Evidence map›Paper›PMID 40056302›Full record

ArticleDigestive diseases and sciences2025

tRF-Pro-CGG Suppresses Cell Proliferation and Promotes Apoptosis in Pancreatic Cancer.

Jikuan Zhu, Xudong Zhang, Tianping Luo, Cailin Xue, Jiadeng Chao, Jun Li, Bei Zhu, Lei Jin, Chunfu Zhu, Xihu Qin

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Article in Digestive diseases and sciences, 2025. 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
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Jikuan ZhuGraduate School of Dalian Medical University, Dalian Medical University, Dalian, 116044, Liaoning Province, China.
Xudong ZhangDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Tianping LuoDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Cailin XueDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Jiadeng ChaoDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Jun LiDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Bei ZhuDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Lei JinDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China. jinlei8016@163.com.
Chunfu ZhuDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.
Xihu QinDepartment of Hepato-Biliary-Pancreatic Surgery, The Affiliated Changzhou No.2 People'S Hospital of Nanjing Medical University, Changzhou, 213003, Jiangsu, China.

Funding

Changzhou Health Commission ZD202023Changzhou Medical Innovation Team CCX201807
6 · The paper itself

Abstract

objectiveThis study aimed to investigate the role of tRNA-derived RNA fragment tRF-Pro-CGG in pancreatic cancer (PC), focusing on its expression levels in PC tissues and cell lines, and its effects on cell proliferation, clonality, migration, invasion, and apoptosis. Additionally, the study explored the potential of tRF-Pro-CGG as a diagnostic biomarker and therapeutic target in PC.

methodsThe expression levels of tRF-Pro-CGG in PC tissues and cell lines were analyzed using next-generation sequencing and quantitative real-time PCR (qRT-PCR). Functional assays, including cell proliferation (CCK-8), colony formation, migration (Transwell), invasion (Matrigel), and apoptosis (flow cytometry), were conducted on PC cell lines (SW1990 and PANC-1) transfected with tRF-Pro-CGG mimic or inhibitor. Dual luciferase reporter assays and Western blotting were used to identify and validate the target gene of tRF-Pro-CGG, CSF1, and its involvement in the PI3K-AKT signaling pathway.

resultstRF-Pro-CGG was significantly downregulated in PC tissues and cell lines compared to normal tissues and cells. Overexpression of tRF-Pro-CGG in SW1990 cells inhibited cell proliferation, clonality, migration, and invasion, while promoting apoptosis. Conversely, inhibition of tRF-Pro-CGG in PANC-1 cells had the opposite effects. Dual luciferase assays confirmed CSF1 as a direct target of tRF-Pro-CGG, and Western blot analysis showed that tRF-Pro-CGG negatively regulated CSF1 expression. Furthermore, tRF-Pro-CGG was found to modulate the PI3K-AKT signaling pathway, with downstream effects on key molecules such as AKT, P-AKT, and PTEN.

conclusiontRF-Pro-CGG acts as a tumor suppressor in pancreatic cancer by inhibiting cell proliferation, migration, invasion, and promoting apoptosis, likely through targeting CSF1 and regulating the PI3K-AKT signaling pathway. These findings suggest that tRF-Pro-CGG could serve as a potential diagnostic biomarker and therapeutic target for pancreatic cancer.

Indexed as

ApoptosisCell ProliferationPancreatic NeoplasmsCell Line, TumorCell MovementFemaleGene Expression Regulation, NeoplasticHumansMaleProto-Oncogene Proteins c-aktSignal TransductionProto-Oncogene Proteins c-aktApoptosisClonalityCSF1Diagnostic biomarkerInvasionMigrationPancreatic cancerProliferationTRF-pro-CGG

Identifiers

PMID40056302

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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.