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p53 family member

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https://www.readbyqxmd.com/read/29030916/identification-and-characterization-of-a-metastatic-suppressor-brms1l-as-a-target-gene-of-p53
#1
Ryota Koyama, Miyuki Tamura, Takafumi Nakagaki, Tomoko Ohashi, Masashi Idogawa, Hiromu Suzuki, Takashi Tokino, Yasushi Sasaki
The tumor suppressor p53 and its family members, p63 and p73, play a pivotal role in the cell fate determination in response to diverse upstream signals. As transcription factors, p53 family proteins regulate a number of genes that are involved in cell-cycle arrest, apoptosis, senescence, and maintenance of genomic stability. Recent studies revealed that p53 family proteins are important for the regulation of cell invasion and migration. Microarray analysis showed that breast cancer metastasis-suppressor 1- like (BRMS1L) is upregulated by p53 family proteins, specifically p53, TAp63γ, and TAp73β...
October 13, 2017: Cancer Science
https://www.readbyqxmd.com/read/28984872/p53-shades-of-hippo
#2
Noa Furth, Yael Aylon, Moshe Oren
The three p53 family members, p53, p63 and p73, are structurally similar and share many biochemical activities. Yet, along with their common fundamental role in protecting genomic fidelity, each has acquired distinct functions related to diverse cell autonomous and non-autonomous processes. Similar to the p53 family, the Hippo signaling pathway impacts a multitude of cellular processes, spanning from cell cycle and metabolism to development and tumor suppression. The core Hippo module consists of the tumor-suppressive MST-LATS kinases and oncogenic transcriptional co-effectors YAP and TAZ...
October 6, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28982757/another-case-for-diet-restriction-tap73-expressing-medulloblastomas-are-stunted-by-glutamine-withdrawal
#3
REVIEW
Marco Napoli, Elsa R Flores
Medulloblastomas are among the most common malignant brain cancers in the pediatric population and consist of at least four distinct subgroups with unique molecular and genetic features and clinical outcomes. In this issue of Genes & Development, Niklison-Chirou and colleagues (pp. 1738-1753) identify the p53 family member and p73 isoform TAp73 as a crucial factor causing glutamine addiction in aggressive medulloblastomas. Their findings pave the way for the use of glutamine restriction as an adjuvant treatment for TAp73-expressing medulloblastomas...
September 1, 2017: Genes & Development
https://www.readbyqxmd.com/read/28978663/distinct-tp73-dapk2-atg5-pathway-involvement-in-ato-mediated-cell-death-versus-atra-mediated-autophagy-responses-in-apl
#4
Magali Humbert, Elena A Federzoni, Mario P Tschan
We have previously demonstrated that the death-associated protein kinase 2 (DAPK2) expression is significantly reduced in acute myeloid leukemia (AML), particularly in acute promyelocytic leukemia (APL) blast cells. In this study, we aimed at further understanding DAPK2 function and regulation during arsenic trioxide (ATO) cytotoxic or all-trans retinoic acid (ATRA) differentiation therapy in APL cells. We found that the p53 family member transactivation domain-p73 isoform (TAp73) binds to and activates the DAPK2 promoter, whereas the dominant-negative ΔNp73 isoform inhibits DAPK2 transcription...
October 4, 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28978123/iaspp-overexpression-is-associated-with-clinical-outcome-in-spinal-chordoma-and-influences-cellular-proliferation-invasion-and-sensitivity-to-cisplatin-in-vitro
#5
Yunlong Ma, Bin Zhu, Xiaoguang Liu, Zhongjun Liu, Liang Jiang, Feng Wei, Miao Yu, Fengliang Wu, Hua Zhou, Nanfang Xu, Xiao Liu, Lei Yong, Yongqiang Wang, Peng Wang, Chen Liang, Guanping He
The oncogenetic function of inhibitory member of the apoptosis stimulating protein of p53 family (iASPP) in chordoma is unclear and remains to elucidate. The expression of iASPP in chordoma tissues and cells, its correlation to clinicopathological parameters and the effect on the patients' prognosis were evaluated. Cellular proliferation, invasion and cisplatin-response were observed after the iASPP knockdown or overexpression in vitro. Co-Immunoprecipitation assay was used to explore the interaction between iASPP and p53...
