SIRT5 indicated poorer overall survival...
October 25, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29115400/global-gene-expression-analysis-combined-with-a-genomics-approach-for-the-identification-of-signal-transduction-networks-involved-in-postnatal-mouse-myocardial-proliferation-and-development
#8
Ruoxin Wang, Chao Su, Xinting Wang, Qiang Fu, Xingjie Gao, Chunyan Zhang, Jie Yang, Xi Yang, Minxin Wei
Mammalian cardiomyocytes may permanently lose their ability to proliferate after birth. Therefore, studying the proliferation and growth arrest of cardiomyocytes during the postnatal period may enhance the current understanding regarding this molecular mechanism. The present study identified the differentially expressed genes in hearts obtained from 24 h‑old mice, which contain proliferative cardiomyocytes; 7‑day‑old mice, in which the cardiomyocytes are undergoing a proliferative burst; and 10‑week‑old mice, which contain growth‑arrested cardiomyocytes, using global gene expression analysis...
November 3, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29113170/screening-of-potential-therapy-targets-for-prostate-cancer-using-integrated-analysis-of-two-gene-expression-profiles
#9
Rui Zhao, Yao Wang, Muchun Zhang, Xinquan Gu, Weihua Wang, Jiufeng Tan, Xin Wei, Ning Jin
The aim of the present study was to analyze potential therapy targets for prostate cancer using integrated analysis of two gene expression profiles. First, gene expression profiles GSE38241 and GSE3933 were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between prostate cancer and normal control samples were identified using the Linear Models for Microarray Data package. Pathway enrichment analysis of DEGs was performed using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes...
November 2017: Oncology Letters
https://www.readbyqxmd.com/read/29109143/microrna-874-mediated-inhibition-of-the-major-g1-s-phase-cyclin-ccne1-is-lost-in-osteosarcomas
#10
Tanushree Ghosh, Akhil Varshney, Praveen Kumar, Manpreet Kaur, Vipin Kumar, Ritu Shekhar, Raksha Devi, Priyanka Priyanka, Md Muntaz Khan, Sandeep Saxena
The tumor microenvironment is characterized by nutrient-deprived conditions in which the cancer cells have to adapt for survival. Serum starvation resembles the growth factor deprivation characteristic of the poorly vascularized tumor microenvironment and has aided in the discovery of key growth regulatory genes and microRNAs (miRNAs) that have a role in the oncogenic transformation. We report here that miR-874 downregulates the major G1/S phase cyclin, cyclin E1 (CCNE1), during serum starvation. Since the adaptation of cancer cells to the tumor microenvironment is vital for subsequent oncogenesis, we tested for miR-874 and CCNE1 interdependence in osteosarcoma cells...
November 6, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29106686/the-identification-of-pivotal-transcriptional-factors-mediating-cell-responses-to-drugs-with-drug-induced-liver-injury-liabilities
#11
Falgun Shah, Alex Medvedev, Anne Mai Wassermann, Marian Brodney, Liying Zhang, Sergei Makarov, Robert V Stanton
Drug-induced liver injury (DILI) is a leading cause of drug attrition during drug development and a common reason for drug withdrawal from the market. The poor predictability of conventional animal-based approaches (Olson et al. 2000) necessitates the development of alternative testing approaches. Body of evidence associates DILI with the induction of stress-response genes in the liver cells (Yuan and Kaplowitz 2013). Here, we set out to identify signal transduction pathways predominantly involved in the regulation of gene transcription by DILI drugs...
November 2, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/29100415/the-e2f-activators-control-multiple-mitotic-regulators-and-maintain-genomic-integrity-through-sgo1-and-bubr1
#12
Miyoung Lee, Yainyrette Rivera-Rivera, Carlos S Moreno, Harold I Saavedra
The E2F1, E2F2, and E2F3a transcriptional activators control proliferation. However, how the E2F activators regulate mitosis to maintain genomic integrity is unclear. Centrosome amplification (CA) and unregulated spindle assembly checkpoint (SAC) are major generators of aneuploidy and chromosome instability (CIN) in cancer. Previously, we showed that overexpression of single E2F activators induced CA and CIN in mammary epithelial cells, and here we show that combined overexpression of E2F activators did not enhance CA...
