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https://www.readbyqxmd.com/read/28211873/the-p53-family-members-have-distinct-roles-during-mammalian-embryonic-development
#1
Jeanine L Van Nostrand, Margot E Bowen, Hannes Vogel, Maria Barna, Laura D Attardi
The p53 tumor suppressor is a member of a multi-protein family, including the p63 and p73 transcription factors. These proteins can bind to the same consensus sites in DNA and activate the same target genes, suggesting that there could be functional redundancy between them. Indeed, double mutant mice heterozygous for any two family member-encoding genes display enhanced cancer phenotypes relative to single heterozygous mutants. However, whether the family members play redundant roles during embryonic development has remained largely unexplored...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28187431/recombinant-adeno-associated-virus-expressing-a-p53-derived-apoptotic-peptide-37aa-inhibits-hcc-cells-growth-in-vitro-and-in-vivo
#2
Hongyong Zhang, Yufeng Wang, Yanxia Bai, Yuan Shao, Jigang Bai, Zhenhua Ma, Qingguang Liu, Shengli Wu
Recent studies have confirmed that a p53-derived apoptotic peptide (37AA) could act as a tumor suppressor inducing apoptosis in multiple tumor cells through derepressing p73. However, the tumor suppressive effects of recombinant adeno-associated virus (rAAV) expressing 37AA on HCC cells are still unknown. In this study, we successfully constructed a recombinant rAAV expressing 37AA. In vitro and in vivo assays showed that transfection of NT4-37AA/rAAV in HCC cells strongly suppressed cell proliferation, induced apoptosis, and up-regulated the cellular expression of p73...
February 6, 2017: Oncotarget
https://www.readbyqxmd.com/read/28134496/p73-g4c14-to-a4t14-polymorphism-is-associated-with-survival-in-advanced-non-small-cell-lung-cancer-patients
#3
Lei Ge, Yang Yang, Yifeng Sun, Wen Xu, Daru Lu, Bo Su
BACKGROUND: p73, a structural and functional homolog of p53, plays an important role in modulating cell cycle arrest. This study investigated the association between p73 G4C14-to-A4T14 polymorphism and survival outcomes in a Chinese population of advanced non-small cell lung cancer (NSCLC) patients treated with platinum agents. METHODS: The p73 G4C14-to-A4T14 polymorphism was genotyped using DNA from blood samples of advanced NSCLC patients (642 in the discovery set and 330 in the replication set)...
January 30, 2017: Thoracic Cancer
https://www.readbyqxmd.com/read/28128397/meta-analysis-of-tp73-polymorphism-and-cervical-cancer
#4
H Feng, L Sui, M Du, Q Wang
The aim of this study was to investigate the tumor protein p73 (TP73) G4C14-A4T14 polymorphism and to perform a meta-analysis to assess TP73 expression in cervical cancer and precancerous tissue. Articles containing data regarding TP73 status in cervical cancer patients and healthy controls were retrieved from PubMed, EMBASE, Cochrane, Chinese Biomedical Literature, and China National Knowledge Infrastructure databases. Then, the quality of the studies was evaluated according to inclusion and exclusion criteria...
January 23, 2017: Genetics and Molecular Research: GMR
https://www.readbyqxmd.com/read/28122957/phosphoglycerate-mutase-1-regulates-dntp-pool-and-promotes-homologous-recombination-repair-in-cancer-cells
#5
Jia Qu, Wenyi Sun, Jie Zhong, Hao Lv, Mingrui Zhu, Jun Xu, Nan Jin, Zuoquan Xie, Minjia Tan, Shu-Hai Lin, Meiyu Geng, Jian Ding, Min Huang
Glycolytic enzymes are known to play pivotal roles in cancer cell survival, yet their molecular mechanisms remain poorly understood. Phosphoglycerate mutase 1 (PGAM1) is an important glycolytic enzyme that coordinates glycolysis, pentose phosphate pathway, and serine biosynthesis in cancer cells. Herein, we report that PGAM1 is required for homologous recombination (HR) repair of DNA double-strand breaks (DSBs) caused by DNA-damaging agents. Mechanistically, PGAM1 facilitates DSB end resection by regulating the stability of CTBP-interacting protein (CtIP)...
