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p53 family member

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https://www.readbyqxmd.com/read/28549975/knockdown-of-epigenetic-transcriptional-co-regulator-brd2a-disrupts-apoptosis-and-proper-formation-of-hindbrain-and-midbrain-hindbrain-boundary-mhb-region-in-zebrafish
#1
Tami Murphy, Heather Melville, Eliza Fradkin, Giana Bistany, Gregory Branigan, Kelly Olsen, Catharine R Comstock, Hayley Hanby, Ellie Garbade, Angela J DiBenedetto
Brd2 is a member of the bromodomain-extraterminal domain (BET) family of proteins and functions as an acetyl-histone-directed transcriptional co-regulator and recruitment scaffold in chromatin modification complexes affecting signal-dependent transcription. While Brd2 acts as a protooncogene in mammalian blood, developmental studies link it to regulation of neuronal apoptosis and epilepsy, and complete knockout of the gene is invariably embryonic lethal. In Drosophila, the Brd2 homolog acts as a maternal effect factor necessary for segment formation and identity and proper expression of homeotic loci, including Ultrabithorax and engrailed...
May 23, 2017: Mechanisms of Development
https://www.readbyqxmd.com/read/28536638/abcc6-knockdown-in-hepg2-cells-induces-a-senescent-like-cell-phenotype
#2
Rocchina Miglionico, Angela Ostuni, Maria Francesca Armentano, Luigi Milella, Elvira Crescenzi, Monica Carmosino, Faustino Bisaccia
BACKGROUND: Pseudoxanthoma elasticum (PXE) is characterized by progressive ectopic mineralization of elastic fibers in dermal, ocular and vascular tissues. No effective treatment exists. It is caused by inactivating mutations in the gene encoding for the ATP-binding cassette, sub-family C member 6 transporter (ABCC6), which is mainly expressed in the liver. The ABCC6 substrate (s) and the PXE pathomechanism remain unknown. Recent studies have shown that overexpression of ABCC6 in HEK293 cells results in efflux of ATP, which is rapidly converted into nucleoside monophosphates and pyrophosphate (PPi)...
2017: Cellular & Molecular Biology Letters
https://www.readbyqxmd.com/read/28534998/proliferation%C3%A2-inhibiting-pathways-in-liver-regeneration-review
#3
Menggang Liu, Ping Chen
Liver regeneration, an orchestrated process, is the primary compensatory mechanism following liver injury caused by various factors. The process of liver regeneration consists of three stages: Initiation, proliferation and termination. Proliferation‑promoting factors, which stimulate the recovery of mitosis in quiescent hepatocytes, are essential in the initiation and proliferation steps of liver regeneration. Proliferation‑promoting factors act as the 'motor' of liver regeneration, whereas proliferation inhibitors arrest cell proliferation when the remnant liver reaches a suitable size...
May 19, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28534990/tumor-suppressor-microrna-34a-inhibits-cell-migration-and-invasion-by-targeting-mmp-2-mmp-9-fndc3b-in-esophageal-squamous-cell-carcinoma
#4
Lan Yang, Xiaoyue Song, Jianbo Zhu, Mei Li, Yu Ji, Fei Wu, Yunzhao Chen, Xiaobin Cui, Jianming Hu, Lianghai Wang, Yuwen Cao, Yutao Wei, Wenjie Zhang, Feng Li
MicroRNAs (miRNAs) are a large family of small, non-coding RNAs that play a pivotal role in tumorigenesis. miR‑34a, which is a member of the miR-34 family, is a downstream target of p53. Increasing evidence shows that miR-34a dysregulation may contribute to tumor development and progression in numerous cancers, including esophageal squamous cell carcinoma (ESCC). However, the mechanism of miR-34a in the regulation of ESCC cells need to be further elucidated because of the complex regulative network of miRNAs...
May 19, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28530640/genetic-regulation-of-the-runx-transcription-factor-family-has-antitumor-effects
#5
Ken Morita, Kensho Suzuki, Shintaro Maeda, Akihiko Matsuo, Yoshihide Mitsuda, Chieko Tokushige, Gengo Kashiwazaki, Junichi Taniguchi, Rina Maeda, Mina Noura, Masahiro Hirata, Tatsuki Kataoka, Ayaka Yano, Yoshimi Yamada, Hiroki Kiyose, Mayu Tokumasu, Hidemasa Matsuo, Sunao Tanaka, Yasushi Okuno, Manabu Muto, Kazuhito Naka, Kosei Ito, Toshio Kitamura, Yasufumi Kaneda, Paul P Liu, Toshikazu Bando, Souichi Adachi, Hiroshi Sugiyama, Yasuhiko Kamikubo
Runt-related transcription factor 1 (RUNX1) is generally considered to function as a tumor suppressor in the development of leukemia, but a growing body of evidence suggests that it has pro-oncogenic properties in acute myeloid leukemia (AML). Here we have demonstrated that the antileukemic effect mediated by RUNX1 depletion is highly dependent on a functional p53-mediated cell death pathway. Increased expression of other RUNX family members, including RUNX2 and RUNX3, compensated for the antitumor effect elicited by RUNX1 silencing, and simultaneous attenuation of all RUNX family members as a cluster led to a much stronger antitumor effect relative to suppression of individual RUNX members...
