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Human endogenous retrovirus (HERV) and solitary long terminal repeats (LTRs) constitute 8% of the human genome. Although most HERV genes are partially deleted and not intact, HERV LTRs comprise features including promoters, enhancers, selective splicer sites and polyadenylation sites in order to regulate the expression of neighboring genes. Owing to the genetic instability of LTRs, their wide distributions along human chromosomes are not only non-random, but are also correlated with gene density. Considerable evidence indicates that HERV LTRs regulate the expression of their adjacent viral and cellular genes in placental development and tumorigenesis. However, the regulatory mechanism of HERV LTRs on the expression of its neighboring cancer-associated genes in human cancers remains to be elucidated. Insertional mutagenesis, recombination and polymorphism are three principal factors of LTR that contribute to its genetic instability. Moreover, genetic instability, hypomethylation, transactivation and the antisense transcript of LTRs enhance the activity of LTRs and regulate the expression of their adjacent genes in human cancers. Therefore, in the present review, we examined the mechanism of HERV LTRs in tumorigenesis in combination with the structure and function of LTRs.

The role of human endogenous retroviral long terminal repeat sequences in human cancer (Review)