scholarly journals The p53 Family: A Role in Lipid and Iron Metabolism

Author(s):  
Kyra Laubach ◽  
Jin Zhang ◽  
Xinbin Chen

The p53 family of tumor suppressors, which includes p53, p63, and p73, has a critical role in many biological processes, such as cell cycle arrest, apoptosis, and differentiation. In addition to tumor suppression, the p53 family proteins also participate in development, multiciliogenesis, and fertility, indicating these proteins have diverse roles. In this review, we strive to cover the relevant studies that demonstrate the roles of p53, p63, and p73 in lipid and iron metabolism.

Tumor Biology ◽  
2017 ◽  
Vol 39 (10) ◽  
pp. 101042831772618 ◽  
Author(s):  
Khuloud Bajbouj ◽  
Jasmin Shafarin ◽  
Maher Y Abdalla ◽  
Iman M Ahmad ◽  
Mawieh Hamad

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Christophe Nicot

Tumor suppressor functions are essential to control cellular proliferation, to activate the apoptosis or senescence pathway to eliminate unwanted cells, to link DNA damage signals to cell cycle arrest checkpoints, to activate appropriate DNA repair pathways, and to prevent the loss of adhesion to inhibit initiation of metastases. Therefore, tumor suppressor genes are indispensable to maintaining genetic and genomic integrity. Consequently, inactivation of tumor suppressors by somatic mutations or epigenetic mechanisms is frequently associated with tumor initiation and development. In contrast, reactivation of tumor suppressor functions can effectively reverse the transformed phenotype and lead to cell cycle arrest or death of cancerous cells and be used as a therapeutic strategy. Adult T-cell leukemia/lymphoma (ATLL) is an aggressive lymphoproliferative disease associated with infection of CD4 T cells by the Human T-cell Leukemia Virus Type 1 (HTLV-I). HTLV-I-associated T-cell transformation is the result of a multistep oncogenic process in which the virus initially induces chronic T-cell proliferation and alters cellular pathways resulting in the accumulation of genetic defects and the deregulated growth of virally infected cells. This review will focus on the current knowledge of the genetic and epigenetic mechanisms regulating the inactivation of tumor suppressors in the pathogenesis of HTLV-I.


Author(s):  
Tongyuan Li ◽  
Ning Kon ◽  
Le Jiang ◽  
Ying Zhao ◽  
Richard Baer ◽  
...  

2020 ◽  
Vol 527 (1) ◽  
pp. 257-263
Author(s):  
Kayoko Nagata ◽  
Keisuke Shindo ◽  
Yusuke Matsui ◽  
Kotaro Shirakawa ◽  
Akifumi Takaori-Kondo

2015 ◽  
Vol 231 (2) ◽  
pp. 357-369 ◽  
Author(s):  
Anup Shrestha ◽  
Saroj Nepal ◽  
Mi Jin Kim ◽  
Jae Hoon Chang ◽  
Sang-Hyun Kim ◽  
...  

Oncogene ◽  
1998 ◽  
Vol 16 (24) ◽  
pp. 3087-3095 ◽  
Author(s):  
Sandra P Frizelle ◽  
Jon Grim ◽  
Joan Zhou ◽  
Pankaj Gupta ◽  
David T Curiel ◽  
...  

Cell ◽  
2012 ◽  
Vol 149 (6) ◽  
pp. 1269-1283 ◽  
Author(s):  
Tongyuan Li ◽  
Ning Kon ◽  
Le Jiang ◽  
Minjia Tan ◽  
Thomas Ludwig ◽  
...  

Oncogene ◽  
1998 ◽  
Vol 17 (20) ◽  
pp. 2619-2627 ◽  
Author(s):  
Masafumi Menjo ◽  
Yoko Kaneko ◽  
Etsuro Ogata ◽  
Kyoji Ikeda ◽  
Makoto Nakanishi

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1769
Author(s):  
Zehuan Liao ◽  
Han Lin Yeo ◽  
Siaw Wen Wong ◽  
Yan Zhao

Cellular senescence is a complex and multistep biological process which cells can undergo in response to different stresses. Referring to a highly stable cell cycle arrest, cellular senescence can influence a multitude of biological processes—both physiologically and pathologically. While phenotypically diverse, characteristics of senescence include the expression of the senescence-associated secretory phenotype, cell cycle arrest factors, senescence-associated β-galactosidase, morphogenesis, and chromatin remodelling. Persistent senescence is associated with pathologies such as aging, while transient senescence is associated with beneficial programmes, such as limb patterning. With these implications, senescence-based translational studies, namely senotherapy and pro-senescence therapy, are well underway to find the cure to complicated diseases such as cancer and atherosclerosis. Being a subject of major interest only in the recent decades, much remains to be studied, such as regarding the identification of unique biomarkers of senescent cells. This review attempts to provide a comprehensive understanding of the diverse literature on senescence, and discuss the knowledge we have on senescence thus far.


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