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https://www.readbyqxmd.com/read/28095325/peroxisome-proliferator-activated-receptor-%C3%AE-activation-inhibits-liver-growth-through-mir-122-mediated-downregulation-of-cmyc
#1
Andrei A Yarushkin, Yuliya A Kazantseva, Vyacheslav S Kobelev, Yuliya A Pustylnyak, Vladimir O Pustylnyak
Although NR1C3 agonists inhibit cell growth, the molecular mechanism of their action has not been thoroughly characterized to date. A recent study demonstrated that NR1C3 can regulate miR-122 by binding to its promoter. Given that miR-122 can indirectly regulate cMyc-mediated promitogenic signaling by targeting E2f1, we hypothesized that NR1C3 activation inhibits hepatocyte proliferation through miR-122-mediated cMyc downregulation. In the present study, we examined if liver hyperplasia induced by a strong chemical mitogen for the liver, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), which is an agonist of NR1I3, can be repressed by NR1C3 activation through miR-122 upregulation...
January 14, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28092370/api5-confers-cancer-stem-cell-like-properties-through-the-fgf2-nanog-axis
#2
K-H Song, H Cho, S Kim, H-J Lee, S J Oh, S R Woo, S-O Hong, H S Jang, K H Noh, C H Choi, J-Y Chung, S M Hewitt, J-H Kim, M Son, S-H Kim, B I Lee, H-C Park, Y-K Bae, T W Kim
Immune selection drives the evolution of tumor cells toward an immune-resistant and cancer stem cell (CSC)-like phenotype. We reported that apoptosis inhibitor-5 (API5) acts as an immune escape factor, which has a significant role in controlling immune resistance to antigen-specific T cells, but its functional association with CSC-like properties remains largely unknown. In this study, we demonstrated for the first time that API5 confers CSC-like properties, including NANOG expression, the frequency of CD44-positive cells and sphere-forming capacity...
January 16, 2017: Oncogenesis
https://www.readbyqxmd.com/read/28074012/reduced-abundance-of-the-e3-ubiquitin-ligase-e6ap-contributes-to-decreased-expression-of-the-ink4-arf-locus-in-non-small-cell-lung-cancer
#3
Cristina Gamell, Twishi Gulati, Yaara Levav-Cohen, Richard J Young, Hongdo Do, Pat Pilling, Elena Takano, Neil Watkins, Stephen B Fox, Prudence Russell, Doron Ginsberg, Brendon J Monahan, Gavin Wright, Alex Dobrovic, Sue Haupt, Ben Solomon, Ygal Haupt
The tumor suppressor p16(INK4a), one protein encoded by the INK4/ARF locus, is frequently absent in multiple cancers, including non-small cell lung cancer (NSCLC). Whereas increased methylation of the encoding gene (CDKN2A) accounts for its loss in a third of patients, no molecular explanation exists for the remainder. We unraveled an alternative mechanism for the silencing of the INK4/ARF locus involving the E3 ubiquitin ligase and transcriptional cofactor E6AP (also known as UBE3A). We found that the expression of three tumor suppressor genes encoded in the INK4/ARF locus (p15(INK4b), p16(INK4a), and p19(ARF)) was decreased in E6AP(-/-) mouse embryo fibroblasts...
January 10, 2017: Science Signaling
https://www.readbyqxmd.com/read/28070831/the-prolyl-oligopeptidase-inhibitor-suam-14746-attenuates-the-proliferation-of-human-breast-cancer-cell-lines-in-vitro
#4
Satoshi Tanaka, Kanayo Suzuki, Minoru Sakaguchi
BACKGROUND: Prolyl oligopeptidase (POP, EC 3.4.1.26) is a serine peptidase that hydrolyzes post-proline peptide bonds in peptides that are <30 amino acids in length. We previously reported that POP inhibition suppressed the growth of NB-1 human neuroblastomas cells and KATO III human gastric cancer cells. POP activity is commonly elevated in many cancers, which includes breast cancer. However, the effect of POP inhibition as a candidate breast cancer therapy is unknown. METHODS: The effects of POP inhibition and knockdown on the proliferation of cultured human estrogen receptor-positive (ER+) MCF7 and T47D, and ER-negative (ER-) MDA-MB-231 breast cancer cell lines and the MCF12A non-tumorigenic epithelial cell line were tested by analyzing their influence on cell proliferation (WST-1 assay), cell viability (trypan blue exclusion assay), and cell cycle arrest (cell cycle analysis, cell cycle regulator proteins expression)...
