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https://www.readbyqxmd.com/read/27911270/saha-and-or-mg132-reverse-the-aggressive-phenotypes-of-glioma-cells-an-in-vitro-and-vivo-study
#1
Xue-Feng Yang, Zhi-Juan Zhao, Jia-Jie Liu, Xiang-Hong Yang, Yang Gao, Shuang Zhao, Shuai Shi, Ke-Qiang Huang, Hua-Chuan Zheng
To elucidate the anti-tumor effects and molecular mechanisms of SAHA (a histone deacetylase inhibitor) and MG132 (a proteasome inhibitor) on the aggressive phenotypes of glioma cells, we treated U87 and U251 cells with SAHA or/and MG132, and detected phenotypes' assays with phenotype-related molecules examined. It was found that SAHA or/and MG132 treatment suppressed proliferation in both concentration- and time-dependent manners, inhibited energy metabolism, migration, invasion and lamellipodia formation, and induced G2 arrest and apoptosis in the glioma cells...
November 29, 2016: Oncotarget
https://www.readbyqxmd.com/read/27901482/hyperglycemia-triggers-hipk2-protein-degradation
#2
Silvia Baldari, Alessia Garufi, Marisa Granato, Laura Cuomo, Giuseppa Pistritto, Mara Cirone, Gabriella D'Orazi
Homeodomain interacting protein kinase-2 (HIPK2) is an evolutionary conserved kinase that modulates several key molecular pathways to restrain tumor growth and induce p53-depending apoptotic cell-death in response to anticancer therapies. HIPK2 silencing in cancer cells leads to chemoresistance and cancer progression, in part due to p53 inhibition. Recently, hyperglycemia has been shown to reduce p53 phosphorylation at serine 46 (Ser46), the target residue of HIPK2, thus impairing p53 apoptotic function. Here we asked whether hyperglycemia could, upstream of p53, target HIPK2...
November 25, 2016: Oncotarget
https://www.readbyqxmd.com/read/27888613/psmc2-is-up-regulated-in-osteosarcoma-and-regulates-osteosarcoma-cell-proliferation-apoptosis-and-migration
#3
Mingzhi Song, Yong Wang, Zhen Zhang, Shouyu Wang
Proteasome 26S subunit ATPase 2 (PSMC2) is a recently identified gene potentially associated with certain human carcinogenesis. However, the expressional correlation and functional importance of PSMC2 in osteosarcoma is still unclear. Current study was focused on elucidating the significance of PSMC2 on malignant behaviors in osteosarcoma including proliferation, apoptosis, colony formation, migration as well as invasion. The high protein levels of PSMC2 in osteosarcoma samples were identified by tissue microarrays analysis...
November 23, 2016: Oncotarget
https://www.readbyqxmd.com/read/27875574/chidamide-inhibits-aerobic-metabolism-to-induce-pancreatic-cancer-cell-growth-arrest-by-promoting-mcl-1-degradation
#4
Mu He, Zhixin Qiao, Yanbing Wang, Qiyuan Kuai, Changlan Li, Yu Wang, Xingwei Jiang, Xuanlin Wang, Weijing Li, Min He, Suping Ren, Qun Yu
Pancreatic cancer is a fatal malignancy worldwide and urgently requires valid therapies. Previous research showed that the HDAC inhibitor chidamide is a promising anti-cancer agent in pancreatic cancer cell lines. In this study, we elucidate a probable underlying anti-cancer mechanism of chidamide involving the degradation of Mcl-1. Mcl-1 is frequently upregulated in human cancers, which has been demonstrated to participate in oxidative phosphorylation, in addition to its anti-apoptotic actions as a Bcl-2 family member...