May 22, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28525372/overexpression-of-a-novel-candidate-oncogene-kif14-correlates-with-tumor-progression-and-poor-prognosis-in-prostate-cancer
#6
Yixiang Zhang, Yeqing Yuan, Pei Liang, Zhaoxia Zhang, Xiaojing Guo, Ligang Xia, Yingying Zhao, Xing-Sheng Shu, Shengkun Sun, Ying Ying, Yingduan Cheng
Prostate cancer (PCa) is the second leading cause of death from cancer in men. The mechanism underlying tumorigenesis and development of PCa is largely unknown. Here, we identified Kinesin family member 14 (KIF14) as a novel candidate oncogene in PCa. We found that KIF14 was overexpressed in multiple PCa cell lines and primary PCa tissues. Knockdown of KIF14 in DU145 and PC3 prostate cancer cells suppressed cell proliferation, induced cell cycle arrest and apoptosis. Transcriptome analysis by RNA-sequencing demonstrated that KIF4 suppression led to transcriptional changes of genes involved in p53 and TGF-beta signaling pathway...
May 2, 2017: Oncotarget
https://www.readbyqxmd.com/read/28521467/upregulation-of-maspin-expression-in-human-cervical-carcinoma-cells-by-transforming-growth-factor-%C3%AE-1-through-the-convergence-of-smad-and-non-smad-signaling-pathways
#7
Ariyaphong Wongnoppavich, Nahathai Dukaew, Sirinthip Choonate, Kongthawat Chairatvit
Mammary serine protease inhibitor (maspin), encoded by the serpin family B member 5 gene, serves as a tumor suppressor through the inhibition of cancer cell invasion and metastasis. Paradoxically, maspin levels are upregulated in a number of types of malignant cells. Therefore, the regulation of maspin expression may depend on the genetic or epigenetic background and the specific microenvironment of carcinoma cells. In the present study, it was demonstrated that transforming growth factor β1 (TGF-β1) induced maspin expression at the transcript and protein levels in the human cervical carcinoma HeLa and human oral squamous carcinoma HSC4 cell lines...
May 2017: Oncology Letters
https://www.readbyqxmd.com/read/28518146/acyl-coa-thioesterase-7-is-involved-in-cell-cycle-progression-via-regulation-of-pkc%C3%AE-p53-p21-signaling-pathway
#8
Seung Hee Jung, Hyung Chul Lee, Hyun Jung Hwang, Hyun A Park, Young-Ah Moon, Bong Cho Kim, Hyeong Min Lee, Kwang Pyo Kim, Yong-Nyun Kim, Byung Lan Lee, Jae Cheol Lee, Young-Gyu Ko, Heon Joo Park, Jae-Seon Lee
Acyl-CoA thioesterase 7 (ACOT7) is a major isoform of the ACOT family that catalyzes hydrolysis of fatty acyl-CoAs to free fatty acids and CoA-SH. However, canonical and non-canonical functions of ACOT7 remain to be discovered. In this study, for the first time, ACOT7 was shown to be responsive to genotoxic stresses such as ionizing radiation (IR) and the anti-cancer drug doxorubicin in time- and dose-dependent manners. ACOT7 knockdown induced cytostasis via activation of the p53-p21 signaling pathway without a DNA damage response...
May 18, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28498467/antibody-to-human-%C3%AE-fetoprotein-inhibits-cell-growth-of-human-hepatocellular-carcinoma-cells-by-resuscitating-the-pten-molecule-in-vitro-experiments
#9
Kiyoshi Ohkawa, Tadashi Asakura, Yutaka Tsukada, Tomokazu Matsuura
It has been proposed that α-fetoprotein (AFP) is a new member of the intracellular signaling molecule family of the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway via interaction with the phosphatase and tensin homolog (PTEN). In this study, the effects of anti-human AFP antibody on the functions of PTEN were examined using an AFP-producing human hepatoma cell line. The antibody caused significant inhibition of cell growth, compared to a normal IgG control, with the accumulation of intracellular immune complexes followed by significant reduction of cytosolic functional AFP...