January 9, 2017: Breast Cancer: the Journal of the Japanese Breast Cancer Society
https://www.readbyqxmd.com/read/28069943/acetylation-promotes-tyrrs-nuclear-translocation-to-prevent-oxidative-damage
#5
Xuanye Cao, Chaoqun Li, Siyu Xiao, Yunlan Tang, Jing Huang, Shuan Zhao, Xueyu Li, Jixi Li, Ruilin Zhang, Wei Yu
Tyrosyl-tRNA synthetase (TyrRS) is well known for its essential aminoacylation function in protein synthesis. Recently, TyrRS has been shown to translocate to the nucleus and protect against DNA damage due to oxidative stress. However, the mechanism of TyrRS nuclear localization has not yet been determined. Herein, we report that TyrRS becomes highly acetylated in response to oxidative stress, which promotes nuclear translocation. Moreover, p300/CBP-associated factor (PCAF), an acetyltransferase, and sirtuin 1 (SIRT1), a NAD(+)-dependent deacetylase, regulate the nuclear localization of TyrRS in an acetylation-dependent manner...
January 9, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28068326/klf4-is-regulated-by-ras-raf-mek-erk-signaling-through-e2f1-and-promotes-melanoma-cell-growth
#6
M Riverso, V Montagnani, B Stecca
Melanoma is the most lethal form of skin cancer and treatment of metastatic melanoma remains challenging. BRAF/MEK inhibitors show only temporary benefit due the occurrence of resistance and immunotherapy is effective only in a subset of patients. To improve patient survival, there is a need to better understand molecular mechanisms that drive melanoma growth and operate downstream of the mitogen activated protein kinase (MAPK) signaling. The Krüppel-like factor 4 (KLF4) is a zinc-finger transcription factor that plays a critical role in embryonic development, stemness and cancer, where it can act either as oncogene or tumor suppressor...
January 9, 2017: Oncogene
https://www.readbyqxmd.com/read/28057797/prmt2-interacts-with-splicing-factors-and-regulates-the-alternative-splicing-of-bcl-x
#7
Mynol I Vhuiyan, Magnolia L Pak, Margaret A Park, Dylan Thomas, Ted M Lakowski, Charles E Chalfant, Adam Frankel
Protein arginine N-methyltransferase 2 (PRMT2) functions in JAK-STAT and Wnt/β-catenin signaling pathways, serves as a nuclear receptor-dependent transcriptional co-activator, and represses NF-κB and E2F1 transcription factor activities to promote apoptosis. We have previously demonstrated that PRMT2 interacts with PRMT1 and increases its activity. Here, we reveal associations using proteomics between the PRMT2 SH3 domain and splicing factors including Src-associated in mitosis 68 kDa protein (SAM68), a PRMT1 substrate and trans-acting factor that mediates BCL-X alternative splicing...
January 5, 2017: Journal of Biochemistry
https://www.readbyqxmd.com/read/28042453/design-and-synthesis-of-selective-small-molecule-inhibitors-of-coactivator-associated-arginine-methyltransferase-1-carm1
#8
H Ü Kaniskan, M S Eram, J Liu, D Smil, M L Martini, Y Shen, V Santhakumar, P J Brown, C Arrowsmith, M Vedadi, J Jin
Coactivator-associated arginine methyltransferase 1 (CARM1) is a type I protein arginine methyltransferase (PRMT) that catalyzes the conversion of arginine into monomethylarginine (MMA) and further into asymmetric dimethylarginine (ADMA). CARM1 methylates histone 3 arginines 17 and 26, as well as numerous non-histone proteins including CBP/p300, SRC-3, NCOA2, PABP1, and SAP49, while also functioning as a coactivator for various proteins that have been linked to cancer such as p53, NF-κβ, β-catenin, E2F1 and steroid hormone receptor ERα...
