TY - JOUR
T1 - New insights into long non-coding rna malat1 in cancer and metastasis
AU - Sun, Yutong
AU - Ma, Li
N1 - Funding Information:
Y.S. is supported by MD Anderson’s Cancer Center Support Grant from the US National Cancer Institute (NCI P30CA016672). L.M. is supported by NCI grants R01CA166051 and R01CA181029 and a Stand Up To Cancer Innovative Research Grant (403235).
Funding Information:
Funding: Y.S. is supported by MD Anderson’s Cancer Center Support Grant from the US National Cancer Institute (NCI P30CA016672). L.M. is supported by NCI grants R01CA166051 and R01CA181029 and a Stand Up To Cancer Innovative Research Grant (403235).
Publisher Copyright:
© 2019 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2019/2
Y1 - 2019/2
N2 - Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However, Malat1 knockout mice develop and grow normally, and do not show alterations in alternative splicing. While MALAT1 was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for MALAT1 is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating MALAT1 have been observed, which led to distinct models for MALAT1′s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study MALAT1′s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA.
AB - Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is one of the most abundant, long non-coding RNAs (lncRNAs) in normal tissues. This lncRNA is highly conserved among mammalian species, and based on in vitro results, has been reported to regulate alternative pre-mRNA splicing and gene expression. However, Malat1 knockout mice develop and grow normally, and do not show alterations in alternative splicing. While MALAT1 was originally described as a prognostic marker of lung cancer metastasis, emerging evidence has linked this lncRNA to other cancers, such as breast cancer, prostate cancer, pancreatic cancer, glioma, and leukemia. The role described for MALAT1 is dependent on the cancer types and the experimental model systems. Notably, different or opposite phenotypes resulting from different strategies for inactivating MALAT1 have been observed, which led to distinct models for MALAT1′s functions and mechanisms of action in cancer and metastasis. In this review, we reflect on different experimental strategies used to study MALAT1′s functions, and discuss the current mechanistic models of this highly abundant and conserved lncRNA.
KW - LncRNA
KW - MALAT1
KW - Metastasis
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U2 - 10.3390/cancers11020216
DO - 10.3390/cancers11020216
M3 - Review article
C2 - 30781877
AN - SCOPUS:85062410566
SN - 2072-6694
VL - 11
JO - Cancers
JF - Cancers
IS - 2
M1 - 216
ER -