Evidence map›Paper›PMID 39083441›Full record

ReviewThe FEBS journal2025

Therapeutic targeting of TGF-β in lung cancer.

Sajjad Aftabi, Amir Barzegar Behrooz, Marco Cordani, Niloufar Rahiman, Mohammadamin Sadeghdoust, Farnaz Aligolighasemabadi, Stephen Pistorius, Seyedeh Hoda Alavizadeh, Nima Taefehshokr, Saeid Ghavami

Abstract readReview
In one paragraph

Review in The FEBS journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Review
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  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Tumorigenesis and Tumor Microenvironment in Lung Cancer.Current issues in molecular biology · 2026
    Review
  13. Review
  14. Article
  15. Journal of stem cells & regenerative medicine · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

10 authors.

Sajjad AftabiDepartment of Human Anatomy and Cell Science, University of Manitoba College of Medicine, Winnipeg, Canada.
Amir Barzegar BehroozDepartment of Human Anatomy and Cell Science, University of Manitoba College of Medicine, Winnipeg, Canada.
Marco CordaniDepartment of Biochemistry and Molecular Biology, Faculty of Biology, Complutense University, Madrid, Spain.
Niloufar RahimanNanotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Iran.
Mohammadamin SadeghdoustDivision of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St. John's, Canada.
Farnaz AligolighasemabadiDepartment of Human Anatomy and Cell Science, University of Manitoba College of Medicine, Winnipeg, Canada.
Stephen PistoriusDepartment of Human Anatomy and Cell Science, University of Manitoba College of Medicine, Winnipeg, Canada.
Seyedeh Hoda AlavizadehNanotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Iran.
Nima TaefehshokrApoptosis Research Centre, Children's Hospital of Eastern Ontario Research Institute, Ottawa, Canada.
Saeid GhavamiDepartment of Human Anatomy and Cell Science, University of Manitoba College of Medicine, Winnipeg, Canada.ORCID 0000-0001-5948-508X

Funding

European Union NextGenerationEU/PRTRMICIU/AEI RYC2021-031003I
6 · The paper itself

Abstract

Transforming growth factor-β (TGF-β) plays a complex role in lung cancer pathophysiology, initially acting as a tumor suppressor by inhibiting early-stage tumor growth. However, its role evolves in the advanced stages of the disease, where it contributes to tumor progression not by directly promoting cell proliferation but by enhancing epithelial-mesenchymal transition (EMT) and creating a conducive tumor microenvironment. While EMT is typically associated with enhanced migratory and invasive capabilities rather than proliferation per se, TGF-β's influence on this process facilitates the complex dynamics of tumor metastasis. Additionally, TGF-β impacts the tumor microenvironment by interacting with immune cells, a process influenced by genetic and epigenetic changes within tumor cells. This interaction highlights its role in immune evasion and chemoresistance, further complicating lung cancer therapy. This review provides a critical overview of recent findings on TGF-β's involvement in lung cancer, its contribution to chemoresistance, and its modulation of the immune response. Despite the considerable challenges encountered in clinical trials and the development of new treatments targeting the TGF-β pathway, this review highlights the necessity for continued, in-depth investigation into the roles of TGF-β. A deeper comprehension of these roles may lead to novel, targeted therapies for lung cancer. Despite the intricate behavior of TGF-β signaling in tumors and previous challenges, further research could yield innovative treatment strategies.

Indexed as

Lung NeoplasmsTransforming Growth Factor betaAnimalsCell ProliferationDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionHumansMolecular Targeted TherapySignal TransductionTumor MicroenvironmentTransforming Growth Factor betachemoresistanceepithelial–mesenchymal transitionimmunotherapylung cancertransforming growth factor‐β

Identifiers

PMID39083441
PMCPMC11970718

What OpenQuestion 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 OpenQuestion graph.