September 1, 2016: MedChemComm
https://www.readbyqxmd.com/read/28042322/chromatin-remodeling-factor-lsh-is-upregulated-by-the-lrp6-gsk3%C3%AE-e2f1-axis-linking-reversely-with-survival-in-gliomas
#9
Desheng Xiao, Jun Huang, Yu Pan, Hao Li, Chunyan Fu, Chao Mao, Yan Cheng, Ying Shi, Ling Chen, Yiqun Jiang, Rui Yang, Yating Liu, Jianhua Zhou, Ya Cao, Shuang Liu, Yongguang Tao
The signaling pathway-based stratification in chromatin modification could predict clinical outcome more reliably than morphology-alone-based classification schemes in gliomas. Here we reported a role of the chromatin-remodeling factor lymphoid-specific helicase (LSH) in gliomas. Among astrocytomas of grade I to III and glioblastoma of grade IV, LSH were almost completely expressed in all cases, and strongly correlated with astrocytomas progression and poor prognosis of patients with astrocytomas and glioblastoma...
2017: Theranostics
https://www.readbyqxmd.com/read/28042030/ectopic-expression-of-the-cdk-inhibitor-p21-cip1-enhances-deregulated-e2f-activity-and-increases-cancer-cell-specific-cytotoxic-gene-expression-mediated-by-the-arf-tumor-suppressor-promoter
#10
Kenta Kurayoshi, Ayumi Shiromoto, Eiko Ozono, Ritsuko Iwanaga, Andrew P Bradford, Keigo Araki, Kiyoshi Ohtani
In cancer treatment, specifically targeting cancer cells is important for optimal therapeutic efficacy. One strategy is to utilize a cancer specific promoter to express a cytotoxic gene or a viral gene required for replication. In this approach, the therapeutic window is dependent on the relative promoter activity in cancer cells versus normal cells. Therefore, a promoter with optimal cancer cell-specificity should be used. The tumor suppressor ARF promoter, which specifically responds to deregulated E2F activity, is a potent candidate...
December 29, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28031235/htp-nutraceutical-screening-for-histone-deacetylase-inhibitors-and-effects-of-hdacis-on-tumor-suppressing-mirnas-by-trichostatin-a-and-grapeseed-vitis-vinifera-in-hela-cells
#11
Elizabeth A Mazzio, Karam F A Soliman
BACKGROUND/AIM: Aggressive tumor malignancies are a consequence of delayed diagnosis, epigenetic/phenotype changes and chemo-radiation resistance. Histone deacetylases (HDACs) are a major epigenetic regulator of transcriptional repression, which are highly overexpressed in advanced malignancy. While original chemotherapy drugs were modeled after phytochemicals elucidated by botanical screenings, HDAC inhibitors (HDACi) such as apicidin, trichostatin A (TSA) and butyrate were discovered as products of fungus and microbes, in particular, gut microbiota...
2, 2017: Cancer Genomics & Proteomics
https://www.readbyqxmd.com/read/28008375/knockdown-of-ewsr1-fli1-expression-alters-the-transcriptome-of-ewing-sarcoma-cells-in-vitro
#12
Jihan Wang, Wenyan Jiang, Yuzhu Yan, Chu Chen, Yan Yu, Biao Wang, Heping Zhao
Ewing sarcoma breakpoint region 1 (EWSR1) fusion with Friend leukemia integration 1 transcription factor (FLI1) induced by a translocation of chromosome 11 with 22 contributes to Ewing sarcoma development. To date, the precise molecular mechanisms about EWSR1/FLI1 involving in Ewing sarcoma development remains to be defined. This study explored the potential critical gene targets of EWSR1/FLI1 knockdown in Ewing sarcoma cells on the gene expression profile based on online dataset, performed Limma algorithm for differentially expressed genes identification, constructed the transcriptional factor (TF)-gene regulatory network based on integrate transcriptional regulatory element database (TRED)...
