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p53 family member

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https://www.readbyqxmd.com/read/28334319/erbb4-acts-as-a-suppressor-in-the-development-of-hepatocellular-carcinoma
#1
Yao Liu, Liming Song, Hengli Ni, Lina Sun, Weijuan Jiao, Lin Chen, Qun Zhou, Tong Shen, Hongxia Cui, Tianming Gao, Jianming Li
ERBB4, one member of the epidermal growth factor receptor (EGFR) family, plays a key role in physiological and pathological processes. Recently, we identified that ERBB4 played a protective role from chronic hepatitis B virus infection. However, the role of ERBB4 in hepatocellular carcinoma (HCC) is still unclear. Here, we explore the role of ERBB4 in the development of HCC using in vitro models, in vivo animal models and clinical samples of HCC. Liver-specific ERBB4 knockout alleles and full ERBB4 except heart knockout mice were used in this study...
March 14, 2017: Carcinogenesis
https://www.readbyqxmd.com/read/28315432/splicing-factors-of-sr-and-hnrnp-families-as-regulators-of-apoptosis-in-cancer
#2
Hanna Kędzierska, Agnieszka Piekiełko-Witkowska
SR and hnRNP proteins were initially discovered as regulators of alternative splicing: the process of controlled removal of introns and selective joining of exons through which multiple transcripts and, subsequently, proteins can be expressed from a single gene. Alternative splicing affects genes involved in all crucial cellular processes, including apoptosis. During cancerogenesis impaired apoptotic control facilitates survival of cells bearing molecular aberrations, contributing to their unrestricted proliferation and chemoresistance...
March 14, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28300573/concomitant-expression-of-ezrin-and-her2-predicts-distant-metastasis-and-poor-prognosis-of-patients-with-salivary-gland-carcinomas
#3
Kazuki Hashimoto, Ryuichi Hayashi, Takashi Mukaigawa, Manabu Yamazaki, Satoshi Fujii
Salivary gland carcinomas (SGCs) exhibit heterogeneous biological behaviors, including the formation of distant metastases, which is a critical event associated with poor prognosis. Ezrin, which is a member of the ezrin-radixin-moesin family of plasma membrane-cytoskeleton linker proteins, may provide a marker for metastasis and poor survival of patients with cancer. The aim of the present study was to investigate the relationship between ezrin expression and the expression of HER2, p53, and Ki-67 as well as clinicopathological factors in SGCs...
March 11, 2017: Human Pathology
https://www.readbyqxmd.com/read/28299666/runx3-and-p53-how-two-tumor-suppressors-cooperate-against-oncogenic-ras
#4
Jung-Won Lee, Andre van Wijnen, Suk-Chul Bae
RUNX family members play pivotal roles in both normal development and neoplasia. In particular, RUNX1 and RUNX2 are essential for determination of the hematopoietic and osteogenic lineages, respectively. RUNX3 is involved in lineage determination of various types of epithelial cells. Analysis of mouse models and human cancer specimens revealed that RUNX3 acts as a tumor suppressor via multiple mechanisms. p53-related pathways play central roles in tumor suppression through the DNA damage response and oncogene surveillance, and RUNX3 is involved in both processes...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28288992/identification-of-a-dna-damage-induced-alternative-splicing-pathway-that-regulates-p53-and-cellular-senescence-markers
#5
Jing Chen, John Crutchley, Dadong Zhang, Kouros Owzar, Michael B Kastan
Cellular responses to DNA damage are critical determinants of cancer development and aging-associated pathogenesis. Here we report a novel DNA damage response pathway that regulates alternative splicing of numerous gene products, including the human tumor suppressor p53, and controls DNA damage-induced cellular senescence. In brief, ionizing irradiation (IR) inhibits the activity of hSMG-1, a phosphoinositide-3-kinase-like kinase (PIKK) family member, reducing the binding of hSMG1 to a specific region of p53 precursor mRNA near exon 9 and promoting the binding of ribosomal protein L26 (RPL26) to p53 pre-mRNA...