February 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28071670/benzyl-isothiocyanate-potentiates-p53-signaling-and-antitumor-effects-against-breast-cancer-through-activation-of-p53-lkb1-and-p73-lkb1-axes
#6
Bei Xie, Arumugam Nagalingam, Panjamurthy Kuppusamy, Nethaji Muniraj, Peter Langford, Balázs Győrffy, Neeraj K Saxena, Dipali Sharma
Functional reactivation of p53 pathway, although arduous, can potentially provide a broad-based strategy for cancer therapy owing to frequent p53 inactivation in human cancer. Using a phosphoprotein-screening array, we found that Benzyl Isothiocynate, (BITC) increases p53 phosphorylation in breast cancer cells and reveal an important role of ERK and PRAS40/MDM2 in BITC-mediated p53 activation. We show that BITC rescues and activates p53-signaling network and inhibits growth of p53-mutant cells. Mechanistically, BITC induces p73 expression in p53-mutant cells, disrupts the interaction of p73 and mutant-p53, thereby releasing p73 from sequestration and allowing it to be transcriptionally active...
January 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28055961/p73-to-the-rescue-role-of-rpl26
#7
Xiao-Xin Sun, Mu-Shui Dai
No abstract text is available yet for this article.
January 24, 2017: Oncotarget
https://www.readbyqxmd.com/read/28054503/inhibition-of-telomerase-using-bibr1532-enhances-doxorubicin-induced-apoptosis-in-pre-b-acute-lymphoblastic-leukemia-cells
#8
Davood Bashash, Mohadeseh Zareii, Ava Safaroghli-Azar, Mir Davood Omrani, Seyed H Ghaffari
OBJECTIVES: Interest into targeting telomerase in cancer has increased by the recent disclosure that elevated telomerase activity is associated with disease recurrence and poor outcome in cancers. In addition, cellular acquisition of unlimited replicative potential, which is closely related to the maintenance of telomeres mostly via the reactivation of telomerase, has been shown to confer loss of sensitivity to a wide range of anti-neoplastic agents. METHODS: To evaluate whether telomerase inhibition using non-nucleosidic inhibitor of telomerase BIBR1532 could enhance cytotoxic effect of doxorubicin in acute lymphoblastic leukemia, Nalm-6 pre-B ALL cells were subjected to combination treatment and subsequent cell viability, growth kinetics, caspase-3 activity, and transcriptional alteration of p73, p21, FOXO3a, c-Myc, hTERT, and other apoptosis-related target genes were investigated...
January 5, 2017: Hematology (Amsterdam, Netherlands)
https://www.readbyqxmd.com/read/28043938/mtorc1-activation-downregulates-fgfr3-and-pth-pthrp-receptor-in-articular-chondrocytes-to-initiate-osteoarthritis
#9
H Zhang, H Wang, C Zeng, B Yan, J Ouyang, X Liu, Q Sun, C Zhao, H Fang, J Pan, D Xie, J Yang, T Zhang, X Bai, D Cai
OBJECTIVE: Articular chondrocyte activation, involving aberrant proliferation and prehypertrophic differentiation, is essential for osteoarthritis (OA) initiation and progression. Disruption of mechanistic target of rapamycin complex 1 (mTORC1) promotes chondrocyte autophagy and survival, and decreases the severity of experimental OA. However, the role of cartilage mTORC1 activation in OA initiation is unknown. In this study, we elucidated the specific role of mTORC1 activation in OA initiation, and identify the underlying mechanisms...
December 31, 2016: Osteoarthritis and Cartilage
https://www.readbyqxmd.com/read/28025428/expression-of-p73-and-trail-in-odontogenic-cysts-and-tumors
#10
Marco Mascitti, Andrea Santarelli, Antonio Zizzi, Maurizio Procaccini, Lorenzo Lo Muzio, Corrado Rubini
Odontogenic tumors are a group of lesions arising from the odontogenic apparatus. Although the mechanism of oncogenesis and tumor progression in these lesions remains unknown, certain proteins, such as those involved in apoptosis, seem to be involved in the differentiation and proliferation of odontogenic epithelial cells. The aim of this study was to analyze the expression of p73 and TNF-related apoptosis-inducing ligand (TRAIL) in odontogenic tumors and cysts, and to clarify changes in the expression of these proteins...
2016: Journal of Oral Science
https://www.readbyqxmd.com/read/27959389/matrine%C3%A2-induced-apoptosis-in-hep3b-cells-via-the-inhibition-of-mdm2
#11
Ning Zhou, Jiequn Li, Ting Li, Guangshun Chen, Zhongqiang Zhang, Zhongzhou Si
Matrine, an alkaloid component derived from the Sophora root, can inhibit cancer cell proliferation and induce autophagy via p53 associated pathways. However, numerous tumor cells lack functional p53 and little is known about the effect of matrine on the p53‑deficient/mutant cancer cells. The present study aimed to assess anticancer effects of matrine in p53‑deficient human Hep3B hepatoma cells. The present results demonstrated that matrine caused Hep3B cell apoptosis by suppressing gene expression of minute double‑mutant (MDM)2...