November 2016: Journal of Bone Oncology
https://www.readbyqxmd.com/read/28007956/upregulation-of-rpa2-promotes-nf-%C3%AE%C2%BAb-activation-in-breast-cancer-by-relieving-the-antagonistic-function-of-menin-on-nf-%C3%AE%C2%BAb-regulated-transcription
#13
Chao-Chung Chen, Chi-Wen Juan, Kuan-Yu Chen, Yi-Chien Chang, Janq-Chang Lee, Ming-Chung Chang
RPA2, a subunit of the heterotrimeric replication protein A (RPA) complex, is overexpressed in various cancers. In this study, we showed a significant RPA2 upregulation in breast cancer tissues and cell lines. Ectopic expression of RPA2 in MCF7 and MDA-MB-231 cells promoted cell proliferation, adhesion, migration and invasion, and induced epithelial-mesenchymal transition (EMT) of MCF7 cells. Ablation of RPA2 in MDA-MB-231 cells induced apoptosis and suppressed colony formation, EMT and invasion. Binding assays indicated that menin, the MEN1 (multiple endocrine neoplasia type 1) tumor suppressor gene product, interacted with RPA2...
December 22, 2016: Carcinogenesis
https://www.readbyqxmd.com/read/28003426/pdk4-deficiency-results-in-expedited-cellular-proliferation-through-e2f1-mediated-increase-of-cyclins
#14
Jonathan P Choiniere, Jianguo Wu, Li Wang
Hepatocellular carcinoma (HCC) is a common form of cancer with prevalence worldwide. There are many factors that lead to the development and progression of HCC. The aim of this study was to identify potential new tumor suppressors and examine their function as cell cycle modulators and investigate their impact on the cyclin family of proteins and cyclin dependent kinases. In this study the pyruvate dehydrogenase kinase 4 (PDK4) gene was shown to have potential tumor suppressor characteristics. PDK4 expression was significantly downregulated in human HCC...
December 21, 2016: Molecular Pharmacology
https://www.readbyqxmd.com/read/27994550/anti-proliferative-and-apoptosis-inducing-effect-of-theabrownin-against-non-small-cell-lung-adenocarcinoma-a549-cells
#15
Feifei Wu, Li Zhou, Wangdong Jin, Weiji Yang, Ying Wang, Bo Yan, Wenlin Du, Qiang Zhang, Lei Zhang, Yonghua Guo, Jin Zhang, Letian Shan, Thomas Efferth
With the highest cancer incidence rate, lung cancer, especially non-small cell lung cancer (NSCLC), is the leading cause of cancer death in the world. Tea (leaves of Camellia sinensis) has been widely used as a traditional beverage beneficial to human health, including anti-NSCLC activity. Theabrownin (TB) is one major kind of tea pigment responsible for the beneficial effects of tea liquor. However, its effect on NSCLC is unknown. The aim of the present study was to evaluate anti-proliferative and apoptosis-inducing effect of TB on NSCLC (A549) cells, using MTT assay, morphological observation (DAPI staining), in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and annexin-V/PI flow cytometry...
