The telomerase RNA subunit (TR) is overexpressed in many tumors; however, the contribution of TR in cancer formation remains elusive. The most frequent clinically diagnosed cancer in the animal kingdom is caused by the highly oncogenic herpesvirus Marek’s disease virus (MDV). MDV encodes a TR (vTR) that plays an important role in virus-induced tumorigenesis and shares 88% sequence identity with its cellular homologue. To determine if the cellular TR possesses pro-oncogenic activity, we replaced vTR with the cellular homologue in the virus genome. Insertion of cellular TR resulted in a strong overexpression in virus infected cells, while virus replication was not affected. Strikingly, cellular TR promoted tumor formation as efficient as vTR, while tumorigenesis was severely impaired in the absence of vTR. Our data provide the first evidence that overexpression of cellular TR can contribute to tumor formation in vivo using this natural virus-host model for herpesvirus-induced oncogenesis.

端粒酶RNA亚基（TR）在许多肿瘤中都过表达。然而，TR在癌症形成中的作用仍然难以捉摸。动物界最常见的临床诊断癌症是由高度致癌的疱疹病毒马立克氏病病毒（MDV）引起的。MDV编码的TR（vTR）在病毒诱导的肿瘤发生中起重要作用，并与其细胞同源物具有88％的序列同一性。为了确定细胞TR是否具有促癌活性，我们用病毒基因组中的细胞同源物替换了vTR。细胞TR的插入导致病毒感染的细胞中强烈的过表达，而病毒复制不受影响。令人惊讶的是，细胞TR可以像vTR一样有效地促进肿瘤形成，而在不存在vTR的情况下，致瘤性受到严重损害。