ArticleCancer research2013
The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells.
Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 988 papers.
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988 citing papers in PubMed, 1,556 citations in OpenAlex.
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- The role of non-coding variants in hereditary cancer syndromes: mechanistic insights and clinical implications.Annals of medicine and surgery (2012) · 2026Review
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- TRNAU1AP and PRPF39 establish integrated control over processing of most abundant human non-coding RNAs.Nature communications · 2026Article
- Noncoding RNAs are indispensable architects and regulators of biomolecular condensates.Non-coding RNA research · 2026Review
- Quercetin Affects Carcinogenic Phenotype of Breast and Lung Cancer Cells Differentially Through Sterol Regulation Mediated by MALAT1 Perturbation.Chemistry, an Asian journal · 2026Article
- State-Aware RNA Biomarkers in Triple-Negative Breast Cancer (TNBC): Integrating Tumor Plasticity, Spatial Architecture, and Temporal Monitoring.International journal of molecular sciences · 2026Review
- Sequence alignment of the primate lineage reveals evolutionary divergence and conserved secondary structural motifs in noncoding RNAs.bioRxiv : the preprint server for biology · 2026Article
928 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
The long noncoding RNA MALAT1 (metastasis-associated lung adenocarcinoma transcript 1), also known as MALAT-1 or NEAT2 (nuclear-enriched abundant transcript 2), is a highly conserved nuclear noncoding RNA (ncRNA) and a predictive marker for metastasis development in lung cancer. To uncover its functional importance, we developed a MALAT1 knockout model in human lung tumor cells by genomically integrating RNA destabilizing elements using zinc finger nucleases. The achieved 1,000-fold MALAT1 silencing provides a unique loss-of-function model. Proposed mechanisms of action include regulation of splicing or gene expression. In lung cancer, MALAT1 does not alter alternative splicing but actively regulates gene expression including a set of metastasis-associated genes. Consequently, MALAT1-deficient cells are impaired in migration and form fewer tumor nodules in a mouse xenograft. Antisense oligonucleotides (ASO) blocking MALAT1 prevent metastasis formation after tumor implantation. Thus, targeting MALAT1 with ASOs provides a potential therapeutic approach to prevent lung cancer metastasis with this ncRNA serving as both predictive marker and therapeutic target. Finally, regulating gene expression, but not alternative splicing, is the critical function of MALAT1 in lung cancer metastasis. In summary, 10 years after the discovery of the lncRNA MALAT1 as a biomarker for lung cancer metastasis, our loss-of-function model unravels the active function of MALAT1 as a regulator of gene expression governing hallmarks of lung cancer metastasis.
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Registered trials
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