September 15, 2017: Oncotarget
https://www.readbyqxmd.com/read/28975366/a-double-dealing-tale-of-p63-an-oncogene-or-a-tumor-suppressor
#6
REVIEW
Yonglong Chen, Yougong Peng, Shijie Fan, Yimin Li, Zhi-Xiong Xiao, Chenghua Li
As a member of tumor suppressor p53 family, p63, a gene encoding versatile protein variant, has been documented to correlate with cancer formation and progression, though it is rarely mutated in cancer patients. However, it has long been controversial on whether p63 is an oncogene or a tumor suppressor. Here, we comprehensively reviewed reports on roles of p63 in development, tumorigenesis and tumor progression. According to data from molecular cell biology, genetic models and clinic research, we conclude that p63 may act as either an oncogene or a tumor suppressor gene in different scenarios: TA isoforms of p63 gene are generally tumor-suppressive through repressing cell proliferation, survival and metastasis; ΔN isoforms, however, may initiate tumorigenesis via promoting cell proliferation and survival, but inhibit tumor metastasis and progression; effects of p63 on tumor formation and progression depend on the context of the whole p53 family, and either amplification or loss of p63 gene locus can break the balance to cause tumorigenesis...
October 3, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28959360/role-of-wild-type-p53-induced-phosphatase-1-in-cancer
#7
Zhi-Peng Wang, Ye Tian, Jun Lin
Wild-type p53-induced phosphatase (Wip1) is a member of the protein phosphatase type 2C family and is an established oncogene due to its dephosphorylation of several tumor suppressors and negative control of the DNA damage response system. It has been reported to dephosphorylate p53, ataxia telangiectasia mutated, checkpoint kinase 1 and p38 mitogen activated protein kinases, forming negative feedback loops to inhibit apoptosis and cell cycle arrest. Wip1 serves a major role in tumorigenesis, progression, invasion, distant metastasis and apoptosis in various types of human cancer...
October 2017: Oncology Letters
https://www.readbyqxmd.com/read/28944886/sulforaphane-induces-p53%C3%A2-deficient-sw480-cell-apoptosis-via-the-ros%C3%A2-mapk-signaling-pathway
#8
Hai Lan, Hongyin Yuan, Congyao Lin
Sulforaphane (SFN) has been revealed to inhibit the growth and induce apoptosis of cancer cells. However, the detailed anticancer effects of SFN on p53‑deficient colon cancer cells has yet to be clearly elucidated. The present study employed p53‑deficient SW480 cells to establish an SFN‑induced in vitro model of apoptosis. The critical events leading to apoptosis were then evaluated in SFN‑treated p53‑deficient SW480 cells, by performing an MTT assay, flow cytometry, western blotting and ELISA. The results demonstrated that SFN at concentrations of 5, 10, 15 and 20 µM induced mitochondria‑associated cell apoptosis, which was further confirmed by disruption of the mitochondrial membrane potential, an increase in the Bax/Bcl‑2 ratio, as well as activation of caspase‑3, ‑7 and ‑9...
November 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28940692/dpff-1-transcription-factor-deficiency-causes-the-aberrant-activation-of-mpk-1-and-meiotic-defects-in-the-caenorhabditis-elegans-germline
#9
Emmanuel Villanueva-Chimal, Laura S Salinas, Laura P Fernández-Cardenas, Gabriela Huelgas-Morales, Alejandro Cabrera-Wrooman, Rosa E Navarro
The d4 family of transcription factors consists of three members in mammals. DPF1/neuro-d4 is expressed mainly in neurons and the peripheral nervous system, and is important for brain development. DPF2/requiem/ubi-d4 is expressed ubiquitously and presumably functions as an apoptotic factor, especially during the deprivation of trophic factors. DPF3/cer-d4 is expressed in neurons and in the heart, and is important for heart development and function in zebrafish. In Drosophila, there is only one member, dd4, whose function is still unknown, but it is expressed in many tissues and is particularly abundant in the brain of developing embryos and in adults...
September 23, 2017: Genesis: the Journal of Genetics and Development
https://www.readbyqxmd.com/read/28937686/serine-392-phosphorylation-modulates-p53-mitochondrial-translocation-and-transcription-independent-apoptosis
#10
Cédric Castrogiovanni, Béranger Waterschoot, Olivier De Backer, Patrick Dumont
The tumor suppressor p53 is a key regulator of apoptosis induced by various cellular stresses. p53 can induce apoptosis by two mechanisms. First, p53 acts as a transcription factor inducing and repressing pro-apoptotic and anti-apoptotic targets genes, respectively. Second, p53 is able to translocate to the mitochondria, where it interacts with BCL-2 family members to induce membrane permeabilization and cytochrome c release. p53 transcriptional activity is regulated by a set of post-translational modifications that have been well documented...