May 3, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28494179/predictive-biomarkers-for-triple-negative-breast-cancer-treated-with-platinum-based-chemotherapy
#10
Juan Jin, Wenwen Zhang, Wenfei Ji, Fang Yang, Xiaoxiang Guan
Treatment of triple negative breast cancer (TNBC) has been a big challenge since it is defined. To date, platinum-based chemotherapy has played a significant role in the treatment of TNBC patients. However, some patients do not respond to platinum salts or gradually develop chemoresistance, resulting in little effect, or even some adverse effects. Here, we review numerous preclinical and clinical investigations to summarize possible mechanisms and potential predictive biomarkers of platinum in TNBC. The homologous recombination deficiency (HRD) resulting from the loss of BRCA function is the main rationale of platinum efficacy in TNBC...
May 11, 2017: Cancer Biology & Therapy
https://www.readbyqxmd.com/read/28481879/cytoplasmic-e3-ubiquitin-ligase-cul9-controls-cell-proliferation-senescence-apoptosis-and-genome-integrity-through-p53
#11
Z Li, Y Xiong
CUL9 is a member of the cullin family of E3 ubiquitin ligases, and it localizes predominantly in the cytoplasm. Deletion of Cul9 in mice results in increased DNA damage, widespread aneuploidy, spontaneous tumor development, accelerated Eμ-Myc-induced lymphomagenesis and susceptibility to carcinogenesis. CUL9 binds to p53 and causes cell apoptosis when ectopically expressed. Whether the function of CUL9 in maintaining genomic integrity and suppressing tumorigenesis is linked to p53 has not been genetically tested...
May 8, 2017: Oncogene
https://www.readbyqxmd.com/read/28480888/hepatic-p63-regulates-steatosis-via-ikk%C3%AE-er-stress
#12
Begoña Porteiro, Marcos F Fondevila, Teresa C Delgado, Cristina Iglesias, Monica Imbernon, Paula Iruzubieta, Javier Crespo, Amaia Zabala-Letona, Johan Fernø, Bárbara González-Terán, Nuria Matesanz, Lourdes Hernández-Cosido, Miguel Marcos, Sulay Tovar, Anxo Vidal, Julia Sánchez-Ceinos, Maria M Malagon, Celia Pombo, Juan Zalvide, Arkaitz Carracedo, Xabier Buque, Carlos Dieguez, Guadalupe Sabio, Miguel López, Patricia Aspichueta, María L Martínez-Chantar, Ruben Nogueiras
p53 family members control several metabolic and cellular functions. The p53 ortholog p63 modulates cellular adaptations to stress and has a major role in cell maintenance and proliferation. Here we show that p63 regulates hepatic lipid metabolism. Mice with liver-specific p53 deletion develop steatosis and show increased levels of p63. Down-regulation of p63 attenuates liver steatosis in p53 knockout mice and in diet-induced obese mice, whereas the activation of p63 induces lipid accumulation. Hepatic overexpression of N-terminal transactivation domain TAp63 induces liver steatosis through IKKβ activation and the induction of ER stress, the inhibition of which rescues the liver functions...
May 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28480326/combining-oncolytic-virotherapy-with-p53-tumor-suppressor-gene-therapy
#13
REVIEW
Christian Bressy, Eric Hastie, Valery Z Grdzelishvili
Oncolytic virus (OV) therapy utilizes replication-competent viruses to kill cancer cells, leaving non-malignant cells unharmed. With the first U.S. Food and Drug Administration-approved OV, dozens of clinical trials ongoing, and an abundance of translational research in the field, OV therapy is poised to be one of the leading treatments for cancer. A number of recombinant OVs expressing a transgene for p53 (TP53) or another p53 family member (TP63 or TP73) were engineered with the goal of generating more potent OVs that function synergistically with host immunity and/or other therapies to reduce or eliminate tumor burden...
June 16, 2017: Molecular Therapy Oncolytics
https://www.readbyqxmd.com/read/28477117/studies-of-atm-kinase-activity-using-engineered-atm-sensitive-to-atp-analogues-atm-as
#14
Masato Enari, Yuko Matsushima-Hibiya, Makoto Miyazaki, Ryo Otomo
Ataxia-telangiectasia mutated (ATM) protein is a member of the phosphatidylinositol 3-phosphate kinase (PI3-K)-related protein kinase (PIKK) family and is implicated in the initiation of signaling pathways following DNA double strand breaks (DSBs) elicited by exposure to ionizing irradiation (IR) or radiomimetic compounds. Loss of function of the ATM gene product results in the human genetic disorder ataxia-telangiectasia (A-T) characterized by neurodegeneration, immunodeficiency, genomic instability, and cancer predisposition...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28471195/-application-of-pla-method-for-detection-of-p53-p63-p73-complexes-in-situ-in-tumour-cells-and-tumour-tissue
#15
V Hrabal, M Nekulová, R Nenutil, J Holčaková, P J Coates, B Vojtěšek
BACKGROUND: PLA (proximity ligation assay) can be used for detection of protein-protein interactions in situ directly in cells and tissues. Due to its high sensitivity and specificity it is useful for detection, localization and quantification of protein complexes with single molecule resolution. One of the mechanisms of mutated p53 gain of function is formation of proten-protein complexes with other members of p53 family - p63 and p73. These interactions influences chemosensitivity and invasivity of cancer cells and this is why these complexes are potential targets of anti-cancer therapy...
