Evidence mapPaperPMID 39623377Full record

ReviewCell communication and signaling : CCS2024

The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.

Mahsa Liaghat, Saeid Ferdousmakan, Seyedeh Haniyeh Mortazavi, Sheida Yahyazadeh, Asrin Irani, Sara Banihashemi, Fatemeh Sadat Seyedi Asl, Abdullatif Akbari, Farnoosh Farzam, Fatemeh Aziziyan and 4 more

Abstract readReview
In one paragraph

Review in Cell communication and signaling : CCS, 2024. 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.

  1. Epithelial-mesenchymal transition and cancer-associated fibroblasts in tumor progression and therapy resistance: mechanistic convergence and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
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  3. International journal of molecular sciences · 2026
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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

14 authors.

Mahsa Liaghat *Department of Medical Laboratory Sciences, Faculty of Medical Sciences, Kazerun Branch, Islamic Azad University, Kazerun, Iran.
Saeid Ferdousmakan *Department of Pharmacy Practice, Nargund College of Pharmacy, Bangalore, 560085, India.
Seyedeh Haniyeh MortazaviNeurosurgery Department of Shiraz University of Medical Sciences, Shiraz, Iran.
Sheida YahyazadehDepartment of Immunology, Faculty of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Asrin IraniDepartment of Biology, Faculty of Basic Sciences, University of Guilan, Rasht, Iran.
Sara BanihashemiDepartment of Bioscience, School of Science and Technology, Nottingham Trent University, Nottingham, UK.
Fatemeh Sadat Seyedi AslMedical School, Tehran University of Medical Sciences, Tehran, Iran.
Abdullatif AkbariNetwork of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran.
Farnoosh FarzamDepartment of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Fatemeh AziziyanNetwork of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran.
Maryam BakhtiyariNetwork of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran.
Mohammad Javad ArghavaniDepartment of Medical Biotechnology, School of Advanced Technologies in Medicine, Fasa University of Medical Sciences, Fasa, Iran.
Hamidreza ZalpoorNetwork of Immunity in Infection, Malignancy & Autoimmunity (NIIMA), Universal Scientific Education & Research Network (USERN), Tehran, Iran. hamidreza.zlpr1998@gmail.com.ORCID http://orcid.org/0000-0002-8057-2804
Mohsen Nabi-AfjadiDepartment of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran. mohsen.nabiafjadi@modares.ac.ir.ORCID http://orcid.org/0000-0001-8243-1530

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intricate cellular process, known as the epithelial-mesenchymal transition (EMT), significantly influences solid tumors development. Changes in cell shape, metabolism, and gene expression linked to EMT facilitate tumor cell invasion, metastasis, drug resistance, and recurrence. So, a better understanding of the intricate processes underlying EMT and its role in tumor growth may lead to the development of novel therapeutic approaches for the treatment of solid tumors. This review article focuses on the signals that promote EMT and metabolism, the intracellular signaling pathways leading to EMT, and the network of interactions between EMT and cancer cell metabolism. Furthermore, the functions of EMT in treatment resistance, recurrence, and metastasis of solid cancers are covered. Lastly, treatment approaches that focus on intracellular signaling networks and metabolic alterations brought on by EMT will be discussed.

Indexed as

Drug Resistance, NeoplasmEpithelial-Mesenchymal TransitionNeoplasm MetastasisNeoplasmsSignal TransductionAnimalsHumansNeoplasm Recurrence, LocalChemotherapy resistanceEMTMetabolic profileMetastasisSolid tumorsTumor recurrence

Identifiers

PMID39623377
PMCPMC11610171

What Socratic 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 Socratic graph.