January 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27957261/p53-p63-and-p73-expression-and-angiogenesis-in-keratocystic-odontogenic-tumors
#12
Soranun Chandrangsu, Kraisorn Sappayatosok
BACKGROUND: Keratocystic odontogenic tumors (KCOTSs) are odontogenic tumors previously referred to as odontogenic keratocysts. Several studies have reported that KCOT behavior is more like that of a benign neoplasm than a cyst. KCOTs are locally destructive and exhibit a high recurrence rate. The objective of this study is to characterize the expression of p53, p63 and p73 in KCOTs together with the relationship between their expression and KCOT angiogenesis and recurrence. MATERIAL AND METHODS: Standard indirect immunohistochemistry using monoclonal antibodies specific to human p53, p63, p73 and CD105 was performed in formalin-fixed paraffin-embedded tissue sections of 39 KCOT samples...
December 2016: Journal of Clinical and Experimental Dentistry
https://www.readbyqxmd.com/read/27919789/unravelling-a-p73-regulated-network-the-role-of-a-novel-p73-dependent-target-mir3158-in-cancer-cell-migration-and-invasiveness
#13
Sotiris Galtsidis, Stella Logotheti, Athanasia Pavlopoulou, Christos P Zampetidis, Georgia Papachristopoulou, Andreas Scorilas, Borek Vojtesek, Vassilis Gorgoulis, Vassilis Zoumpourlis
The transcription factor p73 is homologous to the well-known tumor-suppressor p53. The p73-regulated networks are of significant clinical interest, because they may substitute for impaired p53-regulated networks which are commonly perturbed in cancer. Herein, we aimed to characterize a p73-regulated network that mediates cell migration and restores anti-oncogenic responses in p53-mutant cancer cells. In this study, we demonstrate that p73 regulates a network underlying cell migration, which consists of MIR34A/MIR3158/vimentin/β-catenin/lef1...
December 3, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27902457/tfdp3-confers-chemoresistance-in-minimal-residual-disease-within-childhood-t-cell-acute-lymphoblastic-leukemia
#14
Ming Chu, Kailin Yin, Yujun Dong, Pingzhang Wang, Yun Xue, Peng Zhou, Yuqi Wang, Yuedan Wang
Acquired drug resistance in childhood T-cell acute lymphoblastic leukemia (T-ALL) remains a significant clinical problem. In this study, a novel gene therapy target for childhood T-ALL to overcome chemoresistance was discovered: TFDP3 increased in the minimal residual disease (MRD) positive childhood T-ALL patients. Then, we established a preclinical model of resistance to induction therapy to examine the functional relevance of TFDP3 to chemoresistance in MRD derived from Jurkat/E6-1. Jurkat xenografts in NOD/SCID mice were exposed to a four drug combination (VXLD) of vincristine (VCR), dexamethasone (DEX), L-asparaginase (L-asp) and daunorubicin (DNR)...
January 3, 2017: Oncotarget
https://www.readbyqxmd.com/read/27889317/the-p53-family-coordinates-wnt-and-nodal-inputs-in-mesendodermal-differentiation-of-embryonic-stem-cells
#15
Qiong Wang, Yilong Zou, Sonja Nowotschin, Sang Yong Kim, Qing V Li, Chew-Li Soh, Jie Su, Chao Zhang, Weiping Shu, Qiaoran Xi, Danwei Huangfu, Anna-Katerina Hadjantonakis, Joan Massagué
In this study, we outline a regulatory network that involves the p53 tumor suppressor family and the Wnt pathway acting together with the TGF-β pathway in mesendodermal differentiation of mouse and human embryonic stem cells. Knockout of all three members, p53, p63, and p73, shows that the p53 family is essential for mesendoderm specification during exit from pluripotency in embryos and in culture. Wnt3 and its receptor Fzd1 are direct p53 family target genes in this context, and induction of Wnt signaling by p53 is critical for activation of mesendodermal differentiation genes...
