Evidence map›Paper›PMID 41290994›Full record

ArticleCancer gene therapy2026

Construction of the cancer cell continuum reveals hybrid EMT state driving lung adenocarcinoma aggression.

Qiuhao Qu, Yixin Ma, Chao Huang, Botao Fa, Zhenni Liu, Yuhan Li, Shigao Yang, Zhengtao Xiao

Abstract read
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In one paragraph

Article in Cancer gene therapy, 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. Review
  2. 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

8 authors.

Qiuhao Qu *School of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.
Yixin Ma *School of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.ORCID 0009-0006-9262-8832
Chao Huang *School of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.
Botao FaSchool of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.ORCID 0009-0009-0973-9366
Zhenni LiuSchool of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.
Yuhan LiSchool of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.
Shigao YangSchool of Life Sciences, Anhui Medical University, Hefei, China. yangshigao@ahmu.edu.cn.ORCID 0000-0003-2717-6914
Zhengtao XiaoSchool of basic medical sciences, institute of molecular and translational medicine, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China. zhengtao.xiao@xjtu.edu.cn.ORCID 0000-0002-5535-5381

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32100535National Natural Science Foundation of China (National Science Foundation of China) 32370706National Natural Science Foundation of China (National Science Foundation of China) 82071837National Natural Science Foundation of China (National Science Foundation of China) 82471798
6 · The paper itself

Abstract

The epithelial-to-mesenchymal transition (EMT) is a pivotal cellular process integral to metastasis. Emerging evidence indicates that EMT progresses through a continuum of cellular states, yet the intricate regulatory mechanisms underpinning this transition are not fully elucidated. This study aims to reconstruct the EMT spectrum in lung adenocarcinoma (LUAD) by integrating single-cell RNA sequencing data with advanced cell trajectory inference techniques. We identified five distinct EMT states across 16,310 malignant epithelial cells derived from 10 LUAD patients, encompassing epithelial, mesenchymal, and hybrid epithelial/mesenchymal (E/M) phenotypes. Notably, the hybrid E/M states exhibited the highest metastatic potential and were correlated with a poorer prognosis for patients. By modeling the EMT regulatory network, we evaluated the influence of transcription factor (TF) activation on network stability during cellular state transitions. We identified critical TFs, including TCF7, FOXA1, FOXA2, and SMAD7, which collectively regulate pathways such as TGF-β through both intrinsic EMT-related signaling and the modulation of tumor-associated macrophages. Furthermore, we developed a risk stratification model based on EMT continuum signatures, providing a novel tool for prognostic assessment. Our findings contribute to a comprehensive understanding of EMT-driven tumor evolution and open new avenues for prognostic stratification and targeted therapies in LUAD.

Indexed as

Adenocarcinoma of LungEpithelial-Mesenchymal TransitionLung NeoplasmsGene Expression Regulation, NeoplasticHumansPrognosis

Identifiers

What Socratic holds

Textmetadata
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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.