2017: Klinická Onkologie: Casopis Ceské a Slovenské Onkologické Spolecnosti
https://www.readbyqxmd.com/read/28465493/reduction-oxidation-pathways-involved-in-cancer-development-a-systematic-review-of-literature-reviews
#16
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...
April 16, 2017: Oncotarget
https://www.readbyqxmd.com/read/28464919/the-role-of-apoptosis-repressor-with-a-card-domain-arc-in-the-therapeutic-resistance-of-renal-cell-carcinoma-rcc-the-crucial-role-of-arc-in-the-inhibition-of-extrinsic-and-intrinsic-apoptotic-signalling
#17
Csaba Toth, Sarah Funke, Vanessa Nitsche, Anna Liverts, Viktoriya Zlachevska, Marcia Gasis, Constanze Wiek, Helmut Hanenberg, Csaba Mahotka, Peter Schirmacher, Sebastian Heikaus
BACKGROUND: Renal cell carcinomas (RCCs) display broad resistance against conventional radio- and chemotherapies, which is due at least in part to impairments in both extrinsic and intrinsic apoptotic pathways. One important anti-apoptotic factor that is strongly overexpressed in RCCs and known to inhibit both apoptotic pathways is ARC (apoptosis repressor with a CARD domain). METHODS: Expression and subcellular distribution of ARC in RCC tissue samples and RCC cell lines were determined by immunohistochemistry and fluorescent immunohistochemistry, respectively...
May 2, 2017: Cell Communication and Signaling: CCS
https://www.readbyqxmd.com/read/28460455/ccdc106-promotes-non-small-cell-lung-cancer-cell-proliferation
#18
Xiupeng Zhang, Qin Zheng, Chen Wang, Haijing Zhou, Guiyang Jiang, Yuan Miao, Yong Zhang, Yang Liu, Qingchang Li, Xueshan Qiu, Enhua Wang
Coiled-coil domain containing (CCDC) family members enhance tumor cell proliferation, and high CCDC protein levels correlate with unfavorable prognoses. Limited research demonstrated that CCDC106 may promote the degradation of p53/TP53 protein and inhibit its transactivity. The present study demonstrated that CCDC106 expression correlates with advanced TNM stage (P = 0.008), positive regional lymph node metastasis (P < 0.001), and poor overall survival (P < 0.001) in 183 non-small cell lung cancer cases...
April 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28455242/the-role-of-the-nore1a-tumor-suppressor-in-oncogene-induced-senescence
#19
Thibaut Barnoud, M Lee Schmidt, Howard Donninger, Geoffrey J Clark
The Ras genes are the most frequently mutated oncogenes in human cancer. However, Ras biology is quite complex. While Ras promotes tumorigenesis by regulating numerous growth promoting pathways, activated Ras can paradoxically also lead to cell cycle arrest, death, and Oncogene-Induced Senescence (OIS). OIS is thought to be a critical pathway that serves to protect cells against aberrant Ras signaling. Multiple reports have highlighted the importance of the p53 and Rb tumor suppressors in Ras mediated OIS. However, until recently, the molecular mechanisms connecting Ras to these proteins remained unknown...
April 26, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28454339/puma-decreases-the-growth-of-prostate-cancer-pc-3-cells-independent-of-p53
#20
Zhengfei Shan, Qingzuo Liu, Yuling Li, Jitao Wu, Dekang Sun, Zhenli Gao
PUMA (p53 upregulated modulator of apoptosis), a member of the B-cell lymphoma 2 (Bcl-2) protein family, is a pro-apoptotic protein. PUMA expression is modulated by the tumor suppressor p53. PUMA has a role in rapid cell death via p53-dependent and -independent mechanisms. To evaluate whether p53 is required for PUMA-mediated apoptosis in prostate cancer cells, p53 protein was silenced in human prostate cancer PC-3 cells by using p53 small interfering RNA (siRNA). The interference efficiency of p53 on RNA and protein levels was detected by reverse transcription-quantitative polymerase chain reaction and western blotting...
March 2017: Oncology Letters
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