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MALAT1: A long non-coding RNA highly associated with human cancers
Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a well-known lncRNA associated with numerous diseases, particularly cancer, has received increased attention. The expression of MALAT1 was determined to be upregulated in numerous types of tumors and MALAT1 exhibited effects on tumor c...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6006327/ https://www.ncbi.nlm.nih.gov/pubmed/29928382 http://dx.doi.org/10.3892/ol.2018.8613 |
Sumario: | Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a well-known lncRNA associated with numerous diseases, particularly cancer, has received increased attention. The expression of MALAT1 was determined to be upregulated in numerous types of tumors and MALAT1 exhibited effects on tumor cell proliferation, migration, invasion and apoptosis. The abnormal expression of MALAT1 was identified in almost in every organ of the digestive system. MALAT1 performed an important role in the pathological alterations of organs that are associated with sex hormones and several reproductive system cancers. MALAT1 participates in molecular pathways. In the clinical application of MALAT1, MALAT1 was considered as a potential biomarker for the diagnosis and prediction of cancers, and may also serve as therapeutic target for treatment of specific tumors. This review summarizes the abnormal expression of MALAT1 in cancer, its significant effect on the primary features of cancer, as well as the underlying molecular mechanisms of MALAT1 in various cancers. According to studies on MALAT1, we introduce the upstream and downstream substances associated with the function of MALAT1. These reviewed studies promote the clinical application of MALAT1 in the aspect of diagnosis and treatment of different cancers, and may help point out new study directions for MALAT1. |
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