Evidence map›Paper›PMID 42373804›Full record

ArticleOncogene2026

LncRNA IRENA promotes peripheral T-cell lymphoma progression through scaffolding ARHGEF1 and FMNL1 to modulate RHOA GTPase/MAPK signaling.

Cong Wang, Ming-Ci Cai, Shu Cheng, Song Hu, Yao-Hui Huang, Liang-Juan Zhao, Yao Qin, Yu-Ran Qiu, Hong-Jing Dou, Ye-Hui Tan and 3 more

Abstract read
In one paragraph

Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Cong Wang *Department of Hematology, The First Hospital of Jilin University, Key Laboratory of Hematology Precision Medicine of Jilin Province, Changchun, China.
Ming-Ci Cai *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shu Cheng *Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Song HuShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yao-Hui HuangShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liang-Juan ZhaoShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yao QinShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yu-Ran QiuShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Hong-Jing DouState Key Laboratory of Metal Matrix Composites, School of Materials Science and Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID http://orcid.org/0000-0001-5850-9174
Ye-Hui TanDepartment of Hematology, The First Hospital of Jilin University, Key Laboratory of Hematology Precision Medicine of Jilin Province, Changchun, China.
Su-Jun GaoDepartment of Hematology, The First Hospital of Jilin University, Key Laboratory of Hematology Precision Medicine of Jilin Province, Changchun, China. sjgao@jlu.edu.cn.ORCID http://orcid.org/0000-0002-1090-5802
Jie XiongShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. xiongjie_sih@163.com.ORCID http://orcid.org/0000-0002-7547-5049
Wei-Li ZhaoShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. zhao.weili@yahoo.com.ORCID http://orcid.org/0000-0002-6834-1616

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82101675National Natural Science Foundation of China (National Science Foundation of China) 82130004National Natural Science Foundation of China (National Science Foundation of China) 82270194
6 · The paper itself

Abstract

Peripheral T-cell lymphoma (PTCL) is a highly heterogeneous group of lymphomas, characterized by aggressive behavior and poor outcomes. Investigating the key regulatory long non-coding RNAs (lncRNAs) is helpful to refine current prognostic models and identify novel therapeutic targets in PTCL. Using clinical and transcriptomic data from 172 patients (training cohort) and 36 patients (validation cohort) with newly diagnosed nodal PTCL, this study identified LINC01727 (also known as IRENA) as an independent prognostic marker associated with poor outcomes. Functional assays demonstrated that IRENA significantly promoted tumor growth and inhibited T-lymphoma cell apoptosis, underscoring its oncogenic role in PTCL. Mechanistically, cytoplasmic IRENA acted as a scaffold, enhancing the interactions between Rho guanine nucleotide exchange factor 1 (ARHGEF1) and Formin-like protein 1 (FMNL1), as well as their binding to RHOA. Multi-omics analysis revealed that the scaffolding activity of IRENA established a positive feedback loop, thereby provoking RHOA/MAPK activation. In the murine cell-derived xenograft model, targeting IRENA with an antisense oligonucleotide (ASO) effectively suppressed T-lymphoma growth. This study identifies IRENA as an independent prognostic biomarker for nodal PTCL patients, revealing its role in the self-organizing activation of RHOA GTPase. Targeting the IRENA/RHOA/MAPK signaling axis by ASO may represent a potential therapeutic strategy for PTCL.

Indexed as

ForminsLymphoma, T-Cell, PeripheralrhoA GTP-Binding ProteinRho Guanine Nucleotide Exchange FactorsRNA, Long NoncodingAnimalsApoptosisBiomarkers, TumorCell Line, TumorCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMaleMAP Kinase Signaling SystemBiomarkers, TumorForminsrhoA GTP-Binding ProteinRHOA protein, humanRho Guanine Nucleotide Exchange FactorsRNA, Long Noncoding

Identifiers

PMID42373804
PMCPMC13407170

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.