MALAT-1, a novel noncoding RNA, and thymosin β4 predict metastasis and survival in early-stage non-small cell lung cancer

By P. Ji, Sven Diederichs, Wenbing Wang, S. Böing, R. Metzger, P. Schneider, N. Tidow, B. Brandt, H. Buerger, Etmar Bulk and 4 more. Oncogene, 2003

2,220 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/61de0a826e81f14384e96c2864412b472adcdf6c

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Citations in the corpus

lincRNAs: Genomics, Evolution, and Mechanisms (2013, neutral): “Malat1 is an exceptionally highly expressed, nuclear-retained, single-exon lincRNA that was originally identified in metastatic tumors (Ji et al., 2003).”
Long noncoding RNA in prostate, bladder, and kidney cancer. (2014, background): “The metastasis associated lung adenocarcinoma transcript 1 (MALAT1/NEAT2) [58] is specifically upregulated in bladder, kidney, anda subset of PCas [12,59–61].”
Long noncoding RNAs: functional surprises from the RNA world. (2009, background): “…lung adenocarcinoma transcript 1), also known as NEAT2 (Hutchinson et al. 2007), is a long (;7-kb) ncRNA that is misregulated in many human cancers (Ji et al. 2003; Lin et al. 2007) and was shown previously to be retained specifically in the nucleus in nuclear speckles (Hutchinson et al. 2007),…”
Long Noncoding RNAs: Past, Present, and Future (2013, background): “More recently, MALAT1 has been shown to interact with the PRC1 subunit Cbx4/Pc2 and participate in the shuttling of genes between nuclear compartments for silencing and activation.”
The Nuclear-Retained Noncoding RNA MALAT1 Regulates Alternative Splicing by Modulating SR Splicing Factor Phosphorylation (2010, background): “Originally identified based upon its overexpression in several cancers, the role of MALAT1 in normal cellular physiology remains unknown (Ji et al., 2003; Lin et al., 2006).”
Long Noncoding RNAs in Cardiovascular Diseases (2015, positive): “The study further characterized the function of MALAT1, which was first described as Metastasis Associated in Lung Adenocarcinoma Transcript.74 In endothelial cells, inhibition of MALAT1 by siRNA or LNA GapmeR, which induces RNA degradation by an RNase H-dependent mechanism, promoted migration of ti”
The Genetic Signatures of Noncoding RNAs (2009, background): “Altered expression or splicing in cancer and other diseases [37–49]”
3’ end processing of a long nuclear-retained non-coding RNA yields a tRNA-like cytoplasmic RNA (2008, neutral): “MALAT1 shows broad expression in normal human and mouse tissues (Ji et al., 2003; Hutchinson et al., 2007) and is over-expressed in many human carcinomas, including those of the breast, pancreas, lung, colon, prostate, and liver (Lin et al.”