Multiple overexpressed lncRNAs, including RP11-160H22.5, XLOC-014172, LOC149086, UCA1, WRAP53
, AF085935, uc003wbd, PVT1, uc002mbe.2, PANDAR, SPRY4-IT1, uc001ncr, AX800134, linc00152, and HULC, have been identified to be prospective diagnostic indicators for HCC [19-34].
Mutations in one of 8 genes involved in telomere biology--DKC1, TINF2, TERC, TERT (telomerase reverse transcriptase), NHP2 [NHP2 ribonucleoprotein homolog (yeast)], NOP10 [NOP10 ribonucleoprotein homolog (yeast)], WRAP53 (WD repeat containing, antisense to TP53; formerly TCAB1), and CTC1 (CTS telomere maintenance complex component 1)--can be identified in approximately 50% of patients with clinical features of classic DC, the remainder being as yet uncharacterized (3, 4).
These mutations all participate in telomere maintenance but fall into 3 distinct telomere-maintenance pathways: the telomerase complex, which elongates telomeres in stem cells [disease genes TERC, TERT, DKC1, NOP10, NHP2, and WRAP53 (formerly TCAB1)]; the shelterin complex, which protects telomere ends and regulates telomerase recruitment (disease gene TINF2); and the CTS complex, which participates in telomere replication and regulates telomerase activity at the telomere end (disease gene CTC1) (1).
 Human genes: DKC1, dyskeratosis congenita 1, dyskerin; TINF2, TERF1 (TRF1)-interacting nuclear factor 2; TERC, telomerase RNA component; TERT, telomerase reverse transcriptase; NHP2, NHP2 ribonucleoprotein homolog (yeast); NOP10, NOP10 ribonucleoprotein homolog (yeast); WRAP53 (formerly TCAB1), WD repeat containing, antisense to TP53; CTC1, CTS telomere maintenance complex component 1.
Writing about their work in the journal Molecular Cell, the researchers have revealed the newly identified gene as Wrap53.
They have found that Wrap53 gives rise to a molecule, known as antisense RNA, the presence of which is necessary for the production of sufficient quantities of p53 protein in the event of DNA damage.
Marianne Farnebo, a member of the research team, said that the results suggested that damage to Wrap53 could indirectly cause cancer.
She, thus, said that Wrap53 was a new potential target for future cancer therapies.