Evidence map›Paper›PMID 40176117›Full record

ReviewJournal of translational medicine2025

Epithelial-mesenchymal transition orchestrates tumor microenvironment: current perceptions and challenges.

Yuqi Xie, Xuan Wang, Wenquan Wang, Ning Pu, Liang Liu

Abstract readReview
In one paragraph

Review in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

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  14. Suppression of NGALR impedes TNBC cell survival, proliferation, invasion, and migration through Akt/mTOR and JAK/STAT3 pathway inhibition.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
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  20. Extracellular Vesicles fromNanomaterials (Basel, Switzerland) · 2026
    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

5 authors.

Yuqi XieDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Xuan WangDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Wenquan WangDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Ning PuDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China.
Liang LiuDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, 180 Fenglin Road, Shanghai, 200032, People's Republic of China. liu.liang@zs-hospital.sh.cn.

Funding

Beijing Xisike Clinical Oncology Research Foundation Y-2022METAZQN-0003Beijing Xisike Clinical Oncology Research Foundation Y-Gilead2024-PT-0002Beijing Xisike Clinical Oncology Research Foundation Y-HR2022MS-0251Beijing Xisike Clinical Oncology Research Foundation Y-HR2022QN-0085National Natural Science Foundation of China 82103409National Natural Science Foundation of China 82103417National Natural Science Foundation of China 82272929National Natural Science Foundation of China 82273382National Natural Science Foundation of China 82303443National Natural Science Foundation of China 82473459Program of Shanghai Academic Research Leader 23XD1400600Science and Technology Commission of Shanghai Municipality 24SF1900300Shanghai Municipal Health Commission 201940019Shanghai Municipal Health Commission 20244Y0023Yunnan Provincial Science and Technology Department 202305AF150148
6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) is a critical process in cancer progression, facilitating tumor cells to develop invasive traits and augmenting their migratory capabilities. EMT is primed by tumor microenvironment (TME)-derived signals, whereupon cancer cells undergoing EMT in turn remodel the TME, thereby modulating tumor progression and therapeutic response. This review discusses the mechanisms by which EMT coordinates TME dynamics, including secretion of soluble factors, direct cell contact, release of exosomes and enzymes, as well as metabolic reprogramming. Recent evidence also indicates that cells undergoing EMT may differentiate into cancer-associated fibroblasts, thereby establishing themselves as functional constituents of the TME. Elucidating the relationship between EMT and the TME offers novel perspectives for therapeutic strategies to enhance cancer treatment efficacy. Although EMT-directed therapies present significant therapeutic potential, the current lack of effective targeting approaches-attributable to EMT complexity and its microenvironmental context dependency-underscores the necessity for mechanistic investigations and translational clinical validation.

Indexed as

Epithelial-Mesenchymal TransitionNeoplasmsTumor MicroenvironmentAnimalsHumansEpithelial-mesenchymal transition (EMT)PlasticityTumor microenvironment (TME)Tumor progression

Identifiers

PMID40176117
PMCPMC11963649

What OpenQuestion 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 OpenQuestion graph.