January 5, 2017: Cell Stem Cell
https://www.readbyqxmd.com/read/27884017/the-p53-family-orchestrates-the-regulation-of-metabolism-physiological-regulation-and-implications-for-cancer-therapy
#16
Marco Napoli, Elsa R Flores
The p53 family of transcription factors is essential to counteract tumour formation and progression. Although previously this was exclusively associated with the ability of the p53 family to induce cell cycle arrest and apoptosis, an increasing number of reports have now indisputably demonstrated that the tumour suppressive functions of the p53 family members also rely on their ability to control and regulate cellular metabolism and maintain cellular oxidative homeostasis. Here, we review how each p53 family member, including p63 and p73, controls metabolic pathways in physiological conditions, and how these mechanisms could be exploited to provide anticancer therapeutic opportunities...
January 17, 2017: British Journal of Cancer
https://www.readbyqxmd.com/read/27878984/sulforaphane-induced-apoptosis-in-xuanwei-lung-adenocarcinoma-cell-line-xwlc-05
#17
Lan Zhou, Qian Yao, Yan Li, Yun-Chao Huang, Hua Jiang, Chuan-Qiong Wang, Lei Fan
BACKGROUND: Xuanwei district in Yunnan Province has the highest incidence of lung cancer in China, especially among non-smoking women. Cruciferous vegetables can reduce lung cancer risk by prompting a protective mechanism against respiratory tract inflammation caused by air pollution, and are rich in sulforaphane, which can induce changes in gene expression. We investigated the effect of sulforaphane-induced apoptosis in Xuanwei lung adenocarcinoma cell line (XWCL-05) to explore the value of sulforaphane in lung cancer prevention and treatment...
January 2017: Thoracic Cancer
https://www.readbyqxmd.com/read/27866875/p53-and-p73-regulate-apoptosis-but-not-cell-cycle-progression-in-mouse-embryonic-stem-cells-upon-dna-damage-and-differentiation
#18
Hanbing He, Cheng Wang, Qian Dai, Fengtian Li, Johann Bergholz, Zhonghan Li, Qintong Li, Zhi-Xiong Xiao
Embryonic stem cells (ESCs) are fast proliferating cells capable of differentiating into all somatic cell types. In somatic cells, it is well documented that p53 is rapidly activated upon DNA damage to arrest the cell cycle and induce apoptosis. In mouse ESCs, p53 can also be functionally activated, but the precise biological consequences are not well characterized. Here, we demonstrated that doxorubicin treatment initially led to cell-cycle arrest at G2/M in ESCs, followed by the occurrence of massive apoptosis...
December 13, 2016: Stem Cell Reports
https://www.readbyqxmd.com/read/27865929/g2-m-cell-cycle-arrest-on-ht-29-cancer-cells-and-toxicity-assessment-of-triphenylphosphanegold-i-carbonimidothioates-ph3pau-sc-or-nph-r-me-et-and-ipr-during-zebrafish-development
#19
Kah Kooi Ooi, Chien Ing Yeo, Theventhiran Mahandaran, Kok Pian Ang, Abdah Md Akim, Yoke-Kqueen Cheah, Hoi-Ling Seng, Edward R T Tiekink
Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NPh], R=Me (1), Et (2) and iPr (3), were previously shown to be significantly cytotoxic toward HT-29 cancer cells and to induce cell death by both intrinsic and extrinsic apoptotic pathways whereby 1 activated the p73 gene, and each of 2 and 3 activated p53; 2 also caused apoptotic cell death via the c-Jun N-terminal kinase/mitogen-activated protein kinase pathway. Apoptosis pathways have been further evaluated by mitochondrial cytochrome c measurements and annexin V screening, confirming apoptotic pathways of cell death...
January 2017: Journal of Inorganic Biochemistry
https://www.readbyqxmd.com/read/27835605/meta-analysis-of-dna-methylation-biomarkers-in-hepatocellular-carcinoma
#20
Cheng Zhang, Jinyun Li, Tao Huang, Shiwei Duan, Dongjun Dai, Danjie Jiang, Xinbing Sui, Da Li, Yidan Chen, Fei Ding, Changxin Huang, Gongying Chen, Kaifeng Wang
DNA methylation is an epigenetic mechanism in the pathogenesis of hepatocellular carcinoma (HCC). Here, we conducted a systematic meta-analysis to evaluate the contribution of DNA methylation to the risk of HCC. A total of 2109 publications were initially retrieved from PubMed, Web of Science, Cochrane Library, Embase, CNKI and Wanfang literature database. After a four-step filtration, we harvested 144 case-control articles in the meta-analysis. Our results revealed that 24 genes (carcinoma tissues vs adjacent tissues), 17 genes (carcinoma tissues vs normal tissues) and six genes (carcinoma serums vs normal serums) were significantly hypermethylated in HCC...
November 8, 2016: Oncotarget
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