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Yue Wang, Runping Fang, Ming Cui, Weiying Zhang, Xiao Bai, Huawei Wang, Bowen Liu, Xiaodong Zhang, Lihong Ye
The oncoprotein Yes-associated protein (YAP) in Hippo pathway plays crucial roles in the development of cancer. However, the mechanism of YAP regulation in cancer remains poorly understood. Here, we supposed that the oncoprotein hepatitis B X-interacting protein (HBXIP) might be involved in the modulation of YAP in liver cancer. Interestingly, our data showed that the expression levels of HBXIP were positively associated with those of YAP in clinical hepatocellular carcinoma (HCC) samples by immunohistochemistry (IHC) staining and real-time PCR assays...
October 17, 2016: Cancer Letters
Sagar Uttarkar, Therese Piontek Ellendorff, Sandeep Dukare, Caroline Schomburg, Peter Schlenke, Wolfgang E Berdel, Carsten Muller-Tidow, Thomas J Schmidt, Karl-Heinz Klempnauer
The transcription factor c-Myb is essential for the proliferation of hematopoietic cells and has been implicated in the development of leukemia and other human cancers. Pharmacological inhibition of Myb is therefore emerging as a potential therapeutic strategy for these diseases. By using a Myb reporter cell line we have identified plumbagin and several naphthoquinones as potent low-molecular weight Myb inhibitors. We demonstrate that these compounds inhibit c-Myb by binding to the c-Myb transactivation domain and disrupting the cooperation of c-Myb with the co-activator p300, a major driver of Myb activity...
October 5, 2016: Molecular Cancer Therapeutics
Xuefeng Li, Sisi He, Rongpeng Li, Xikun Zhou, Shuang Zhang, Min Yu, Yan Ye, Yongsheng Wang, Canhua Huang, Min Wu
MicroRNAs (miRNAs) play critical roles in various biological processes, including cell proliferation, development and host defence. However, the molecular mechanism for miRNAs in regulating bacterial-induced inflammation remains largely unclear. Here, we report that miR-301b augments pro-inflammatory response during pulmonary infection, and caffeine suppresses the effect of miR-301b and thereby augments respiratory immunity. LPS treatment or Pseudomonas aeruginosa infection induces miR-301b expression via a TLR4/MyD88/NF-κB pathway...
August 8, 2016: Nature Microbiology
C Chen, K-Y Jia, H-L Zhang, J Fu
OBJECTIVE: In this study, we explored the regulative effect of miR-195 on c-myb expression and also investigated the role of miR-195 and c-myb in cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) injury. MATERIALS AND METHODS: QRT-PCR analysis was performed to measure mature miR-195 expression. H9c2 cells were transfected for miR-195 overexpression or knockdown or c-myb overexpression using Lipofectamine 2000. The cells were subjected to H/R treatment and following flow cytometric analysis of active caspase-3 or florescent study of reactive oxygen species (ROS) generation...
August 2016: European Review for Medical and Pharmacological Sciences
Junfang Zhang, Bingshe Han, Xiaoxia Li, Juraj Bies, Penglei Jiang, Richard P Koller, Linda Wolff
The c-Myb transcription factor is a major regulator that controls differentiation and proliferation of hematopoietic progenitor cells, which is frequently deregulated in hematological diseases, such as lymphoma and leukemia. Understanding of the mechanisms regulating the transcription of c-myb gene is challenging as it lacks a typical promoter and multiple factors are involved. Our previous studies identified some distal regulatory elements in the upstream regions of c-myb gene in murine myeloid progenitor M1 cells, but the detailed mechanisms still remain unclear...
2016: Cell Death & Disease
Christina Kyrousi, Maria-Eleni Lalioti, Eleni Skavatsou, Zoi Lygerou, Stavros Taraviras
Ependymal cells are multiciliated cells located in the wall of the lateral ventricles of the adult mammalian brain and are key components of the subependymal zone niche, where adult neural stem cells reside. Through the movement of their motile cilia, ependymal cells control the cerebrospinal fluid flow within the ventricular system from which they receive secreted molecules and morphogens controlling self-renewal and differentiation decisions of adult neural stem cells. Multiciliated ependymal cells become fully differentiated at postnatal stages however they are specified during mid to late embryogenesis from a population of radial glial cells...
2016: Neurogenesis (Austin, Tex.)
Noah I Hornick, Ben Doron, Sherif Abdelhamed, Jianya Huan, Christina A Harrington, Rongkun Shen, Xiaolu A Cambronne, Santhosh Chakkaramakkil Verghese, Peter Kurre
Exosomes are paracrine regulators of the tumor microenvironment and contain complex cargo. We previously reported that exosomes released from acute myeloid leukemia (AML) cells can suppress residual hematopoietic stem and progenitor cell (HSPC) function indirectly through stromal reprogramming of niche retention factors. We found that the systemic loss of hematopoietic function is also in part a consequence of AML exosome-directed microRNA (miRNA) trafficking to HSPCs. Exosomes isolated from cultured AML or the plasma from mice bearing AML xenografts exhibited enrichment of miR-150 and miR-155...
