Prekomjerna ekspresija PVT1 može dovesti do tumorigeneze na tri načina. Preuređivanje fuzijomDNK PVT1 i onkogenskog tumorskog supresora moglo bi dovesti do disregulacije onkogena ili supresije tumora, što je na kraju dovodi do tumorigeneze. Zatim, ekspresija miRNK kodiranih putem PVT1 može smanjiti regulaciju gena za suzbijanje tumora, uzrokujući tumorigenezu. Konačno, povećanje interakcije MYC s PVT1 može takođđer dovesti do tumorigeneze.[8]
Nadekspresija PVT1 koji se nalazi u regiji 8q24.21 povezana je s mnogim tipovima raka kod ljudi [8] disregulacijom određenih različitih gena u različitim tipovima raka. Naprimjer, prekomjerna ekspresija PVT1 u raku prostate snižava ekspresiju gena miR-146a, što dovodi do smanjenja nivoa miR-146a u ćeliji, putem metilacijaCpG-otoka na promotorskoj regiji, podstičući suzbijanje ćelija raka apoptozom.[9] Nadalje, pokazalo se da aktivnost lncPVT1 i s njim povezanih mikroRNK utiče na otpornost na hemoterapiju u više tipova raka epigenetičkom regulacijom ili direktnom represijom drugih nekodiranih transkripata.[10]
^ abCui M, You L, Ren X, Zhao W, Liao Q, Zhao Y (februar 2016). "Long non-coding RNA PVT1 and cancer". Biochemical and Biophysical Research Communications. 471 (1): 10–14. doi:10.1016/j.bbrc.2015.12.101. PMID26850852.
Oh JH, Yang JO, Hahn Y, Kim MR, Byun SS, Jeon YJ, Kim JM, Song KS, Noh SM, Kim S, Yoo HS, Kim YS, Kim NS (decembar 2005). "Transcriptome analysis of human gastric cancer". Mammalian Genome. 16 (12): 942–954. doi:10.1007/s00335-005-0075-2. PMID16341674. S2CID69278.
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