CGE-2015v3n14 - page 8

Cancer Genetics and Epigenetics 2015, Vol.3, No.14, 1-5
4
tools, the secrets of interaction and mechanism
between epigenome and structural genomic variation
will gradually emerge from the water.
5 Conclusion
More and more researches confirmed that the
mechanism of genetic and epigenetic influence
each other and cooperate to promoter oncogenic
transformation in a variety of ways. The can cer
genome and epigenome affect and cooperate with
each other to achieve similar results, such as
the inactivation of tumor suppressor genes mentioned
above such as p53, BRAF, IDH1, RB by either
mutation or hypermethylation of promoter regions.
On the one hand, global DNA hypomethylation can
induce human genomic instability, which gives a more
chance for the mutation of the oncogene, the
methylation status of LINE-1 is closely associated
with chromosomal stability. On the other hand,
hypermehtylation can increase the mutation rate of
tumor suppressor genes such as hypermethylation of
promoter region produced a favorable condition for
inactivation mutant of the BRAF in the colorectal
cancer.
Many questions remind in this field such as altered
methylation patterns in cancer cell genomes: Cause or
consequence? There is such a point that DNA
methylation is considered as a consolidating rather
than an initiating event in tumor suppressor gene
inactivation. Somatic inactivation of X chromosome
in female, where DNA hypermethylation of promoter
CpG islands is after inactivation not before (71, 95,
108). Another major question is how to investigate the
mechanistic basis for well-known examples of
disruption of epigenetic control. Therefore, the
identification of epigenetic drivers must rely more on
the analysis of transcriptional consequences and most
importantly functional experimental validation of the
effect of epigenetic genes inactivation on cellular
proliferation, immortality, angiogenesis, cell death,
invasion and metastasis affected.
Acknowledgements
This work was supported by National Natural Science
Foundation of China (grants 61403112, 31371334).
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