Evidence map›Paper›PMID 41328768›Full record

ArticleThoracic cancer2025

Fucosyltransferase 8-Derived Circular RNA Drives M2 Polarization of Macrophages Through ENO1-TNF Signaling Axis to Promote Lung Cancer Progression.

Yang Ren, Yidan Shen, Qingguo Wu, Peng Zhang, Lei Wang, Feng Li, Yinzhong Shen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. 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

7 authors.

Yang RenDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0001-5584-8963
Yidan ShenDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Qingguo WuDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Peng ZhangDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Lei WangDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Feng LiDepartment of Respiratory Disease and Critical Care Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Yinzhong ShenDepartment of Infection and Immunity, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.

Funding

Shanghai hospital development center SHDC22024317Shanghai Public Health Clinical Center KY-GW-2021-15
6 · The paper itself

Abstract

backgroundLung cancer, representing a predominant form of pulmonary malignancy, demonstrates significant disease burden and poor clinical outcomes. Circular RNAs (circRNAs) have emerged as critical regulators in various cancers, including lung cancer. However, the specific roles and mechanisms of circRNAs in lung cancer remain largely unexplored.

methodsDifferential circRNA expression was analyzed using GEO datasets GSE101586 and GSE112214. CircFUT8 was prioritized for its upregulation in lung cancer tissues. In vitro and in vivo functional experiments evaluated its effects on cell proliferation, apoptosis, migration, and invasion. RNA pull-down, immunofluorescence, and western blotting assessed interactions with ENO1. Macrophage polarization was examined via cocultures and flow cytometry.

resultsCircFUT8 (hsa_circ_0003028) was significantly upregulated in lung cancer tissues, correlating with advanced stages and poor prognosis. It enhanced lung cancer cell proliferation, migration, and invasion while inhibiting apoptosis in cellular and animal models. Mechanistically, circFUT8 directly binds ENO1 to form an RNA-protein complex, promoting M2 macrophage polarization. Silencing circFUT8 reversed these effects by suppressing ENO1 and M2 polarization, inhibiting tumor progression. Moreover, ENO1 promotes TNF signaling through glycolytic metabolites.

conclusionsOur findings highlight the critical role of circFUT8 in lung cancer progression through its regulation of M2 macrophage polarization via interaction with ENO1. The findings suggest that circFUT8 may serve as both a diagnostic marker and a promising therapeutic target in lung cancer management. This study first identified the regulating oncogenic role of circFUT8 in lung cancer progression and the microenvironment.

Indexed as

DNA-Binding ProteinsFucosyltransferasesLung NeoplasmsMacrophagesPhosphopyruvate HydrataseRNA, CircularTumor Necrosis Factor-alphaTumor Suppressor ProteinsAnimalsApoptosisBiomarkers, TumorCell MovementCell ProliferationDisease ProgressionFemaleHumansBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanFucosyltransferasesPhosphopyruvate HydrataseRNA, CircularTumor Necrosis Factor-alphaTumor Suppressor ProteinscircFUT8ENO1lung cancermacrophages

Identifiers

PMID41328768
PMCPMC12670297

What Socratic holds

Textmetadata
LicenceCC BY
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.