scholarly journals Genetic screens reveal mechanisms for the transcriptional regulation of tissue-specific genes in normal cells and tumors

2019 ◽  
Vol 47 (7) ◽  
pp. 3407-3421
Author(s):  
Ikrame Naciri ◽  
Marthe Laisné ◽  
Laure Ferry ◽  
Morgane Bourmaud ◽  
Nikhil Gupta ◽  
...  
2007 ◽  
Vol 39 (6) ◽  
pp. 730-732 ◽  
Author(s):  
Duncan T Odom ◽  
Robin D Dowell ◽  
Elizabeth S Jacobsen ◽  
William Gordon ◽  
Timothy W Danford ◽  
...  

Open Biology ◽  
2017 ◽  
Vol 7 (3) ◽  
pp. 160338 ◽  
Author(s):  
Christine A. Armstrong ◽  
Kazunori Tomita

Aberrant activation of telomerase occurs in 85–90% of all cancers and underpins the ability of cancer cells to bypass their proliferative limit, rendering them immortal. The activity of telomerase is tightly controlled at multiple levels, from transcriptional regulation of the telomerase components to holoenzyme biogenesis and recruitment to the telomere, and finally activation and processivity. However, studies using cancer cell lines and other model systems have begun to reveal features of telomeres and telomerase that are unique to cancer. This review summarizes our current knowledge on the mechanisms of telomerase recruitment and activation using insights from studies in mammals and budding and fission yeasts. Finally, we discuss the differences in telomere homeostasis between normal cells and cancer cells, which may provide a foundation for telomere/telomerase targeted cancer treatments.


2016 ◽  
Vol 14 (05) ◽  
pp. 1644001 ◽  
Author(s):  
Fangzhou Shen ◽  
Jian Li ◽  
Ying Zhu ◽  
Zhuo Wang

Cancer cells have different metabolism in contrast to normal cells. The advancement in omics measurement technology enables the genome-wide characterization of altered cellular processes in cancers, but the metabolic flux landscape of cancer is still far from understood. In this study, we compared the well-reconstructed tissue-specific models of five cancers, including breast, liver, lung, renal, and urothelial cancer, and their corresponding normal cells. There are similar patterns in majority of significantly regulated pathways and enriched pathways in correlated reaction sets. But the differences among cancers are also explicit. The renal cancer demonstrates more dramatic difference with other cancer models, including the smallest number of reactions, flux distribution patterns, and specifically correlated pathways. We also validated the predicted essential genes and revealed the Warburg effect by in silico simulation in renal cancer, which are consistent with the measurements for renal cancer. In conclusion, the tissue-specific metabolic model is more suitable to investigate the cancer metabolism. The similarity and heterogenicity of metabolic reprogramming in different cancers are crucial for understanding the aberrant mechanisms of cancer proliferation, which is fundamental for identifying drug targets and biomarkers.


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