Evidence map›Paper›PMID 35442152›Full record

ArticleBioengineered2022

The biological behavior of tRNA-derived fragment tRF-Leu-AAG in pancreatic cancer cells.

Shizhen Sui, Zhihuai Wang, Xiaohan Cui, Lei Jin, Chunfu Zhu

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The Roles of tRNA-Derived Fragments in Cancer: Updates and Perspectives.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Emerging roles of tRNA-derived small RNAs in cancer biology.Experimental & molecular medicine · 2023
    Review
  15. tRNA-derived fragments (tRFs) in cancer.Journal of cell communication and signaling · 2023
    Review
  16. Review
  17. Article
  18. Inhibition of tiRNA-Gly-GCC ameliorates neointimal formationFrontiers in cardiovascular medicine · 2023
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Shizhen SuiGraduate School of Dalian Medical University, Dalian Medical University, Dalian, Liaoning, China.
Zhihuai WangGraduate School of Dalian Medical University, Dalian Medical University, Dalian, Liaoning, China.
Xiaohan CuiDepartment of Hepatobiliary Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Lei JinDepartment of Hepatobiliary Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Chunfu ZhuDepartment of Hepatobiliary Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Dalian Medical University · CNNanjing Medical University · CNChangzhou No.2 People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer (PC) is a life-threatening cancer with increasing incidence in developed countries. Reports indicate that tRNA-derived fragments (tRFs) are possible therapeutic targets and biomarkers for cancer treatment. Nonetheless, the effect of tRF-Leu-AAG on PC is unclear. This study aims to explore the role of tRF-Leu-AAG and upstream frameshift mutant 1 (UPF1) in the development of PC and its potential underlying mechanisms. High-throughput second-generation sequencing techniques were used to detect the expression of tRFs in cancerous and adjacent normal tissues from PC patients. The role of tRF-Leu-AAG proliferation in PC cells was investigated via the Cell Counting Kit-8 (CCK8) assay. The effect of tRF-Leu-AAG on the invasion and migration ability of PC cells was also determined by the transwell assay. Thereafter, the downstream target genes of tRF-Leu-AAG were comprehensively predicted using bioinformatics analysis databases. We also used the Dual-Luciferase Reporter assay to assess the nexus between tRF-Leu-AAG and UPF1. Eventually, Western Blot was used to validate the expression of UPF1 in PC cells. A total of 33 tRF expressions significantly varied from PC patients. RT-qPCR confirmed that the expression of tRF-Leu-AAG was observably up-regulated in PC cells as compared to the control cells. Importantly, knockdown of tRF-Leu-AAG observably inhibited cell proliferation, migration, and invasion. Furthermore, according to the predicted frameshift database results, the UPF1 acted as downstream target genes for tRF-Leu-AAG and significantly down-regulated UPF1 expression.

Indexed as

Pancreatic NeoplasmsRNA, Transfer, LeuCell ProliferationHigh-Throughput Nucleotide SequencingHumansReal-Time Polymerase Chain ReactionRNA HelicasesTrans-ActivatorsRNA HelicasesRNA, Transfer, LeuTrans-ActivatorsUPF1 protein, humanPancreatic cancertRNA-derived fragmentsUPF1

Identifiers

PMID35442152
PMCPMC9161985
OpenAlexW4224252969

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Registered trials

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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.