Evidence map›Paper›PMID 41937164›Full record

ArticleCellular & molecular biology letters2026

A tRNA-derived fragment tRF3019a promotes LUAD metastasis by stabilizing hnRNPK and enhancing MYH11 expression.

Xin Li, Weifang Cui, Zhangjie Wang, Danyao Chen, Zhenyu Kuang, Junjie Jiang, Yuwei Lai, Xiongzhou Zhang, Chaojun Duan, Chunfang Zhang and 1 more

Abstract read
In one paragraph

Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
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1 · What the graph read from it

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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.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Xin LiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Weifang CuiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhangjie WangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Danyao ChenDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Zhenyu KuangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Junjie JiangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Yuwei LaiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Xiongzhou ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China.
Chaojun DuanDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. duancjxy@csu.edu.cn.
Chunfang ZhangDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. zhcf3801@csu.edu.cn.
Xizhe LiDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, 410008, Hunan, China. lixizhe@csu.edu.cn.

Funding

National Multidisciplinary Cooperative Diagnosis and Treatment Capacity Building Project for Major Diseases (Lung Cancer) of China No. z027002National Natural Science Foundation of China No. 82172655National Natural Science Foundation of China No. 82203833National Natural Science Foundation of China No. 82372935
6 · The paper itself

Abstract

backgroundtRNA-derived fragments (tRFs) have been shown to play important regulatory roles in cancer biology. However, the impact of tRFs on lung adenocarcinoma (LUAD) remains largely unexplored.

methodsThe differential expression of tRF3019a, a tRNA fragment derived from tRNA-Ala (AGC), was identified through database mining and subsequently validated by quantitative reverse transcription PCR (qRT–PCR) in pathological tissues obtained from 100 patients with LUAD. The role of tRF3019a in LUAD metastasis was assessed through both in vitro and in vivo experiments. A comprehensive investigation of its regulatory function involved RNA pulldown assays, mass spectrometry, RNA immunoprecipitation (RIP), western blotting, chromatin immunoprecipitation (ChIP), co-immunoprecipitation (Co-IP), and rescue assays.

resultstRF3019a expression was significantly elevated in LUAD tumor tissues and was associated with advanced disease stage and metastatic progression. Higher tRF3019a expression correlated with shorter overall survival and disease-free survival. Functionally, tRF3019a enhanced LUAD cell migration and invasion both in vitro and in vivo. Mechanistically, tRF3019a interacted with heterogeneous nuclear ribonucleoprotein K (hnRNPK) and inhibited its ubiquitin-mediated proteasomal degradation, leading to increased hnRNPK protein stability. This was accompanied by changes in epithelial–mesenchymal transition (EMT)-associated markers, including increased N-cadherin and vimentin and decreased E-cadherin. Furthermore, tRF3019a enhanced hnRNPK-associated transcriptional regulation of the myosin heavy chain 11 (MYH11) gene, contributing to the pro-metastatic phenotype of LUAD cells.

conclusionstRF3019a promotes LUAD progression and metastasis by stabilizing hnRNPK and enhancing hnRNPK-associated transcriptional regulation of MYH11. These findings identify a previously unrecognized tRF3019a–hnRNPK–MYH11 regulatory axis involved in LUAD metastasis.

Indexed as

Adenocarcinoma of LungHeterogeneous-Nuclear Ribonucleoprotein KLung NeoplasmsMyosin Heavy ChainsRNA, TransferAnimalsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansMaleMiceMice, NudeMiddle AgedHeterogeneous-Nuclear Ribonucleoprotein KHNRNPK protein, humanMyosin Heavy ChainsRNA, TransferhnRNPKLUADMYH11tRNA-derived fragmentsUbiquitination

Identifiers

PMID41937164
PMCPMC13277126

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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.