2016: PloS One
https://www.readbyqxmd.com/read/27852045/different-bcr-abl-protein-suppression-patterns-as-a-converging-trait-of-chronic-myeloid-leukemia-cell-adaptation-to-energy-restriction
#5
Silvia Bono, Matteo Lulli, Vito Giuseppe D'Agostino, Federico Di Gesualdo, Rosa Loffredo, Maria Grazia Cipolleschi, Alessandro Provenzani, Elisabetta Rovida, Persio Dello Sbarba
BCR/Abl protein drives the onset and progression of Chronic Myeloid Leukemia (CML). We previously showed that BCR/Abl protein is suppressed in low oxygen, where viable cells retain stem cell potential. This study addressed the regulation of BCR/Abl protein expression under oxygen or glucose shortage, characteristic of the in vivo environment where cells resistant to tyrosine kinase inhibitors (TKi) persist. We investigated, at transcriptional, translational and post-translational level, the mechanisms involved in BCR/Abl suppression in K562 and KCL22 CML cells...
November 12, 2016: Oncotarget
https://www.readbyqxmd.com/read/27833612/15-deoxy-%C3%AE-12-14-prostaglandin-j2-modifies-components-of-the-proteasome-and-inhibits-inflammatory-responses-in-human-endothelial-cells
#6
Simone Marcone, Paul Evans, Desmond J Fitzgerald
15-Deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2) is an electrophilic lipid mediator derived from PGD2 with potent anti-inflammatory effects. These are likely to be due to the covalent modification of cellular proteins, via a reactive α,β-unsaturated carbonyl group in its cyclopentenone ring. This study was carried out to identify novel cellular target(s) for covalent modification by 15d-PGJ2 and to investigate the anti-inflammatory effects of the prostaglandin on endothelial cells (EC). The data presented here show that 15d-PGJ2 modifies and inhibits components of the proteasome and consequently inhibits the activation of the NF-κB pathway in response to TNF-α...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27814632/implication-of-cd38-gene-in-autophagic-degradation-of-collagen-i-in-mouse-coronary-arterial-myocytes
#7
Jun-Xiang Bao, Qin-Fang Zhang, Mi Wang, Min Xia, Krishna M Boini, Erich Gulbins, Yang Zhang, Pin-Lan Li
Collagen deposition is a hallmark of atherosclerosis. Although compromised collagen I degradation has been implied in the pathogenesis of atherosclerosis, the molecular mechanisms are still unclear. Thus, we determined the role of CD38, an enzyme involved in cellular calcium modulation and autophagic flux, in the regulation of collagen I degradation in coronary arterial myocytes (CAMs).In primary cultured CAMs from CD38(-/-) mice, collagen I protein accumulation but not mRNA abundance was significantly increased compared with cells from CD38(+/+) mice either under control or upon TGF-Beta stimulation...
January 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/27813130/p-glycoprotein-inhibition-sensitizes-human-breast-cancer-cells-to-proteasome-inhibitors
#8
Rahul R Deshmukh, Seongho Kim, Yasmine Elghoul, Q Ping Dou
Although effective for the treatment of hematological malignancies, the FDA approved proteasome inhibitors bortezomib and carfilzomib have limited efficacy in solid tumors including triple negative breast cancer (TNBC). Chemotherapy is the only option for treating TNBC due to the absence of specific therapeutic targets. Therefore, development of new TNBC therapeutic strategies has been warranted. We studied whether P-glycoprotein (P-gp) inhibition could sensitize TNBC cells to proteasome inhibitors. When verapamil, a P-gp inhibitor, was combined with the proteasome inhibitor MG132, bortezomib or carfilzomib, the cytotoxic effects and apoptosis in TNBC MDA-MB-231 cells were enhanced, compared to each treatment alone...
