Evidence map›Paper›PMID 41413713›Full record

ArticleOncogene2026

IRF2BPL transcriptionally regulates IGFBP2 to promote tumor progression and suppresses immune cell infiltration in esophageal squamous cell carcinoma.

Yueguang Wu, Heyang Cui, Longlong Wang, Ning Ding, Yongjia Weng, Yikun Cheng, Shanshan Bi, Heng Xiao, Mingwei Gao, Huijuan Liu and 3 more

Abstract read
PubMed Publisher
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. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Yueguang Wu *Cancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Heyang Cui *Department of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, SAR, PR China.
Longlong WangCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.ORCID http://orcid.org/0000-0002-6508-1804
Ning DingCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Yongjia WengCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Yikun ChengCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Shanshan BiCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Heng XiaoKey Laboratory of Cellular Physiology of the Ministry of Education, Department of Pathology, Shanxi Medical University, Taiyuan, Shanxi, PR China.
Mingwei GaoCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Huijuan LiuKey Laboratory of Cellular Physiology of the Ministry of Education, Department of Pathology, Shanxi Medical University, Taiyuan, Shanxi, PR China.
Qiqin SongCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China.
Weimin ZhangInstitute of Cancer Research, Shenzhen Bay Laboratory, Shenzhen, PR China. zhangweimin@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-3348-9813
Yongping CuiCancer Institute, Shenzhen Peking University-the Hong Kong University of Science and Technology (PKU-HKUST) Medical Center, Shenzhen, PR China. cuiyp@sphmc.org.ORCID http://orcid.org/0000-0002-5961-4125

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82103143National Natural Science Foundation of China (National Science Foundation of China) 82203286National Natural Science Foundation of China (National Science Foundation of China) 82302916National Natural Science Foundation of China (National Science Foundation of China) 82341024National Natural Science Foundation of China (National Science Foundation of China) U21A20372
6 · The paper itself

Abstract

Numerous ubiquitination-related proteases (URPs) have been identified as facilitators of disease progression through the disruption of ubiquitination homeostasis in substrate proteins. Notably, some URPs have exhibited non-classical biological functions. In this study, we experimentally elucidate the role of the E3 ubiquitin ligase IRF2BPL as transcriptional activator that promotes malignant phenotypes in esophageal squamous cell carcinoma (ESCC) and inhibits the infiltration of various immune cells within the tumor microenvironment. Specifically, we found that IRF2BPL is highly expressed in ESCC cells and promotes IGFBP2 transcription, thereby facilitating ESCC development both in vivo and in vitro. Moreover, the chemical drug ONC201 was shown to effectively impede ESCC progression induced by the hyperactive IRF2BPL-IGFBP2 axis in tumor cells. Collectively, our findings verified that the IRF2BPL-IGFBP2 axis plays a critical role in enhancing ESCC progression by increasing the malignancy of ESCC cells and fostering an immune-deficient tumor microenvironment. Targeting the IRF2BPL-IGFBP2 axis may represent a promising therapeutic strategy for ESCC.

Indexed as

Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaInsulin-Like Growth Factor Binding Protein 2Ubiquitin-Protein LigasesAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceTumor MicroenvironmentIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2Ubiquitin-Protein LigasesE3 ubiquitin ligaseIGFBP2Immune infiltrationIRF2BPLONC201Transcriptional regulation

Identifiers

What Socratic holds

Textmetadata
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.