September 22, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28931858/loss-of-p73-in-ependymal-cells-during-the-perinatal-period-leads-to-aqueductal-stenosis
#11
Masashi Fujitani, Ryohei Sato, Toshihide Yamashita
The p53 family member p73 plays a critical role in brain development. p73 knockout mice exhibit a number of deficits in the nervous system, such as neuronal death, hydrocephalus, hippocampal dysgenesis, and pheromonal defects. Among these phenotypes, the mechanisms of hydrocephalus remain unknown. In this study, we generated a p73 knock-in (KI) mutant mouse and a conditional p73 knockout mouse. The homozygous KI mutants showed aqueductal stenosis. p73 was expressed in the ependymal cell layer and several brain areas...
September 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28926586/sox14-activates-the-p53-signaling-pathway-and-induces-apoptosis-in-a-cervical-carcinoma-cell-line
#12
Danijela Stanisavljevic, Isidora Petrovic, Vladanka Vukovic, Marija Schwirtlich, Marija Gredic, Milena Stevanovic, Jelena Popovic
SOX14 is a member of the SOX family of transcription factors mainly involved in the regulation of neural development. Recently, it became evident that SOX14 is one of four hypermethylated genes in cervical carcinoma, considered as a tumor suppressor candidate in this type of malignancy. In this paper we elucidated the role of SOX14 in the regulation of malignant properties of cervical carcinoma cells in vitro. Functional analysis performed in HeLa cells revealed that SOX14 overexpression decreased viability and promoted apoptosis through altering the expression of apoptosis related genes...
2017: PloS One
https://www.readbyqxmd.com/read/28919777/synaptotagmin-7-is-overexpressed-in-hepatocellular-carcinoma-and-regulates-hepatocellular-carcinoma-cell-proliferation-via-chk1-p53-signaling
#13
Hao Jin, Geliang Xu, Qiang Zhang, Qing Pang, Meifang Fang
BACKGROUND: Synaptotagmin-7 (Syt-7) is a member of the synaptotagmin (Syt) family, which plays an important role in many physiological and pathological processes. However, to the best of our knowledge, there is no study describing its function in tumors, particularly in hepatocellular carcinoma (HCC). Therefore, in this study, we examined the role of Syt-7 in HCC and attempted to elucidate its underlying mechanism. MATERIALS AND METHODS: We examined the expression levels of Syt-7 in HCC cell lines and normal hepatocytes by real-time quantitative polymerase chain reaction analysis...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/28919418/the-nampt-e2f2-sirt1-axis-promotes-proliferation-and-inhibits-p53-dependent-apoptosis-in-human-melanoma-cells
#14
Hailong Zhao, Weiwei Tang, Xiaowen Chen, Siyu Wang, Xianyan Wang, Haiyan Xu, Lijuan Li
Melanoma is the most common primary malignant neoplasm in adults, causing more deaths than any other skin cancer, necessitating the development of new target-based approaches. Current evidence suggests SIRT1, the mammalian nicotinamide adenine dinucleotide (NAD(+))-dependent protein deacetylase, and nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD(+) biosynthetic enzyme, together comprise a novel systemic regulatory network to play a pivotal role in cell proliferation and apoptosis. Nevertheless, how the regulation of this cofactor interfaces with signal transduction network remains poorly understood in melanoma...
November 4, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28918507/the-muscle-regulatory-transcription-factor-myod-participates-with-p53-to-directly-increase-the-expression-of-the-pro-apoptotic-bcl2-family-member-puma
#15
Terri J Harford, Greg Kliment, Girish C Shukla, Crystal M Weyman
The muscle regulatory transcription factor MyoD is a master regulator of skeletal myoblast differentiation. We have previously reported that MyoD is also necessary for the elevated expression of the pro-apoptotic Bcl2 family member PUMA, and the ensuing apoptosis, that occurs in a subset of myoblasts induced to differentiate. Herein, we report the identification of a functional MyoD binding site within the extended PUMA promoter. In silico analysis of the murine PUMA extended promoter revealed three potential MyoD binding sites within 2 kb of the transcription start site...
