Although metastasis-associated lung adenocarcinoma transcript (MALAT)-1 is known 
to be consistently upregulated in several epithelial malignancies, little is 
known about its function or regulation. We therefore examined the relationship 
between MALAT-1 expression and candidate modulators such as DNA tumor virus 
oncoproteins human papillomavirus (HPV)-16 E6 and E7, BK virus T antigen 
(BKVTAg), mouse polyoma virus middle T antigen (MPVmTAg) and tumor suppressor 
genes p53 and pRb. Using suppressive subtractive hybridization (SSH) and 
real-time reverse transcriptase polymerase chain reaction (RT-PCR) assays, 
MALAT-1 was shown to be increased in viral oncongene-expressing salivary gland 
biopsies from humans and mice. The results also indicated that MALAT-1 
transcripts and promoter activity were increased in vitro when viral 
oncongene-expressing plasmids were introduced into different cell types. These 
same viral oncogenes in addition to increasing MALAT-1 transcription have also 
been shown to inhibit p53 and/or pRb function. In p53 mutant or inactive cell 
lines MALAT-1 was also shown to be highly upregulated. We hypothesize that there 
is a correlation between MALAT-1 over-expression and p53 deregulation. In 
conclusion, we show that disruption of p53, by both polyoma and papilloma 
oncoproteins appear to play an important role in the up-regulation of MALAT-1. 
MALAT-1 might therefore represent a biomarker for p53 deregulation within 
malignancies.