November 4, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27813087/antiglioma-effects-of-n6-isopentenyladenosine-an-endogenous-isoprenoid-end-product-through-the-downregulation-of-epidermal-growth-factor-receptor
#9
Elena Ciaglia, Mario Abate, Chiara Laezza, Simona Pisanti, Mario Vitale, Vincenzo Seneca, Giovanni Torelli, Silvia Franceschelli, Giuseppe Catapano, Patrizia Gazzerro, Maurizio Bifulco
Malignant gliomas are highly dependent on the isoprenoid pathway for the synthesis of lipid moieties critical for cell proliferation. The isoprenoid derivative N6-isopentenyladenosine (iPA) displays pleiotropic biological effects, including a direct anti-tumor activity in several tumor models. The antiglioma effects of iPA was then explored in U87MG cells both in vitro and grafted in mice and the related molecular mechanism confirmed in primary derived patients' glioma cells. iPA powerfully inhibited tumor cell growth and induced caspase-dependent apoptosis through a mechanism involving a marked accumulation of the pro-apoptotic BIM protein and inhibition of EGFR...
November 3, 2016: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/27806100/transcriptional-activation-of-pericentromeric-satellite-repeats-and-disruption-of-centromeric-clustering-upon-proteasome-inhibition
#10
Theona Natisvili, Cihangir Yandim, Raquel Silva, Giulia Emanuelli, Felix Krueger, Sathiji Nageshwaran, Richard Festenstein
Heterochromatinisation of pericentromeres, which in mice consist of arrays of major satellite repeats, are important for centromere formation and maintenance of genome stability. The dysregulation of this process has been linked to genomic stress and various cancers. Here we show in mice that the proteasome binds to major satellite repeats and proteasome inhibition by MG132 results in their transcriptional de-repression; this de-repression is independent of cell-cycle perturbation. The transcriptional activation of major satellite repeats upon proteasome inhibition is accompanied by delocalisation of heterochromatin protein 1 alpha (HP1α) from chromocentres, without detectable change in the levels of histone H3K9me3, H3K4me3, H3K36me3 and H3 acetylation on the major satellite repeats...
2016: PloS One
https://www.readbyqxmd.com/read/27774335/n-acetylcysteine-in-combination-with-igf-1-enhances-neuroprotection-against-proteasome-dysfunction-induced-neurotoxicity-in-sh-sy5y-cells
#11
Benxu Cheng, Pinki Anand, Anxiu Kuang, Feroz Akhtar, Virginia L Scofield
Ubiquitin proteasome system (UPS) dysfunction has been implicated in the development of many neuronal disorders, including Parkinson's disease (PD). Previous studies focused on individual neuroprotective agents and their respective abilities to prevent neurotoxicity following a variety of toxic insults. However, the effects of the antioxidant N-acetylcysteine (NAC) on proteasome impairment-induced apoptosis have not been well characterized in human neuronal cells. The aim of this study was to determine whether cotreatment of NAC and insulin-like growth factor-1 (IGF-1) efficiently protected against proteasome inhibitor-induced cytotoxicity in SH-SY5Y cells...
2016: Parkinson's Disease
https://www.readbyqxmd.com/read/27770661/pim-2-protects-h9c2-cardiomyocytes-from-hypoxia-reoxygenation-induced-apoptosis-via-downregulation-of-bim-expression
#12
Yan Xu, Yawei Xing, Yanjie Xu, Chahua Huang, Huihui Bao, Kui Hong, Xiaoshu Cheng
We know that silencing Bim, a pro-apoptosis protein, significantly attenuates glucose and oxygen-deprived induced apoptosis in cardiomyocytes. However, the mechanisms underlying the regulation of the Bim activation in the heart have remained unknown. Pim-2 is one of three Pim serine/threonine kinase family members thought to be involved in cell survival and proliferation. H9c2 cardiomyocytes were subjected to a hypoxia/reoxygenation (H/R) condition in vitro, mimicking ischemic/reperfusion injury in vivo. H/R augmented the expression of Bim, Cyt C, and Pim-2 and induced H9c2 cell apoptosis...
