The Impact of Mutant p53 in the Non-Coding RNA World

Long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), micro RNAs (miRNAs), and extracellular RNAs (exRNAs) are new groups of RNAs with regulation activities that have low or no protein-coding ability. Emerging evidence suggests that deregulated expression of these non-coding RNAs is associated w...

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Bibliographic Details
Published in:Biomolecules (Basel, Switzerland) Switzerland), 2020-03, Vol.10 (3), p.472
Main Author: Di Agostino, Silvia
Format: Article
Language:English
Subjects:
cancer
circular rna (circrnas)
Epigenesis, Genetic
extracellular rna (exrnas)
gain-of-function
Gene Expression Regulation, Neoplastic
Humans
long non-coding rna (lncrnas)
Methods
micro rna (mirnas)
mutant p53
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Review
RNA sequencing
RNA, Neoplasm - genetics
RNA, Neoplasm - metabolism
RNA, Untranslated - genetics
RNA, Untranslated - metabolism
Tumor Suppressor Protein p53 - genetics
Tumor Suppressor Protein p53 - metabolism
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Summary:Long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), micro RNAs (miRNAs), and extracellular RNAs (exRNAs) are new groups of RNAs with regulation activities that have low or no protein-coding ability. Emerging evidence suggests that deregulated expression of these non-coding RNAs is associated with the induction and progression of diverse tumors throughout epigenetic, transcriptional, and post-transcriptional modifications. A consistent number of non-coding RNAs (ncRNAs) has been shown to be regulated by p53, the most important tumor suppressor of the cells frequently mutated in human cancer. It has been shown that some mutant p53 proteins are associated with the loss of tumor suppressor activity and the acquisition of new oncogenic functions named gain-of-function activities. In this review, we highlight recent lines of evidence suggesting that mutant p53 is involved in the expression of specific ncRNAs to gain oncogenic functions through the creation of a complex network of pathways that influence each other.
ISSN:2218-273X
2218-273X
DOI:10.3390/biom10030472