2016: Science Signaling
A L Ho, L Dunn, E J Sherman, M G Fury, S S Baxi, R Chandramohan, S Dogan, L G T Morris, G D Cullen, S Haque, C S Sima, A Ni, C R Antonescu, N Katabi, D G Pfister
BACKGROUND: Recurrent/metastatic adenoid cystic carcinoma (ACC) is an incurable disease with no standard treatments. The majority of ACCs express the oncogenic transcription factor MYB (also c-myb), often in the context of a MYB gene rearrangement. This phase II trial of the tyrosine kinase inhibitor (TKI) axitinib (Pfizer) tested the hypothesis that targeting pathways activated by MYB can be therapeutically effective for ACC. PATIENTS AND METHODS: This is a minimax two-stage, phase II trial that enrolled patients with incurable ACC of any primary site...
October 2016: Annals of Oncology: Official Journal of the European Society for Medical Oncology
Huihui Li, Jinhui Hai, Jiang Zhou, Gu Yuan
C-myb proto-oncogene is a potential therapeutic target for some human solid tumors and leukemias. A long cytosine-rich sequence, which locates the downstream of the transcription initiation site, is demonstrated to fold into an intramolecular i-motif DNA using electrospray ionization mass spectrometry (ESI-MS) and circular dichroism (CD) spectroscopy. Effects of factors, including the pH value, the number of C:C(+) dimers, the concentration of buffer, the molecular crowding condition, and the coexistence of the complementary DNA, on the formation and the structural stability of the i-motif DNA are systematically studied...
September 2016: Journal of Photochemistry and Photobiology. B, Biology
W Liu, M Wu, Z Huang, J Lian, J Chen, T Wang, A Y H Leung, Y Liao, Z Zhang, Q Liu, K Yen, S Lin, L I Zon, Z Wen, Y Zhang, W Zhang
The c-MYB transcription factor is a key regulator of hematopoietic cell proliferation and differentiation, and dysregulation of c-MYB activity often associates with various hematological disorders. Yet, its pathogenic role remains largely unknown due to lack of suitable animal models. Here, we report a detail characterization of a c-myb-gfp transgenic zebrafish harboring c-Myb hyperactivity (named c-myb(hyper)). This line exhibits abnormal granulocyte expansion that resembles human myelodysplastic syndrome (MDS) from embryonic stage to adulthood...
July 26, 2016: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
Raúl Esteban Ithuralde, Adrián Enrique Roitberg, Adrián Gustavo Turjanski
Intrinsically disordered proteins (IDPs) are a set of proteins that lack a definite secondary structure in solution. IDPs can acquire tertiary structure when bound to their partners; therefore, the recognition process must also involve protein folding. The nature of the transition state (TS), structured or unstructured, determines the binding mechanism. The characterization of the TS has become a major challenge for experimental techniques and molecular simulations approaches since diffusion, recognition, and binding is coupled to folding...
July 20, 2016: Journal of the American Chemical Society
Kazumi Nakano, Kaoru Uchimaru, Atae Utsunomiya, Kazunari Yamaguchi, Toshiki Watanabe
PURPOSE: Adult T-cell leukemia/lymphoma (ATLL) is an aggressive human T-cell malignancy induced by human T-lymphotrophic virus-1 (HTLV-1) infection. The genetic alterations in infected cells that lead to transformation have not been completely elucidated, thus hindering the identification of effective therapeutic targets for ATL. Here, we present the first assessment of MYB proto-oncogene dysregulation in ATL and an exploration of its role in the onset of ATL. EXPERIMENTAL DESIGN: We investigated the expression patterns of MYB splicing variants in ATL...
June 15, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
Femke Heindryckx, François Binet, Markella Ponticos, Krista Rombouts, Joey Lau, Johan Kreuger, Pär Gerwins
ER stress results in activation of the unfolded protein response and has been implicated in the development of fibrotic diseases. In this study, we show that inhibition of the ER stress-induced IRE1α signaling pathway, using the inhibitor 4μ8C, blocks TGFβ-induced activation of myofibroblasts in vitro, reduces liver and skin fibrosis in vivo, and reverts the fibrotic phenotype of activated myofibroblasts isolated from patients with systemic sclerosis. By using IRE1α(-/-) fibroblasts and expression of IRE1α-mutant proteins lacking endoribonuclease activity, we confirmed that IRE1α plays an important role during myofibroblast activation...
