Genes, Tumor Suppressor

Publication Title: 
The Journal of Pathology

The proliferative lifespan of normal mammalian cells is limited by intrinsic controls, which desensitize the cell-cycle machinery to extrinsic stimulation after a given number of cell divisions. One underlying clock driving this process of 'replicative senescence' is the progressive erosion of chromosome telomeres, which occurs with each round of DNA replication. This appears to trigger growth inhibition via activation of the tumour suppressor gene (TSG) product, p53, and the consequent up-regulation of the cell-cycle inhibitor p21WAF1.

Author(s): 
Wynford-Thomas, D.
Publication Title: 
The EMBO journal

Telomere shortening in normal human cells causes replicative senescence, a p53-dependent growth arrest state, which is thought to represent an innate defence against tumour progression. However, although it has been postulated that critical telomere loss generates a 'DNA damage' signal, the signalling pathway(s) that alerts cells to short dysfunctional telomeres remains only partially defined.

Author(s): 
Gire, VÈronique
Roux, Pierre
Wynford-Thomas, David
Brondello, Jean-Marc
Dulic, Vjekoslav
Publication Title: 
Mechanisms of Ageing and Development

An association between aging/longevity and cancer has long been suggested, yet the evolutionary and molecular links between these complicated traits remain elusive. Here, we analyze the relationship between longevity- and cancer-associated genes/proteins (LAGs/LAPs and CAGs/CAPs, respectively). Specifically, we address the following questions: (1) to what extent the CAGs and LAGs are evolutionary conserved and how they (or their orthologs) are related to each other in diverse species?

Author(s): 
Budovsky, Arie
Tacutu, Robi
Yanai, Hagai
Abramovich, Amir
Wolfson, Marina
Fraifeld, Vadim
Publication Title: 
Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA

OBJECTIVE: To explore a method for rapid construction of a full-length cDNA library of human glioma tissues using switching mechanism at 5' end of RNA transcript (SMART). METHODS: The total RNA was extracted from several samples of human glioma tissues and the mRNA was subsequently separated. Multiple mRNA samples were mixed to be used as the template for the first-strand cDNA synthesis.

Author(s): 
Tu, Yan-yang
Xu, Ru-xiang
Yang, Zhi-lin
Jiang, Xiao-dan
Wu, Shu-guang
Chen, Yi-zhao
Cai, Ying-qian
Du, Mou-xuan
Gao, Yang
Publication Title: 
Cancer Letters

We showed previously that inactivation of TSC2 induces death in cancer cells lacking the Retinoblastoma (Rb) tumor suppressor under stress conditions, suggesting that inactivation of TSC2 can potentially be used as an approach to specifically kill cancers that have lost WT Rb. As Rb is often inactivated in cancers by overexpression of cyclin D1, loss of p16(ink4a) cdk inhibitor, or expression of viral oncoproteins, it will be interesting to determine if such functional inactivation of Rb would similarly sensitize cancer cells to TSC2 inactivation induced cell death.

Author(s): 
Danos, Arpad M.
Liao, Yang
Li, Xuan
Du, Wei
Publication Title: 
Genes & Development

Metabolism generates oxygen radicals, which contribute to oncogenic mutations. Activated oncogenes and loss of tumor suppressors in turn alter metabolism and induce aerobic glycolysis. Aerobic glycolysis or the Warburg effect links the high rate of glucose fermentation to cancer. Together with glutamine, glucose via glycolysis provides the carbon skeletons, NADPH, and ATP to build new cancer cells, which persist in hypoxia that in turn rewires metabolic pathways for cell growth and survival.

Author(s): 
Dang, Chi V.
Publication Title: 
Cell Cycle (Georgetown, Tex.)

CDK8 is either amplified or mutated in a variety of human cancers, and CDK8 functions as an oncoprotein in melanoma and colorectal cancers. Previously, we reported that loss or reduction of CDK8 results in aberrant fat accumulation in Drosophila and mammals, suggesting that CDK8 plays an important role in inhibiting lipogenesis.

Author(s): 
Gu, Weiting
Wang, Chenguang
Li, Weihua
Hsu, Fu-Ning
Tian, Lifeng
Zhou, Jie
Yuan, Cunzhong
Xie, Xiao-Jun
Jiang, Tao
Addya, Sankar
Tai, Yanhong
Kong, Beihua
Ji, Jun-yuan
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