March 13, 2017: Cancer Discovery
https://www.readbyqxmd.com/read/28273808/role-of-ul3-in-multidrug-resistance-in-p53-mutated-lung-cancer-cells
#6
Annapina Russo, Assunta Saide, Silvia Smaldone, Raffaella Faraonio, Giulia Russo
Cancer is one of the most common causes of death among adults. Chemotherapy is crucial in determining patient survival and quality of life. However, the development of multidrug resistance (MDR) continues to pose a significant challenge in the management of cancer. In this study, we analyzed the role of human ribosomal protein uL3 (formerly rpL3) in multidrug resistance. Our studies revealed that uL3 is a key determinant of multidrug resistance in p53-mutated lung cancer cells by controlling the cell redox status...
March 3, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28265066/resistance-mechanisms-to-tp53-mdm2-inhibition-identified-by-in-vivo-piggybac-transposon-mutagenesis-screen-in-an-arf-mouse-model
#7
Emilie A Chapeau, Agnieszka Gembarska, Eric Y Durand, Emeline Mandon, Claire Estadieu, Vincent Romanet, Marion Wiesmann, Ralph Tiedt, Joseph Lehar, Antoine de Weck, Roland Rad, Louise Barys, Sebastien Jeay, Stephane Ferretti, Audrey Kauffmann, Esther Sutter, Armelle Grevot, Pierre Moulin, Masato Murakami, William R Sellers, Francesco Hofmann, Michael Rugaard Jensen
Inhibitors of double minute 2 protein (MDM2)-tumor protein 53 (TP53) interaction are predicted to be effective in tumors in which the TP53 gene is wild type, by preventing TP53 protein degradation. One such setting is represented by the frequent CDKN2A deletion in human cancer that, through inactivation of p14ARF, activates MDM2 protein, which in turn degrades TP53 tumor suppressor. Here we used piggyBac (PB) transposon insertional mutagenesis to anticipate resistance mechanisms occurring during treatment with the MDM2-TP53 inhibitor HDM201...
March 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28255269/diallyl-trisulfide-inhibits-growth-of-nci-h460-in-vitro-and-in-vivo-and-ameliorates-cisplatin-induced-oxidative-injury-in-the-treatment-of-lung-carcinoma-in-xenograft-mice
#8
Xiaoyan Jiang, Xiaosong Zhu, Na Liu, Hongya Xu, Zhongxi Zhao, Siying Li, Shanzhong Li, Jianhua Cai, Jimin Cao
Diallyl trisulfide (DATS), an organosulfuric component of garlic oil, exhibits potential anticancer and chemopreventive effects. Cisplatin (DDP), a common chemotherapeutic agent, has provided great therapeutic contributions to treating solid tumors, but with serious side effects. Here, we verified the anti-tumor properties of DATS on lung cancer in vitro and in vivo, and evaluated synergistic effects of DATS combined with DDP on the NCI-H460 xenograft model. Significantly decreased cell viabilities, cell cycle G1 arrest, and apoptosis induction were observed in DATS treated NCI-H460 cells (p<0...
2017: International Journal of Biological Sciences
https://www.readbyqxmd.com/read/28240971/phase-i-trial-of-the-human-double-minute-2-inhibitor-mk-8242-in-patients-with-advanced-solid-tumors
#9
Andrew J Wagner, Udai Banerji, Amit Mahipal, Neeta Somaiah, Heather Hirsch, Craig Fancourt, Amy O Johnson-Levonas, Raymond Lam, Amy K Meister, Giuseppe Russo, Clayton D Knox, Shelonitda Rose, David S Hong
Purpose To evaluate MK-8242 in patients with wild-type TP53 advanced solid tumors. Patients and Methods MK-8242 was administered orally twice a day on days 1 to 7 in 21-day cycles. The recommended phase II dose (RP2D) was determined on the basis of safety, tolerability, pharmacokinetics (PK), and by mRNA expression of the p53 target gene pleckstrin homology-like domain, family A, member 3 ( PHLDA3). Other objectives were to characterize the PK/pharmacodynamic (PD) relationship, correlate biomarkers with response, and assess tumor response...