September 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/29091720/loss-of-the-caenorhabditis-elegans-pocket-protein-lin-35-reveals-muvb-s-innate-function-as-the-repressor-of-dream-target-genes
#13
Paul D Goetsch, Jacob M Garrigues, Susan Strome
The DREAM (Dp/Retinoblastoma(Rb)-like/E2F/MuvB) transcriptional repressor complex acts as a gatekeeper of the mammalian cell cycle by establishing and maintaining cellular quiescence. How DREAM's three functional components, the E2F-DP heterodimer, the Rb-like pocket protein, and the MuvB subcomplex, form and function at target gene promoters remains unknown. The current model invokes that the pocket protein links E2F-DP and MuvB and is essential for gene repression. We tested this model by assessing how the conserved yet less redundant DREAM system in Caenorhabditis elegans is affected by absence of the sole C...
November 2017: PLoS Genetics
https://www.readbyqxmd.com/read/29072692/mir-99a-reveals-two-novel-oncogenic-proteins-e2f2-and-emr2-and-represses-stemness-in-lung-cancer
#14
Andrea Feliciano, Yoelsis Garcia-Mayea, Luz Jubierre, Cristina Mir, Manuela Hummel, Josep Castellvi, Javier Hernández-Losa, Rosanna Paciucci, Irene Sansano, Yilin Sun, Santiago Ramón Y Cajal, Hiroshi Kondon, Aroa Soriano, Miguel Segura, Alex Lyakhovich, Matilde E LLeonart
Lung cancer is one of the most aggressive tumours with very low life expectancy. Altered microRNA expression is found in human tumours because it is involved in tumour growth, progression and metastasis. In this study, we analysed microRNA expression in 47 lung cancer biopsies. Among the most downregulated microRNAs we focussed on the miR-99a characterisation. In vitro experiments showed that miR-99a expression decreases the proliferation of H1650, H1975 and H1299 lung cancer cells causing cell cycle arrest and apoptosis...
October 26, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/29072058/p16ink4a-expression-in-cervical-lesions-correlates-with-histologic-grading-a-tertiary-level-medical-facility-based-retrospective-study
#15
Usha Sarma, Ira Biswas, Alakananda Das, Gokul Chandra Das, Chandan Saikia, Bidula Sarma
p16INK4a is a tumor-suppressor protein and cyclin-dependent kinase (cdk) inhibitor that blocks cdk4- and cdk6-mediated pRb phosphorylation to inhibit E2F-dependent transcription and cell-cycle progression. Because the E7 protein of high-risk HPVs inactivates pRB, the resulting overexpression of p16INK4a may be a good marker for infection with high risk HPV types. Immunostaining of p16INK4a allows precise identification of even small CIN or cervical cancer lesions in biopsy sections and can help reduce inter-observer variation in the histopathological interpretation of cervical biopsy specimens...
October 26, 2017: Asian Pacific Journal of Cancer Prevention: APJCP
https://www.readbyqxmd.com/read/29059406/dynamic-site-specific-recruitment-of-rbp2-by-pocket-protein-p130-modulates-h3k4-methylation-on-e2f-responsive-promoters
#16
Zaffer Ullah Zargar, Mallikharjuna Rao Kimidi, Shweta Tyagi
The Histone 3 lysine 4 methylation (H3K4me3) mark closely correlates with active transcription. E2F-responsive promoters display dynamic changes in H3K4 methylation during the course of cell cycle progression. However, how and when these marks are reset, is not known. Here we show that the retinoblastoma binding protein RBP2/KDM5A, capable of removing tri-methylation marks on H3K4, associates with the E2F4 transcription factor via the pocket protein-p130-in a cell-cycle-stage specific manner. The association of RBP2 with p130 is LxCxE motif dependent...