September 16, 2017: Apoptosis: An International Journal on Programmed Cell Death
https://www.readbyqxmd.com/read/28895255/ubr2-enriched-in-p53-mbmmsc-exosome-promoted-gastric-cancer-progression-via-wnt-%C3%AE-catenin-pathway
#16
Jiahui Mao, Zhaofeng Liang, Bin Zhang, Huan Yang, Xia Li, Hailong Fu, Xu Zhang, Yongmin Yan, Wenrong Xu, Hui Qian
The deficiency or mutation of p53 has been known to be linked to several types of cancers. Mesenchymal stem cell (MSC) is an important component in tumor microenvironment and exosomes secreted by MSCs can transfer bioactive molecules including proteins and nucleic acid to another cells in tumor microenvironment to influence the progress of tumor. However, whether the state of p53 in MSCs can impact the bioactive molecule secretion of exosomes to promote cancer progression and the regulatory mechanism remain elusive...
September 12, 2017: Stem Cells
https://www.readbyqxmd.com/read/28881698/reduction-oxidation-pathways-involved-in-cancer-development-a-systematic-review-of-literature-reviews
#17
REVIEW
Xīn Gào, Ben Schöttker
Oxidative stress results from an imbalance of the reactive oxygen species/reactive nitrogen species (ROS/RNS) production and the oxidants defense system. Extensive research during the last decades has revealed that oxidative stress can mediate cancer initiation and development by leading not only to molecular damage but also to a disruption of reduction-oxidation (redox) signaling. In order to provide a global overview of the redox signaling pathways, which play a role in cancer formation, we conducted a systematic literature search in PubMed and ISI Web of Science and identified 185 relevant reviews published in the last 10 years...
August 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28827783/ccdc3-a-new-p63-target-involved-in-regulation-of-liver-lipid-metabolism
#18
Wenjuan Liao, Hongbing Liu, Yiwei Zhang, Ji Hoon Jung, Jiaxiang Chen, Xiaohua Su, Yeong C Kim, Elsa R Flores, San Ming Wang, Malwina Czarny-Ratajczak, Wen Li, Shelya X Zeng, Hua Lu
TAp63, a member of the p53 family, has been shown to regulate energy metabolism. Here, we report coiled coil domain-containing 3 (CCDC3) as a new TAp63 target. TAp63, but not ΔNp63, p53 or p73, upregulates CCDC3 expression by directly binding to its enhancer region. The CCDC3 expression is markedly reduced in TAp63-null mouse embryonic fibroblasts and brown adipose tissues and by tumor necrosis factor alpha that reduces p63 transcriptional activity, but induced by metformin, an anti-diabetic drug that activates p63...
August 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28794999/modulation-of-the-p53-family-network-by-rna-binding-proteins
#19
Chris Lucchesi, Jin Zhang, Xinbin Chen
Since its discovery more than three decades ago, tumor suppressor p53 has been shown to play pivotal roles in both maintaining genomic integrity and tumor suppression. p53 functions as a transcription factor responding to a multitude of cellular stressors, regulating the transcription of many genes involved in cell-cycle arrest, senescence, autophagy, and apoptosis. Extensive work has revealed that p53 is one of the most commonly mutated tumor suppressor genes. The last three decades have demonstrated that p53 activity is controlled through transcriptional regulation and posttranslational modifications...
December 2016: Translational Cancer Research
https://www.readbyqxmd.com/read/28794159/p63%C3%AE-protein-up-regulates-heat-shock-protein-70-expression-via-e2f1-transcription-factor-1-promoting-wasf3-wave3-mmp9-signaling-and-bladder-cancer-invasion
#20
Honglei Jin, Qipeng Xie, Xirui Guo, Jiheng Xu, Annette Wang, Jingxia Li, Junlan Zhu, Xue-Ru Wu, Haishan Huang, Chuanshu Huang
Bladder cancer (BC) is the sixth most common cancer in the United States and is the number one cause of death among patients with urinary system malignancies. This makes the identification of invasive regulator(s)/effector(s) as the potential therapeutic targets for managing BC a high priority. p63 is a member of the p53 family of tumor suppressor genes/proteins, plays a role in the differentiation of epithelial tissues, and is believed to function as a tumor suppressor. However, it remains unclear whether and how p63 functions in BC cell invasion after tumorigenesis...
September 22, 2017: Journal of Biological Chemistry
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