February 27, 2017: Journal of Clinical Oncology: Official Journal of the American Society of Clinical Oncology
https://www.readbyqxmd.com/read/28218651/proteome-characteristics-of-non-alcoholic-steatohepatitis-liver-tissue-and-associated-hepatocellular-carcinomas
#10
Anna Kakehashi, Vasily E Stefanov, Naomi Ishii, Takahiro Okuno, Hideki Fujii, Kazuaki Kawai, Norifumi Kawada, Hideki Wanibuchi
To uncover mechanisms of nonalcoholic steatohepatitis (NASH) associated hepatocarcinogenesis, we compared the proteomes of human NASH-associated liver biopsies, resected hepatocellular carcinomas (HCCs) and HCCs of HCV⁺ patients with normal liver tissue of patients with gastrointestinal tumor metastasis, in formalin-fixed paraffin-embedded samples obtained after surgery in our hospital during the period from 2006 to 2011. In addition, proteome analysis of liver tumors in male STAM NASH-model mice was performed...
February 17, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28212736/tap73-upregulates-il-1%C3%AE-in-cancer-cells-potential-biomarker-in-lung-and-breast-cancer
#11
Polina Vikhreva, Varvara Petrova, Tarik Gokbulut, Ilias Pestlikis, Mara Mancini, Nicola Di Daniele, Richard A Knight, Gerry Melino, Ivano Amelio
p73 is a transcription factor belonging to the p53 tumour suppressor family. p73(-/-) mice exhibit a range of phenotypes including neurological, reproductive and inflammatory defects. Although the role of p73 in the control of genomic stability explains part of these phenotypes, a clear mechanism of how p73 participates in the inflammatory response is still elusive. Interleukin-1β (IL-1β) has a crucial role in mediating the inflammatory response. Because of its high potency to induce inflammation, the activation and secretion of IL-1β is tightly regulated by large protein complexes, named inflammasomes...
January 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28212728/metabolic-pathways-regulated-by-p63
#12
REVIEW
Eleonora Candi, Artem Smirnov, Emanuele Panatta, Anna Maria Lena, Flavia Novelli, Mara Mancini, Giuditta Viticchiè, Maria Cristina Piro, Nicola Di Daniele, Margherita Annicchiarico-Petruzzelli, Gerry Melino
The transcription factor p63 belongs to the p53-family and is a master regulator of proliferative potential, lineage specification, and differentiation in epithelia during development and tissue homeostasis. In cancer, p63 contribution is isoform-specific, with both oncogenic and tumour suppressive roles attributed, for ΔNp63 and TAp63, respectively. Recently, p53 and TAp73, in line with other tumour suppressor genes, have emerged as important regulators of energy metabolism and metabolic reprogramming in cancer...
January 15, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28211873/the-p53-family-members-have-distinct-roles-during-mammalian-embryonic-development
#13
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/28193839/metformin-promotes-amp-activated-protein-kinase-independent-suppression-of-%C3%AE-np63%C3%AE-and-inhibits-cancer-cell-viability
#14
Yong Yi, Deshi Chen, Juan Ao, Shengnan Sun, Min Wu, Xiaorong Li, Johann Bergholz, Yujun Zhang, Zhi-Xiong Xiao
The blood-glucose modifier metformin is used to treat type II diabetes and has also been shown to possess anti-cancer activities. Recent studies indicate that glucose deprivation can greatly enhance metformin-mediated inhibition of cell viability, but the molecular mechanism involved in this inhibition is unclear. In this study, we report that under glucose deprivation metformin inhibited expression of ΔNp63α, a p53 family member involved in cell adhesion pathways, resulting in disruption of cell-matrix adhesion and in subsequent apoptosis in human squamous carcinoma cells...
February 13, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28178647/enhancement-of-trail-induced-apoptosis-by-5-fluorouracil-requires-activating-bax-and-p53-pathways-in-trail-resistant-lung-cancers
#15
Uddin Md Nazim, Rasheduzzaman Md, You-Jin Lee, Dai-Wu Seol, Sang-Youel Park
Lung cancer, especially lung adenocarcinoma, is one of the main causes of death worldwide. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a primary anticancer agent and a member of the tumor necrosis factor family that selectively induces apoptosis in various tumor cells, but not in normal cells. Combination chemotherapy can be used for treating specific cancer types even at progressive stages. In the present study, we observed that 5-fluorouracil, which exerts anticancer effects by inhibiting tumor cell proliferation, enhanced TRAIL-induced apoptosis of TRAIL-resistant human adenocarcinoma A549 cells...