October 20, 2017: Nucleic Acids Research
https://www.readbyqxmd.com/read/29050203/loss-of-egr1-a-human-del5q-gene-accelerates-bcr-abl-driven-chronic-myelogenous-leukemia
#17
Silvia Maifrede, Andrew Magimaidas, Xiaojin Sha, Kaushiki Mukherjee, Dan A Liebermann, Barbara Hoffman
There is substantial evidence that early growth response-1 (Egr1) gene, a zinc-finger transcription factor, behaves as a tumor suppressor in leukemia. This includes reports from this laboratory that constitutive Egr1 overrides leukemia conferred by deregulated c-Myc or E2F-1 in the M1 myeloid leukemic cell line by promoting differentiation. To investigate the effect of Egr1 on the initiation and progression of Chronic Myelogenous Leukemia (CML), lethally irradiated syngeneic wild type mice were reconstituted with bone marrow (BM) from either wild type or Egr1 null mice transduced with a 210-kD BCR-ABL-expressing MSCV-retrovirus (bone marrow transplantation {BMT})...
September 19, 2017: Oncotarget
https://www.readbyqxmd.com/read/29039555/mir-363-inhibits-the-growth-migration-and-invasion-of-hepatocellular-carcinoma-cells-by-regulating-e2f3
#18
Junfeng Ye, Wei Zhang, Songyang Liu, Yahui Liu, Kai Liu
A growing body of evidence suggests that microRNA-363 (miR-363) plays crucial roles in tumor progression, development and metastasis, and confer resistance to chemotherapeutic drugs in several types of cancers. However, the biological function and underlying molecular mechanism of miR-363 in hepatocellular carcinoma (HCC) have not been fully elucidated. In the present study, we investigated the biological function and mechanism of miR-363 in the regulation of HCC progression. We found that miR-363 was downregulated in HCC cell lines and tissues, and a low expression level of miR-363 was associated with tumor differentiation, TNM stage and lymph node metastasis...
October 10, 2017: Oncology Reports
https://www.readbyqxmd.com/read/29025894/nascent-rna-sequencing-reveals-a-dynamic-global-transcriptional-response-at-genes-and-enhancers-to-the-natural-medicinal-compound-celastrol
#19
Noah Dukler, Gregory T Booth, Yi-Fei Huang, Nathaniel Tippens, Colin T Waters, Charles G Danko, John T Lis, Adam Siepel
Most studies of responses to transcriptional stimuli measure changes in cellular mRNA concentrations. By sequencing nascent RNA instead, it is possible to detect changes in transcription in minutes rather than hours and thereby distinguish primary from secondary responses to regulatory signals. Here, we describe the use of PRO-seq to characterize the immediate transcriptional response in human cells to celastrol, a compound derived from traditional Chinese medicine that has potent anti-inflammatory, tumor-inhibitory, and obesity-controlling effects...
November 2017: Genome Research
https://www.readbyqxmd.com/read/29023247/mir-449a-a-potential-therapeutic-agent-for-cancer
#20
He Yong-Ming, Ji Ai-Jun, Xu Xiao-Yue, Lu Jian-Wei, Yu Chen, Chen Ye
MicroRNAs (miRNAs) have been reported to be associated with cancer progression and carcinogenesis. They are small, highly conserved, noncoding RNA molecules consisting of 19-25 nucleotides. By binding to complementary binding sites within the 3'-untranslated region of target mRNAs, miRNAs inhibit the translation of mRNAs or promote their degradation. miRNAs play critical roles in cancer initiation and development by functioning either as oncogenes or as tumor suppressors. Similarly, several studies have shown that miRNAs are involved in regulating various biological processes, including apoptosis, proliferation, cellular differentiation, signal transduction, and carcinogenesis...
November 2017: Anti-cancer Drugs
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