December 2016: Environmental Toxicology and Pharmacology
https://www.readbyqxmd.com/read/27766434/mg132-plus-apoptosis-antigen-1-apo-1-antibody-cooperate-to-restore-p53-activity-inducing-autophagy-and-p53-dependent-apoptosis-in-hpv16-e6-expressing-keratinocytes
#13
Alfredo Lagunas-Martínez, Enrique García-Villa, Magaly Arellano-Gaytán, Carla O Contreras-Ochoa, Jisela Dimas-González, María E López-Arellano, Vicente Madrid-Marina, Patricio Gariglio
The E6 oncoprotein can interfere with the ability of infected cells to undergo programmed cell death through the proteolytic degradation of proapoptotic proteins such as p53, employing the proteasome pathway. Therefore, inactivation of the proteasome through MG132 should restore the activity of several proapoptotic proteins. We investigated whether in HPV16 E6-expressing keratinocytes (KE6 cells), the restoration of p53 levels mediated by MG132 and/or activation of the CD95 pathway through apoptosis antigen-1 (APO-1) antibody are responsible for the induction of apoptosis...
October 20, 2016: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/27761169/characterization-of-the-novel-mutant-a78t-herg-from-a-long-qt-syndrome-type-2-patient-instability-of-the-mutant-protein-and-stabilization-by-heat-shock-factor-1
#14
Takehito Kondo, Ichiro Hisatome, Shouichi Yoshimura, Endang Mahati, Tomomi Notsu, Peili Li, Kazuhiko Iitsuka, Masaru Kato, Kazuyoshi Ogura, Junichiro Miake, Takeshi Aiba, Wataru Shimizu, Yasutaka Kurata, Shinji Sakata, Naoe Nakasone, Haruaki Ninomiya, Akira Nakai, Katsumi Higaki, Yasushi Kawata, Yasuaki Shirayoshi, Akio Yoshida, Kazuhiro Yamamoto
BACKGROUND: The human ether-a-go-go-related gene (HERG) encodes the α-subunit of rapidly activating delayed-rectifier potassium channels. Mutations in this gene cause long QT syndrome type 2 (LQT2). In most cases, mutations reduce the stability of the channel protein, which can be restored by heat shock (HS). METHODS: We identified the novel mutant A78T-HERG in a patient with LQT2. The purpose of the current study was to characterize this mutant protein and test whether HS and heat shock factors (HSFs) could stabilize the mutant protein...
October 2016: Journal of Arrhythmia
https://www.readbyqxmd.com/read/27746171/characterization-of-cadmium-chloride-induced-bip-accumulation-in-xenopus-laevis-a6-kidney-epithelial-cells
#15
Cody S Shirriff, John J Heikkila
Endoplasmic reticulum (ER) stress can result in the accumulation of unfolded/misfolded protein in the ER lumen, which can trigger the unfolded protein response (UPR) resulting in the activation of various genes including immunoglobulin-binding protein (BiP; also known as glucose-regulated protein 78 or HSPA5). BiP, an ER heat shock protein 70 (HSP70) family member, binds to unfolded protein, inhibits their aggregation and re-folds them in an ATP-dependent manner. While cadmium, an environmental contaminant, was shown to induce the accumulation of HSP70 in vertebrate cells, less information is available regarding the effect of this metal on BiP accumulation or function...
October 13, 2016: Comparative Biochemistry and Physiology. Toxicology & Pharmacology: CBP
https://www.readbyqxmd.com/read/27733367/depletion-of-vacuolar-protein-sorting-associated-protein-35-is-associated-with-increased-lysosomal-degradation-of-aquaporin-2
#16
Mi Suk Lee, Hyo-Jung Choi, Eui-Jung Park, Hye-Jeong Park, Tae-Hwan Kwon
The carboxyl terminus of aquaporin-2 (AQP2c) undergoes posttranslational modifications, including phosphorylation and ubiquitination, in the process of regulating aquaporin-2 (AQP2) translocation and protein abundance. We aimed to identify novel proteins interacting with AQP2c. Recombinant AQP2c protein was made in Escherichia coli BL21 (DE3) cells by exploiting the pET32 TrxA fusion system. Lysates of rat kidney inner medullary collecting duct (IMCD) tubule suspensions interacted with rat AQP2c bound to Ni(2+)-resin were subjected to LC-MS/MS proteomic analysis...