February 2, 2017: Oncotarget
https://www.readbyqxmd.com/read/28165047/relevance-of-mortalin-to-cancer-cell-stemness-and-cancer-therapy
#16
Chae-Ok Yun, Priyanshu Bhargava, Youjin Na, Jung-Sun Lee, Jihoon Ryu, Sunil C Kaul, Renu Wadhwa
Mortalin/mtHsp70 is a member of Hsp70 family of proteins. Enriched in a large variety of cancers, it has been shown to contribute to the process of carcinogenesis by multiple ways including inactivation of tumor suppressor p53 protein, deregulation of apoptosis and activation of EMT signaling. In this study, we report that upregulation of mortalin contributes to cancer cell stemness. Several cancer cell stemness markers, such as ABCG2, OCT-4, CD133, ALDH1, CD9, MRP1 and connexin were upregulated in mortalin-overexpressing cells that showed higher ability to form spheroids...
February 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28119237/betulinic-acid-promotes-trail-function-on-liver-cancer-progression-inhibition-through-p53-caspase-3-signaling-activation
#17
Ying Xu, Jing Li, Qian-Jun Li, Yan-Ling Feng, Feng Pan
Betulinic acid (BA), isolated from the tree bark, is a pentacyclic triterpenoid, showing inhibitory role in cancer cells. However, the effects of BA treatment on liver cancer have little to be known. Thus, the study is conducted to explore the in vitro and in vivo role of BA in liver cancer. And the interactions between BA and tumor necrosis factor-related apoptosis-inducing ligand of APO2, also known as TRAIL, were investigated in liver cancer cells. A synergistic effect of BA and APO2 combination on apoptosis induction in liver cancer cells was observed...
April 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28115244/identification-expression-pattern-and-functional-characterization-of-as-kip2-in-diapause-embryo-restarting-process-of-artemia-sinica
#18
Mengchen Zhang, Feng Yao, Tong Qin, Lin Hou, Xiangyang Zou
Proper control of the cellular processes requires a variety of regulatory proteins that are involved in the cell cycle, proliferation and apoptosis. Cyclin-dependent kinase inhibitor (CKI) negatively regulates transcription and arrests the cell cycle in G1 phase. KIP2 is a member of CKI family, which could inhibit proliferation by tight-binding with several cyclin-CDK complexes. During the embryonic development of the brine shrimp, Artemia sinica, KIP2 plays a key role in the cell cycle regulation, but the specific mechanisms remain unknown...
April 15, 2017: Gene
https://www.readbyqxmd.com/read/28114432/tfdp3-regulates-epithelial-mesenchymal-transition-in-breast-cancer
#19
Kailin Yin, Yanchen Liu, Ming Chu, Yuedan Wang
Breast cancer remains a lethal disease to women due to lymph node metastasis, the tumor microenvironment, secondary resistance and other unknown factors. Several important transcription factors involved in this disease, such as PTEN, p53 and beta-catenin, have been identified and researched in-depth as candidates for targeted therapy in breast cancer. TFDP3 is a new, promising candidate for transcriptional regulation in breast cancer, although it was first identified in hepatocellular carcinoma. Here, we demonstrate that TFDP3 is expressed in a variety of malignancies, normal testis tissue and breast cancer cell lines and thus provide evidence that TFDP3 is a cancer-testis antigen...
2017: PloS One
https://www.readbyqxmd.com/read/28108301/pfkfb3-a-direct-target-of-p63-is-required-for-proliferation-and-inhibits-differentiation-in-epidermal-keratinocytes
#20
Robert B Hamanaka, Gökhan M Mutlu
p63 is a transcription factor essential for epidermal development and homeostasis. p63 is a member of the p53 family of transcription factors, which are increasingly understood to be regulators of cellular metabolism. How p63 regulates metabolism in epidermal keratinocytes is incompletely understood, and it is unknown whether glycolytic regulation is essential to maintain the balance between proliferation and differentiation within the epidermis. We found that p63 promotes glycolytic metabolism in epidermal keratinocytes...
January 17, 2017: Journal of Investigative Dermatology
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