ArticleCell death discovery2025
Identification of tRF-29-79MP9P9NH525 as a biomarker and tumor suppressor of gastric cancer via regulating KIF14/AKT pathway.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- tRF-27-87R8WP9N1E5 serves as a prognostic biomarker and tumor suppressor in gastric cancer by targeting the WNT4 pathway via Ago2.Oncogene · 2026Article
- tRF and gastric cancer: molecular mechanism exploration and novel strategies for precision diagnosis and therapy.Journal of translational medicine · 2026Review
- tRF-34-P4R8YP9LON4VHM may serve as a promising potential diagnostic biomarker for hepatocellular carcinoma.Scientific reports · 2026Article
- KIF14 in cancer biology: implications for diagnosis and therapy.Clinical & experimental metastasis · 2026Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
Abstract
Gastric cancer (GC) is one of the most common malignancies with a poor prognosis. The development of novel biomarkers is of utmost importance to screen patients with GC. Molecular mechanism study of GC may provide a research basis for the development of targeted drugs. We identified tRF-29-79MP9P9NH525 (tRF-29) as a GC-associated tRNA-derived fragment (tRF). The specific hair-pin structure reverse primer and amplification primers were first designed and then applied for tRF-29 quantification. Receiver operator characteristic curve, Kaplan-Meier survival curve, and multivariate Cox analysis were applied to analyze the diagnostic and prognostic values of tRF-29 in GC. Ethynyl-2'-deoxyuridine, cell cloning, Transwell assay, and flow cytometry were used to detect the effects of tRF-29 on proliferation, migration, and cell cycle distribution of GC cells. Xenograft tumor formation in NOD-SCID mice was applied in determining tRF-29's effects on tumor growth. Fluorescence in situ hybridization, dual luciferase reporter assay, Western blot, immunohistochemistry, and RNA-binding protein immunoprecipitation were conducted to explore the molecular mechanism underlying tRF-29 regulating GC development. It was found that tissue tRF-29 showed effective diagnostic efficiency in GC and could discriminate different gastric mucosa. Besides, plasma tRF-29 improved GC diagnostic values of common tumor markers and had prognostic values in GC. tRF-29 was found to suppress proliferation and cell cycle progression. tRF-29 inhibited the growth of xenograft tumors. Mechanically, tRF-29 exerted Kinesin family member 14 (KIF14) mRNA destabilization by combining with argonaute 2 (Ago2) and regulated AKT/P27 pathway. In conclusion, tRF-29 inhibited GC progression by combining with Ago2 and regulated AKT/P27 pathway by silencing KIF14 expression. In normal cells, tRF-29, derived from tRNA-ValACC, targets the 3'UTR region of KIF14 mRNA by forming RNA silencing complex with Ago2. Reduced KIF14 results in less phospholation of AKT. Subsequently, the expression of P27 is increased, while the expression of MMP-2 is decreased. Finally, the cell cycle is arrested, and the cell proliferation is suppressed, as well as the metastasis is inhibited. In gastric cancer cells, due to the downregulated of tRF-29, the expression of KIF14 is increased, thus the cell proliferation and metastasis are promoted via AKT pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.