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P. Ji, S. Diederichs, W. Wang, S. Boing, R. Metzger, P. M. Schneider, N. Tidow, B. Brandt, H. Buerger, E. Bulk, M. Thomas, W. E. Berdel, H. Serve and C. Muller-Tidow, “MALAT-1, a Novel Noncoding RNA, and Thymosin Beta4 Predict Metastasis and Survival in Early-Stage Non-Small Cell Lung Cancer,” Oncogene, Vol. 22, No. 39, 2003, pp. 8031-8041. doi:10.1038/sj.onc.1206928

has been cited by the following article:

• TITLE: Correlation of Transcription of MALAT-1, a Novel Noncoding RNA, with Deregulated Expression of Tumor Suppressor p53 in Small DNA Tumor Virus Models

  AUTHORS: Liesl K. Jeffers, Kaiwen Duan, Lesley G. Ellies, William T. Seaman, Raquel A. Burger-Calderon, Luda B. Diatchenko, Jennifer Webster-Cyriaque

  KEYWORDS: p53; MALAT-1; Transcription; BK Virus; Polyoma Virus; Papillomavirus; HPV

  JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.3, May 27, 2013

  ABSTRACT: 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.