scholarly journals Jab1 (COPS5) as an Emerging Prognostic, Diagnostic and Therapeutic Biomarker for Human Cancer

2021 ◽  
Vol 12 (5) ◽  
pp. 7001-7011
Keyword(s):  
Cell Cycle ◽  
Dna Damage Response ◽  
Cancer Progression ◽  
Tumor Suppressors ◽  
Human Cancer ◽  
Cancer Biomarkers ◽  
Activation Domain ◽  
Inhibitory Compounds ◽  
Damage Response ◽  
Cancer Cell Survival

Jab1 (C-Jun activation domain-binding protein-1) has been reported to be critically involved in regulating apoptosis, cell proliferation, cell cycle, thereby affecting numerous pathways, DDR (DNA damage response) regulation, and genomic instability. Jab1 (CSN5) dysregulation has been positively associated with oncogenesis via activating oncogenes and deactivating various tumor suppressors. Jab1 overexpression has been reported in several tumor forms, illuminating its potent efficacy in cancer progression and metastasis. Jab1 has instigated prompt research interest in elucidating inhibitors of numerous oncoproteins and oncogenes for chemotherapeutics. Our review has presented strong evidence for presenting the significance of Jab1 overexpression in numerous carcinomas and its involvement in modulating various signaling pathways for cancer cell survival. This review may project a new way for utilizing Jab1 as a strong target for developing potent inhibitory compounds targeting Jab1 that could be further utilized in chemoprevention with limited side effects. Altogether this review further confirmed the crucial involvement of Jab1 in carcinogenesis and tumorigenesis, displaying the strong potential of Jab1 as one of the potent cancer biomarkers.

scholarly journals ADAR1 Transcriptome editing promotes breast cancer progression through the regulation of cell cycle and DNA damage response

2020 ◽  
Vol 1867 (8) ◽  
pp. 118716 ◽  
Author(s):  
Eduardo A. Sagredo ◽  
Alfredo I. Sagredo ◽  
Alejandro Blanco ◽  
Pamela Rojas De Santiago ◽  
Solange Rivas ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Damage Response ◽  
Regulation Of Cell Cycle

scholarly journals ATM: Main Features, Signaling Pathways, and Its Diverse Roles in DNA Damage Response, Tumor Suppression, and Cancer Development

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 845
Author(s):  
Liem Minh Phan ◽  
Abdol-Hossein Rezaeian
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Signaling Pathways ◽  
Dna Damage Response ◽  
Cancer Development ◽  
Cellular Processes ◽  
Cycle Arrest ◽  
Damage Response ◽  
Cancer Cell Survival

ATM is among of the most critical initiators and coordinators of the DNA-damage response. ATM canonical and non-canonical signaling pathways involve hundreds of downstream targets that control many important cellular processes such as DNA damage repair, apoptosis, cell cycle arrest, metabolism, proliferation, oxidative sensing, among others. Of note, ATM is often considered a major tumor suppressor because of its ability to induce apoptosis and cell cycle arrest. However, in some advanced stage tumor cells, ATM signaling is increased and confers remarkable advantages for cancer cell survival, resistance to radiation and chemotherapy, biosynthesis, proliferation, and metastasis. This review focuses on addressing major characteristics, signaling pathways and especially the diverse roles of ATM in cellular homeostasis and cancer development.

Dissecting the Role of Thyrotropin in the DNA Damage Response in Human Thyrocytes after 131I, γ Radiation and H2O2

2019 ◽  
Vol 105 (3) ◽  
pp. 839-853
Author(s):  
Aglaia Kyrilli ◽  
David Gacquer ◽  
Vincent Detours ◽  
Anne Lefort ◽  
Frédéric Libert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Damage Response ◽  
Iodide Uptake ◽  
Transcriptomic Response ◽  
Uptake Inhibition ◽  
Γ Radiation ◽  
Damage Response

Abstract Background The early molecular events in human thyrocytes after 131I exposure have not yet been unravelled. Therefore, we investigated the role of TSH in the 131I-induced DNA damage response and gene expression in primary cultured human thyrocytes. Methods Following exposure of thyrocytes, in the presence or absence of TSH, to 131I (β radiation), γ radiation (3 Gy), and hydrogen peroxide (H2O2), we assessed DNA damage, proliferation, and cell-cycle status. We conducted RNA sequencing to profile gene expression after each type of exposure and evaluated the influence of TSH on each transcriptomic response. Results Overall, the thyrocyte responses following exposure to β or γ radiation and to H2O2 were similar. However, TSH increased 131I-induced DNA damage, an effect partially diminished after iodide uptake inhibition. Specifically, TSH increased the number of DNA double-strand breaks in nonexposed thyrocytes and thus predisposed them to greater damage following 131I exposure. This effect most likely occurred via Gα q cascade and a rise in intracellular reactive oxygen species (ROS) levels. β and γ radiation prolonged thyroid cell-cycle arrest to a similar extent without sign of apoptosis. The gene expression profiles of thyrocytes exposed to β/γ radiation or H2O2 were overlapping. Modulations in genes involved in inflammatory response, apoptosis, and proliferation were observed. TSH increased the number and intensity of modulation of differentially expressed genes after 131I exposure. Conclusions TSH specifically increased 131I-induced DNA damage probably via a rise in ROS levels and produced a more prominent transcriptomic response after exposure to 131I.

WDNfinder: A method for minimum driver node set detection and analysis in directed and weighted biological network

2017 ◽  
Vol 15 (05) ◽  
pp. 1750021 ◽  
Author(s):  
Yanshuo Chu ◽  
Zhenxing Wang ◽  
Rongjie Wang ◽  
Ningyi Zhang ◽  
Jie Li ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Biological Networks ◽  
Domain Knowledge ◽  
Human Cancer ◽  
Accurate Analysis ◽  
Response Network ◽  
Public Data ◽  
Damage Response ◽  
Structural Controllability

Structural controllability is the generalization of traditional controllability for dynamical systems. During the last decade, interesting biological discoveries have been inferred by applied structural controllability analysis to biological networks. However, false positive/negative information (i.e. nodes and edges) widely exists in biological networks that documented in public data sources, which can hinder accurate analysis of structural controllability. In this study, we propose WDNfinder, a comprehensive analysis package that provides structural controllability with consideration of node connection strength in biological networks. When applied to the human cancer signaling network and p53-mediate DNA damage response network, WDNfinder shows high accuracy on essential nodes prediction in these networks. Compared to existing methods, WDNfinder can significantly narrow down the set of minimum driver node set (MDS) under the restriction of domain knowledge. When using p53-mediate DNA damage response network as illustration, we find more meaningful MDSs by WDNfinder. The source code is implemented in python and publicly available together with relevant data on GitHub: https://github.com/dustincys/WDNfinder .

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