2016: EMBO Molecular Medicine
Nasimudeen R Jabir, Chelapram K Firoz, Ashish Bhushan, Shams Tabrez, Mohammad A Kamal
Cancer is one of the leading cause of death worldwide. In view of ever increasing number associated with cancer related death, there is an urgent need to find out a novel compound especially of natural origin (better efficacy, low or no toxicity and cost effective) that could serve against the treatment of all forms of cancer. Currently available treatment options related with cancer have their certain limitations especially in case of solid tumors. In search of natural anticancer compound, alkaloids in general have been exploited by the scientist working in this field of research...
May 20, 2016: Anti-cancer Agents in Medicinal Chemistry
Yihao Li, Ke Jin, Gabi W van Pelt, Hans van Dam, Xiao Yu, Wilma E Mesker, Peter Ten Dijke, Fangfang Zhou, Long Zhang
The molecular underpinnings of aggressive breast cancers remain mainly obscure. Here we demonstrate that activation of the transcription factor c-Myb is required for the prometastatic character of basal breast cancers. An analysis of breast cancer patients led us to identify c-Myb as an activator of Wnt/β-catenin signaling. c-Myb interacted with the intracellular Wnt effector β-catenin and coactivated the Wnt/β-catenin target genes Cyclin D1 and Axin2 Moreover, c-Myb controlled metastasis in an Axin2-dependent manner...
June 1, 2016: Cancer Research
Peng Deng, Ling Chen, Zheng Liu, Ping Ye, Sihua Wang, Jie Wu, Yufeng Yao, Yuan Sun, Xiaofan Huang, Linyun Ren, Anchen Zhang, Ke Wang, Chuangyan Wu, Zhang Yue, Xuezeng Xu, Manhua Chen
BACKGROUND/AIMS: Cardiac fibrosis is the primary cause of deteriorated cardiac function in various cardiovascular diseases. Numerous studies have demonstrated that microRNAs (miRNAs) are critical regulators of myocardial fibrosis. Specifically, many studies have reported that miR-150 is downregulated in cardiovascular diseases, such as acute myocardial infarction (AMI), myocardial hypertrophy and myocardial fibrosis. However, the exact role of miR-150 in these pathological processes remains unknown...
2016: Cellular Physiology and Biochemistry
Eric A Shikatani, Mark Chandy, Rickvinder Besla, Cedric C Li, Abdul Momen, Omar El-Mounayri, Clinton S Robbins, Mansoor Husain
OBJECTIVE: Vascular smooth muscle cells (VSMCs) are believed to dedifferentiate and proliferate in response to vessel injury. Recently, adventitial progenitor cells were implicated as a source of VSMCs involved in vessel remodeling. c-Myb is a transcription factor known to regulate VSMC proliferation in vivo and differentiation of VSMCs from mouse embryonic stem cell-derived progenitors in vitro. However, the role of c-Myb in regulating specific adult vascular progenitor cell populations was not known...
July 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
Changchun Xiao, Dinis Pedro Calado, Gunther Galler, To-Ha Thai, Heide Christine Patterson, Jing Wang, Nikolaus Rajewsky, Timothy P Bender, Klaus Rajewsky
No abstract text is available yet for this article.
May 5, 2016: Cell
Yi-Han Dai, Liang-Yi Hung, Ruo-Yu Chen, Chien-Hsien Lai, Kung-Chao Chang
Diffuse large B-cell lymphoma (DLBCL), the most common lymphoma, shows either no response or development of resistance to further treatment in 30% of the patients that warrants the development of novel drugs. We have reported that ON 01910.Na (rigosertib), a multikinase inhibitor, is selectively cytotoxic for DLBCL and induces more hyperphosphorylation and sumoylation of Ran GTPase-activating protein 1 (RanGAP1) in DLBCL cells than in non-neoplastic lymphoblastoid cell line. However, the exact mechanism of rigosertib-induced cell death in DLBCL remains to be clarified...
September 2016: Translational Research: the Journal of Laboratory and Clinical Medicine
Lucie Pekarčíková, Lucia Knopfová, Petr Beneš, Jan Šmarda
The c-Myb transcription factor is important for maintenance of immature cells of many tissues including colon epithelium. Overexpression of c-Myb occurring in colorectal carcinomas (CRC) as well as in other cancers often marks poor prognosis. However, the molecular mechanism explaining how c-Myb contributes to progression of CRC has not been fully elucidated. To address this point, we investigated the way how c-Myb affects sensitivity of CRC cells to anticancer drugs. Using CRC cell lines expressing exogenous c-myb we show that c-Myb protects CRC cells from the cisplatin-, oxaliplatin-, and doxorubicin-induced apoptosis, elevates reactive oxygen species via up-regulation of NOX1, and sustains the pro-survival p38 MAPK pathway...
August 2016: Cellular Signalling
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