December 1, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27701455/regulation-of-hbegf-by-micro-rna-for-survival-of-developing-human-trophoblast-cells
#17
Chandni V Jain, Philip Jessmon, Brian A Kilburn, Meritxell Jodar, Edward Sendler, Stephen A Krawetz, D Randall Armant
INTRODUCTION: The growth factor HBEGF is upregulated post-transcriptionally in the low O2 environment of the human placenta during the first 10 weeks of pregnancy. We have examined the possible roles of HBEGF turnover and micro-RNA (miRNA) in its regulation by O2 in human first trimester trophoblast. METHODS: HTR-8/SVneo trophoblast cells were cultured at 2% or 20% O2. The cells were transfected with a dual luciferase reporter construct (psiCHECK-2) containing no insert (control), the HBEGF 3' untranslated region (3'UTR), or sub-regions of the 3'UTR, as well as with siRNA for DGCR8...
2016: PloS One
https://www.readbyqxmd.com/read/27696626/ubiquitin-proteasome-dependent-degradation-of-tbp-like-protein-is-prevented-by-direct-binding-of-tfiia
#18
Momoko Isogai, Hidefumi Suzuki, Ryo Maeda, Taka-Aki Tamura
Although the majority of gene expression is driven by TATA-binding protein (TBP)-based transcription machinery, it has been reported that TBP-related factors (TRFs) are also involved in the regulation of gene expression. TBP-like protein (TLP), which is one of the TRFs and exhibits the highest affinity to TFIIA among known proteins, has recently been showed to have significant roles in gene regulation. However, how the level of TLP is maintained in vivo has remained unknown. In this study, we explored the mechanism by which TLP protein is turned over in vivo and the factor that maintains the amount of TLP...
November 2016: Genes to Cells: Devoted to Molecular & Cellular Mechanisms
https://www.readbyqxmd.com/read/27693582/proteasome-inhibitor-mg132-impairs-autophagic-flux-through-compromising-formation-of-autophagosomes-in-bombyx-cells
#19
Ming-Ming Ji, Jae Man Lee, Hiroaki Mon, Jian Xu, Tsuneyuki Tatsuke, Takahiro Kusakabe
MG132 has been used as a proteasome inhibitor on Bombyx cells, but its physiological effects on autophagy still have not been elucidated. In this study, we find that the lipidated BmAtg8, BmAtg8-PE as an autophagosomal marker protein, is only localized to membranes. Then we established systems to monitor autophagic flux in Bombyx cells: Induction of autophagy reduces exogenous BmAtg8 and exogenous BmAtg8-PE, facilitates formation of autophagosomes indicated by green EGFP-BmAtg8 puncta after cotreatment by Rapamycin and Bafilomycin A1, and causes accumulation of free EGFP from EGFP-BmAtg8 cleavage in autolysosomes...
October 28, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27681126/suppression-of-host-innate-immune-response-by-hepatitis-c-virus-via-induction-of-autophagic-degradation-of-traf6
#20
Stephanie T Chan, Jiyoung Lee, Mansi Narula, J-H James Ou
: Tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6) is an important adaptor molecule that mediates the TNFR family and interleukin-1 (IL-1)/Toll-like receptor (TLR) signaling cascades. These pathways are important for the host to control viral infections. In this report, we demonstrated that hepatitis C virus (HCV) depleted TRAF6 from its host cells through a posttranslational mechanism. This depletion was independent of proteasomes, as it was not affected by the proteasome inhibitor MG132, but it was suppressed by bafilomycin A1, which led to the association of TRAF6 with autophagosomes...
December 1, 2016: Journal of Virology
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