Evidence map›Paper›PMID 26743180›Full record

ReviewCell adhesion & migration2016

The tumor microenvironment: An irreplaceable element of tumor budding and epithelial-mesenchymal transition-mediated cancer metastasis.

Hui Li, Fangying Xu, Si Li, Anjing Zhong, Xianwen Meng, Maode Lai

Open access · goldAbstract readReview
In one paragraph

Review in Cell adhesion & migration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% of its field
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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. EMT and cancer: what clinicians should know.Nature reviews. Clinical oncology · 2025
    Review
  6. Article
  7. Article
  8. Significance of Malic Enzyme 1 in Cancer: A Review.Current issues in molecular biology · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
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  15. Review
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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

6 authors at 2 institutions in 1 country.

Hui Lia Department of Pathology , School of Medicine, Zhejiang University , Hangzhou , China.
Fangying Xua Department of Pathology , School of Medicine, Zhejiang University , Hangzhou , China.
Si Lia Department of Pathology , School of Medicine, Zhejiang University , Hangzhou , China.
Anjing Zhonga Department of Pathology , School of Medicine, Zhejiang University , Hangzhou , China.
Xianwen Mengc State Key Laboratory of Plant Physiology and Biochemistry, Department of Bioinformatics, College of Life Sciences, Zhejiang University , Hangzhou , China.
Maode Laia Department of Pathology , School of Medicine, Zhejiang University , Hangzhou , China.
Zhejiang University · CNState Key Laboratory of Plant Physiology and Biochemistry

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor budding occurs at the invasive front of cancer; the tumor cells involved have metastatic and stemness features, indicating a poor prognosis. Tumor budding is partly responsible for cancer metastasis, and its initiation is based on the epithelial-mesenchymal transition (EMT) process. The EMT process involves the conversion of epithelial cells into migratory and invasive cells, and is a profound event in tumorigenesis. The EMT, associated with the formation of cancer stem cells (CSCs) and resistance to therapy, results from a combination of gene mutation, epigenetic regulation, and microenvironmental control. Tumor budding can be taken to represent the EMT in vivo. The EMT process is under the influence of the tumor microenvironment as well as tumor cells themselves. Here, we demonstrate that the tumor microenvironment dominates EMT development and impacts cancer metastasis, as well as promotes CSC formation and mediates drug resistance. In this review, we mainly discuss components of the microenvironment, such as the extracellular matrix (ECM), inflammatory cytokines, metabolic products, and hypoxia, that are involved in and impact on the acquisition of tumor-cell motility and dissemination, the EMT, metastatic tumor-cell formation, tumor budding and CSCs, and cancer metastasis, including subsequent chemo-resistance. From our point of view, the tumor microenvironment now constitutes a promising target for cancer therapy.

Indexed as

Epithelial-Mesenchymal TransitionTumor MicroenvironmentAnimalsExtracellular MatrixHumansInflammationNeoplasm MetastasisNeoplasmscancer metastasisdrug resistanceepithelial-mesenchymal transitionmicroenvironmenttumor budding

Identifiers

PMID26743180
PMCPMC4986710
OpenAlexW2226483342

What OpenQuestion 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 OpenQuestion graph.