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Cited by 484

The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.

Role of EMT in Metastasis and Therapy Resistance

Open access
Smith, Bethany, Bhowmick, Neil·2016·Journal of Clinical Medicine

Abstract

Epithelial–mesenchymal transition (EMT) is a complex molecular program that regulates changes in cell morphology and function during embryogenesis and tissue development. EMT also contributes to tumor progression and metastasis. Cells undergoing EMT expand out of and degrade the surrounding microenvironment to subsequently migrate from the primary site. The mesenchymal phenotype observed in fibroblasts is specifically important based on the expression of smooth muscle actin (α-SMA), fibroblast growth factor (FGF), fibroblast-specific protein-1 (FSP1), and collagen to enhance EMT. Although EMT is not completely dependent on EMT regulators such as Snail, Twist, and Zeb-1/-2, analysis of upstream signaling (i.e., TGF-β, EGF, Wnt) is necessary to understand tumor EMT more comprehensively. Tumor epithelial–fibroblast interactions that regulate tumor progression have been identified during prostate cancer. The cellular crosstalk is significant because these events influence therapy response and patient outcome. This review addresses how canonical EMT signals originating from prostate cancer fibroblasts contribute to tumor metastasis and recurrence after therapy.

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Crossref · 10.3390/jcm5020017

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Metadata

Authors
Smith, B., & Bhowmick, N.
Venue
Journal of Clinical Medicine
Publisher
MDPI AG
Published
2016-01-27
Volume
5
Issue
2
Pages
17
ISSN
2077-0383 (ISSN-L)
OpenAlex
W2258531487
Cited by
484
References
10
FWCI
31.68
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Role of EMT in Metastasis and Therapy Resistance. https://app.cochat.ai/papers/10.3390/jcm5020017
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Smith, B., & Bhowmick, N. (2016). Role of EMT in Metastasis and Therapy Resistance. Journal of Clinical Medicine. https://doi.org/10.3390/jcm5020017

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.