Abstract
tRNA-derived fragments (tRFs) are a new classification of small non-coding RNAs (sncRNAs) derived from the specific cleavage of precursors and mature tRNAs. Accumulating recent evidence has shown that tRFs are frequently abnormal in several cancers. Nevertheless, the role of tRFs in gastric cancer and its mechanism remain unclear. In this study, we found abnormal expression of tRF-3017A (derived from tRNA-Val-TAC) in gastric cancer tissues and cell lines and confirmed its effect on promoting the invasion and migration of gastric cancer cells through functional experiments in vitro. Analysis of clinicopathologic data showed patients with higher tRF-3017A were associated with significantly higher lymph node metastasis. Mechanistic investigation implies that tRF-3017A regulates the tumor suppressor gene NELL2 through forming the RNA-induced silencing complex (RISC) with Argonaute (AGO) proteins. In this study, we found that higher tRF-3017A were associated with significantly higher lymph node metastasis in gastric cancer patients and the tRF-3017A may play a role in promoting the migration and invasion of gastric cancer cells by silencing tumor suppressor NELL2.
Highlights
Gastric cancer (GC) is one of the most common human cancers, which is the second leading cause of cancer death worldwide, and its global burden is increasing [1, 2]
We found that higher tRNA-derived fragments (tRFs)-3017A were associated with significantly higher lymph node metastasis in gastric cancer patients and the tRF-3017A may play a role in promoting the migration and invasion of gastric cancer cells by silencing tumor suppressor NELL2
According to the tRF&tiRNA PCR array data, we analyzed the differential expression of tRNA fragments and found that six were upregulated and 12 were downregulated in GC tissues compared with noncancerous adjacent tissues (NATs)
Summary
Gastric cancer (GC) is one of the most common human cancers, which is the second leading cause of cancer death worldwide, and its global burden is increasing [1, 2]. Increasing studies have shown that tRFs aren’t products from random degradation. Instead they are producted by specific cleavage of multiple pretRNAs and mature tRNAs by different ribonucleases [8,9,10,11]. Dicer and ANG cleave tRF in Gastric Cancer specific tRNAs and produce shorter tRFs [16]. TRFs can regulate tumor progression by competitive binding of RNA binding proteins [22,23,24]. Another study reported that a specific tRNA-derived small RNA (tsRNA) named LeuCAG 3’ tsRNA binds to mRNAs of ribosomal proteins to enhance efficient translation [27]. Much attention has been paid to these tRNA derivatives for cancer predictor and therapeutic targets [20]
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