2016: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27991597/sirt1-regulates-glial-progenitor-proliferation-and-regeneration-in-white-matter-after-neonatal-brain-injury
#16
Beata Jablonska, Marcin Gierdalski, Li-Jin Chew, Teresa Hawley, Mackenzie Catron, Arturo Lichauco, Juan Cabrera-Luque, Tracy Yuen, David Rowitch, Vittorio Gallo
Regenerative processes in brain pathologies require the production of distinct neural cell populations from endogenous progenitor cells. We have previously demonstrated that oligodendrocyte progenitor cell (OPC) proliferation is crucial for oligodendrocyte (OL) regeneration in a mouse model of neonatal hypoxia (HX) that reproduces diffuse white matter injury (DWMI) of premature infants. Here we identify the histone deacetylase Sirt1 as a Cdk2 regulator in OPC proliferation and response to HX. HX enhances Sirt1 and Sirt1/Cdk2 complex formation through HIF1α activation...
December 19, 2016: Nature Communications
https://www.readbyqxmd.com/read/27983535/e2f-transcription-factors-associated-with-up-regulated-genes-in-glioblastoma
#17
Flávia S Donaires, Paulo R D V Godoy, Giovana S Leandro, Elza T Sakamoto-Hojo
BACKGROUND: Glioblastoma corresponds to the most common and malignant brain tumor in adults. Patients have a median survival of approximately one year from diagnosis due to poor response to therapy. OBJECTIVE: We applied bioinformatics approaches to predict transcription factors (TF) that are deregulated in glioblastoma in an attempt to point out molecular targets for therapy. METHODS: Up-regulated genes in glioblastoma selected from public microarray data were submitted to two TF association analyses...
December 9, 2016: Cancer Biomarkers: Section A of Disease Markers
https://www.readbyqxmd.com/read/27981611/grb14-inhibition-triggers-insulin-induced-mouse-hepatocyte-proliferation-and-is-associated-with-hepatocellular-carcinoma
#18
Lucille Morzyglod, Michèle Caüzac, Lucie Popineau, Pierre-Damien Denechaud, Luis Fajas, Bruno Ragazzon, Véronique Fauveau, Julien Planchais, Mireille Vasseur-Cognet, Laetitia Fartoux, Olivier Scatton, Olivier Rosmorduc, Sandra Guilmeau, Catherine Postic, Chantal Desdouets, Christèle Desbois-Mouthon, Anne-Françoise Burnol
: Metabolic diseases such as obesity and type 2 diabetes are recognized as independent risk factors for hepatocellular carcinoma (HCC). Hyperinsulinemia, a hallmark of these pathologies, is suspected to be involved in HCC development. The molecular adapter Grb14 is an inhibitor of insulin receptor (IR) catalytic activity, highly expressed in the liver. To study its involvement in hepatocyte proliferation we specifically inhibited its liver expression using an shRNA strategy in mice. Enhanced insulin signaling upon Grb14 downregulation (Grb14i) was accompanied by a transient induction of S phase entrance by quiescent hepatocytes, indicating that Grb14 is a potent repressor of cell division...
December 16, 2016: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
https://www.readbyqxmd.com/read/27940962/rb-localizes-to-dna-double-strand-breaks-and-promotes-dna-end-resection-and-homologous-recombination-through-the-recruitment-of-brg1
#19
Renier Vélez-Cruz, Swarnalatha Manickavinayaham, Anup K Biswas, Regina Weaks Clary, Tolkappiyan Premkumar, Francesca Cole, David G Johnson
The retinoblastoma (RB) tumor suppressor is recognized as a master regulator that controls entry into the S phase of the cell cycle. Its loss leads to uncontrolled cell proliferation and is a hallmark of cancer. RB works by binding to members of the E2F family of transcription factors and recruiting chromatin modifiers to the promoters of E2F target genes. Here we show that RB also localizes to DNA double-strand breaks (DSBs) dependent on E2F1 and ATM kinase activity and promotes DSB repair through homologous recombination (HR), and its loss results in genome instability...
November 15, 2016: Genes & Development
https://www.readbyqxmd.com/read/27940439/repetitive-dna-elements-are-silenced-by-rb-mediated-ezh2-recruitment
#20
(no author information available yet)
RB-E2F1 recruits EZH2 to repetitive sequences, promoting repression via H3K27me3 deposition.
January 2017: Cancer Discovery
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