Epigenetics: Unravelling the cancer code

Brower, Vicki

doi:10.1038/471s12a

Cited by 56 publications

(35 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Data mining of studies on the epigenetic regulation of carcinogenesis and metabolism has provided invaluable insights for human diseases. [39][40][41] A follow-up study should compare the binding patterns of SET1 and gene expression patterns in stressed endothelial cells on a genomewide scale. Once the role of SET1 in endothelial function is certified, a targeted therapy that aims at limiting the expression or activity of SET1 in endothelial cells may provide a new solution for the intervention of dilative cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Histone Methyltransferase SET1 Mediates Angiotensin II–Induced Endothelin-1 Transcription and Cardiac Hypertrophy in Mice

Yang

Weng

et al. 2015

ATVB

View full text Add to dashboard Cite

Objective— Endothelin-1 is a potent vasoconstrictor derived from vascular endothelium. Elevated endothelin-1 levels are observed in a host of cardiovascular pathologies including cardiomyopathy. The epigenetic mechanism responsible for endothelin-1 induction in these pathological processes remains elusive. Approach and Results— We report here that induction of endothelin-1 expression in endothelial cells by angiotensin II (Ang II) was accompanied by the accumulation of histone H3K4 trimethylation, a preeminent histone modification for transcriptional activation, on the endothelin-1 promoter. In the meantime, Ang II stimulated the expression and the occupancy of Suv, Ez, and Trithorax domain 1 (SET1), a mammalian histone H3K4 trimethyltransferase, on the endothelin-1 promoter, both in vitro and in vivo. SET1 was recruited to the endothelin-1 promoter by activating protein 1 (c-Jun/c-Fos) and synergized with activating protein 1 to activate endothelin-1 transcription in response to Ang II treatment. Knockdown of SET1 in endothelial cells blocked Ang II–induced endothelin-1 synthesis and abrogated hypertrophy of cultured cardiomyocyte. Finally, endothelial-specific depletion of SET1 in mice attenuated Ang II–induced pathological hypertrophy and cardiac fibrosis. Conclusions— Our data suggest that SET1 epigenetically activates endothelin-1 transcription in endothelial cells, thereby contributing to Ang II–induced cardiac hypertrophy. As such, screening of small-molecule compound that inhibits SET1 activity will likely offer a new therapeutic solution to the treatment of cardiomyopathy.

show abstract

Section: Discussionmentioning

confidence: 99%

Histone Methyltransferase SET1 Mediates Angiotensin II–Induced Endothelin-1 Transcription and Cardiac Hypertrophy in Mice

Yang

Weng

et al. 2015

ATVB

View full text Add to dashboard Cite

show abstract

“…Although recent progress in cancer genomics has been rapid during the past few years, it only provides a glimpse of what may occur as dictated by the genetic code (Brower, 2011). In reality, scientists still need to measure what is happening in a patient in real time, which means finding tell-tale proteins as a clue to the biological processes of cancer development (Cao et al, 2011).…”

Section: Role Of Proteomics In Cancer Researchmentioning

confidence: 99%

Implementation of Proteomics for Cancer Research: Past, Present, and Future

Karimi

Shahrokni²,

Ranjbar³

2014

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Cancer is the leading cause of the death, accounts for about 13% of all annual deaths worldwide. Many different fields of science are collaborating together studying cancer to improve our knowledge of this lethal disease, and find better solutions for diagnosis and treatment. Proteomics is one of the most recent and rapidly growing areas in molecular biology that helps understanding cancer from an omics data analysis point of view. The human proteome project was officially initiated in 2008. Proteomics enables the scientists to interrogate a variety of biospecimens for their protein contents and measure the concentrations of these proteins. Current necessary equipment and technologies for cancer proteomics are mass spectrometry, protein microarrays, nanotechnology and bioinformatics. In this paper, we provide a brief review on proteomics and its application in cancer research. After a brief introduction including its definition, we summarize the history of major previous work conducted by researchers, followed by an overview on the role of proteomics in cancer studies. We also provide a list of different utilities in cancer proteomics and investigate their advantages and shortcomings from theoretical and practical angles. Finally, we explore some of the main challenges and conclude the paper with future directions in this field.

show abstract

“…Why the same environmental factors cause different changes in human genome among individuals is a question for scientists searching unique combinations of factors leading to cancer (Brower, 2011). There is a growing body of evidence that many cancers are not caused by mutations in genes, but by chemical modifications that alter the way genes function.…”

Section: Introductionmentioning

confidence: 99%

“…Chemical modifications of genes are called epigenetic changes. Epidemiological studies have shown that diet and lifestyle may cause such changes (Brower, 2011).…”

Section: Introductionmentioning

confidence: 99%