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Adv Exp Med Biol. 2016;927:137-72. doi: 10.1007/978-981-10-1498-7_5.

Noncoding RNAs in Growth and Death of Cancer Cells.

Author information

1
Second Military Medical University, 800 Xiangyin Road, Shanghai, China.
2
Second Military Medical University, 800 Xiangyin Road, Shanghai, China. liushanrong01@126.com.

Abstract

The mammalian genomes are mostly comprised of noncoding genes. And mammalian genomes are characterized by pervasive expression of different types of noncoding RNAs (ncRNAs). In sharp contrast to previous collections, these ncRNAs show strong purifying selection evolutionary conservation. Previous studies indicated that only a small fraction of the mammalian genome codes for messenger RNAs destined to be translated into peptides or proteins, and it is generally assumed that a large portion of transcribed sequences-including pseudogenes and several classes of ncRNAs-do not give rise to peptides or proteins. However, ribosome profiling suggests that ribosomes occupy many regions of the transcriptome thought to be noncoding. Moreover, these observations highlight a potentially large and complex set of biologically regulated translational events from transcripts formerly thought to lack coding potential. Furthermore, accumulating evidence from previous studies has suggested that the novel translation products exhibit temporal regulation similar to that of proteins known to be involved in many biological activity processes. In this review, we focus on the coding potential of noncoding genes and ncRNAs. We also sketched the possible mechanisms for their coding activities. Overall, our review provides new insights into the word of central dogma and is an expansive resource of functional annotations for biomedical research. At last, the outcome of the majority of the translation events and their potential biological purpose remain an intriguing topic for future investigation.

KEYWORDS:

Apoptosis; Autophagy; Cancer cells; Cell cycle; Necrosis; Noncoding RNA; Proliferation

PMID:
27376734
DOI:
10.1007/978-981-10-1498-7_5
[Indexed for MEDLINE]

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