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, 37 (1), 101

The Dysregulation of tRNAs and tRNA Derivatives in Cancer


The Dysregulation of tRNAs and tRNA Derivatives in Cancer

Shi-Qiong Huang et al. J Exp Clin Cancer Res.


Transfer RNAs (tRNAs), traditionally considered to participate in protein translation, were interspersed in the entire genome. Recent studies suggested that dysregulation was observed in not only tRNAs, but also tRNA derivatives generated by the specific cleavage of pre- and mature tRNAs in the progression of cancer. Accumulating evidence had identified that certain tRNAs and tRNA derivatives were involved in proliferation, metastasis and invasiveness of cancer cell, as well as tumor growth and angiogenesis in several malignant human tumors. This paper reviews the importance of the dysregulation of tRNAs and tRNA derivatives during the development of cancer, such as breast cancer, lung cancer, and melanoma, aiming at a better understanding of the tumorigenesis and providing new ideas for the treatment of these cancers.

Keywords: Breast cancer; Lung cancer; Melanoma; tRNA; tRNA derivatives.

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Competing interests

The authors declare that they have no competing interests.

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Fig. 1
Fig. 1
Different types of tRNA derivatives came from the cleavage of pre-tRNAs and mature tRNAs. tsRNAs were generated in the nucleus as a consequence of the pre-tRNA 3′ end cleavage. tiRNAs were generated as a consequence of angiogenin cleaving the anti-codon loop of the mature tRNA. tRFs were formed by Dicer at D-loop, T-loop and other positions of the nucleic acid ribozyme through cleavage of the mature tRNA
Fig. 2
Fig. 2
The overexpression of tRNAs regulated the progression of cancer acting on different ways: Ras, c-myc and TERT promoted the transcription of tRNA genes by binding to pol III. a The overexpression of tRNA activated the RSK1/MSK2 signaling pathway, thus influencing cell proliferation and cell apoptosis. b Overexpressed tRNA promoted the ability of invasion and metastasis by enhancing stability and translation of transcripts enriched for their cognate codons. c The overexpression of tRNA regulated the progression of cancer by increasing the secretion of integrin and type II collagen
Fig. 3
Fig. 3
tRNA derivatives exerted their effects through different pathways. a tRNA derivatives promoted cell proliferation and the progression of G0/G1 cell cycle by regulating the expression of AURKA. b Both tRNA derivatives and endogenous oncogene transcripts competed with YBX1, suppressing the progression of cancer and preventing the translation of eIF4G/A. c tRNA derivatives promoted the translation of ribosomal protein mRNAs, subsequently enhancing cell proliferation and viability

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    1. Ghildiyal M, Zamore PD. Small silencing RNAs: an expanding universe. Nat Rev Genet. 2009;10:94–108. doi: 10.1038/nrg2504. - DOI - PMC - PubMed
    1. Cech TR, Steitz JA. The noncoding RNA revolution-trashing old rules to forge new ones. Cell. 2014;157:77–94. doi: 10.1016/j.cell.2014.03.008. - DOI - PubMed
    1. Kawaji H, Nakamura M, Takahashi Y, Sandelin A, Katayama S, Fukuda S, Daub CO, Kai C, Kawai J, Yasuda J, Carninci P, Hayashizaki Y. Hidden layers of human small RNAs. BMC Genomics. 2008;9:157. doi: 10.1186/1471-2164-9-157. - DOI - PMC - PubMed
    1. Cole C, Sobala A, Lu C, Thatcher SR, Bowman A, Brown JW, Green PJ, Barton GJ, Hutvagner G. Filtering of deep sequencing data reveals the existence of abundant dicer-dependent small RNAs derived from tRNAs. RNA (New York, NY) 2009;15:2147–2160. doi: 10.1261/rna.1738409. - DOI - PMC - PubMed
    1. Tycowski KT, You ZH, Graham PJ, Steitz JA. Modification of U6 spliceosomal RNA is guided by other small RNAs. Mol Cell. 1998;2:629–638. doi: 10.1016/S1097-2765(00)80161-6. - DOI - PubMed

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