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Updated: Jul 1, 2025
Detection of a Circulating MicroRNA Custom Panel in Patients with Metastatic Colorectal Cancer
Published on: March 14, 2019
The tsRNAs (tRFdb-3013a/b) serve as novel biomarkers for colon adenocarcinomas
Lihong Tan1, Xiaoling Wu1, Zhurong Tang2
1Chongqing Medical and Pharmaceutical College, Chongqing 401331, China.
Abstract:
The tsRNAs (tRNA-derived small RNAs) are a novel class of small non-coding RNAs derived from transfer-RNAs. Colon adenocarcinoma (COAD) is the most malignant intestinal tumor. This study focused on the identification and characterization of tsRNA biomarkers in colon adenocarcinomas. Data processing and bioinformatic analyses were performed with the packages of R and Python software. The cell proliferation, migration and invasion abilities were determined by CCK-8 and transwell assays. Luciferase reporter assay was used to test the binding of tsRNA with its target genes. With computational methods, we identified the tRNA fragments profiles within COAD datasets, and discriminated forty-two differentially expressed tsRNAs between paired colon adenocarcinomas and non-tumor controls. Among the fragments derived from the 3' end of tRNA-His-GUG (a histidyl-transfer-RNA), tRFdb-3013a and tRFdb-3013b (tRFdb-3013a/b) were notably decreased in colon and rectum adenocarcinomas, especially, tRFdb-3013a/b might tend to be down-regulated in patients with lymphatic or vascular invasion present. The clinical survival of colorectal adenocarcinoma patients with low tRFdb-3013a/b expression was significantly worse than that of high expression patients. In colon adenocarcinoma cells, tRFdb-3013a could have inhibited cell proliferations, and reduced cell migration and invasion abilities. The enrichment analyses showed that most of tRFdb-3013a correlated-genes were enriched in the extracellular matrix associated GO terms, phagosome pathway, and a GSEA molecular signature pathway. Additionally, the 3'UTR of ST3GAL1 mRNA was predicted to contain the binding site of tRFdb-3013a/b, tRFdb-3013a/b might directly target and regulate ST3GAL1 expression in colon adenocarcinomas. These results suggested that tRFdb-3013a/b might serve as novel biomarkers for diagnosis and prognosis of colon adenocarcinomas, and act a key player in the progression of colon adenocarcinomas.
Insights
Novel tRNA-derived small RNAs (tsRNAs) were identified as potential biomarkers for colon adenocarcinoma (COAD). Specifically, decreased tRFdb-3013a/b expression correlates with worse prognosis and inhibited tumor progression in COAD patients.
Area of Science:
- Molecular Biology
- Oncology
- Bioinformatics
Background:
- Colon adenocarcinoma (COAD) is a major cause of cancer mortality.
- tRNA-derived small RNAs (tsRNAs) are emerging as critical regulators in various cancers.
- The role of tsRNAs in COAD pathogenesis remains largely unexplored.
Purpose of the Study:
- To identify and characterize tsRNA biomarkers for colon adenocarcinoma.
- To investigate the functional role of specific tsRNAs in COAD progression.
- To explore the potential of tsRNAs as diagnostic and prognostic indicators for COAD.
Main Methods:
- Bioinformatic analysis of COAD datasets using R and Python.
- Experimental validation of cell proliferation, migration, and invasion using CCK-8 and transwell assays.
- Luciferase reporter assays to confirm tsRNA-target gene interactions.
Main Results:
- Forty-two differentially expressed tsRNAs were identified between COAD and non-tumor tissues.
- tRFdb-3013a/b, derived from tRNA-His-GUG, were significantly decreased in COAD, particularly with advanced invasion.
- Lower tRFdb-3013a/b expression correlated with poorer patient survival and inhibited COAD cell proliferation, migration, and invasion.
- tRFdb-3013a/b potentially targets ST3GAL1 mRNA, regulating its expression in COAD.
Conclusions:
- tRFdb-3013a/b show promise as novel biomarkers for COAD diagnosis and prognosis.
- These tsRNAs may play a crucial role in the progression of colon adenocarcinomas.
- Targeting tRFdb-3013a/b could offer new therapeutic strategies for COAD.
