The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Epithelial–mesenchymal transition (EMT) is an essential process in normal embryonic development and tissue regeneration. However, aberrant reactivation of EMT is associated with malignant properties of tumor cells during cancer progression and metastasis, including promoted migration and invasiveness, increased tumor stemness, and enhanced resistance to chemotherapy and immunotherapy. EMT is tightly regulated by a complex network which is orchestrated with several intrinsic and extrinsic factors, including multiple transcription factors, post-translational control, epigenetic modifications, and noncoding RNA-mediated regulation. In this review, we described the molecular mechanisms, signaling pathways, and the stages of tumorigenesis involved in the EMT process and discussed the dynamic non-binary process of EMT and its role in tumor metastasis. Finally, we summarized the challenges of chemotherapy and immunotherapy in EMT and proposed strategies for tumor therapy targeting EMT.

Related collections

Most cited references 310

Record: found
Abstract: found
Article: not found

Epithelial-mesenchymal transitions in development and disease.

Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)

The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.

0 comments Cited 3759 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Molecular mechanisms of epithelial-mesenchymal transition.

Samy Lamouille, Jian Xu, Rik Derynck (2014)

The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which are finely regulated at the transcriptional, translational and post-translational levels. The reprogramming of gene expression during EMT, as well as non-transcriptional changes, are initiated and controlled by signalling pathways that respond to extracellular cues. Among these, transforming growth factor-β (TGFβ) family signalling has a predominant role; however, the convergence of signalling pathways is essential for EMT.

0 comments Cited 1730 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The basics of epithelial-mesenchymal transition.

Raghu Kalluri, Robert Weinberg (2009)

The origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions.

0 comments Cited 1426 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Xiawei Wei: xiaweiwei@scu.edu.cn

Journal

Journal ID (nlm-ta): J Hematol Oncol

Journal ID (iso-abbrev): J Hematol Oncol

Title: Journal of Hematology & Oncology

Publisher: BioMed Central (London )

ISSN (Electronic): 1756-8722

Publication date (Electronic): 8 September 2022

Publication date PMC-release: 8 September 2022

Publication date Collection: 2022

Volume: 15

Electronic Location Identifier: 129

Affiliations

GRID grid.13291.38, ISNI 0000 0001 0807 1581, Laboratory of Aging Research and Cancer Drug Target, State Key Laboratory of Biotherapy, National Clinical Research Center for Geriatrics, West China Hospital, , Sichuan University, ; Chengdu, China

Article

Publisher ID: 1347

DOI: 10.1186/s13045-022-01347-8

PMC ID: 9461252

PubMed ID: 36076302

SO-VID: e6b395fc-16dc-4f69-9a82-47d6e51302b0

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 6 May 2022

Date accepted : 30 August 2022

Funding

Funded by: National Science Foundation for Excellent Young Scholars

Award ID: 32122052

Award Recipient : Xiawei Wei

Funded by: National Natural Science Foundation Regional Innovation and Development

Award ID: U19A2003

Award Recipient : Xiawei Wei

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: epithelial–mesenchymal transition,metastasis,tumor stemness,circulating tumor cells

Data availability:

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: epithelial–mesenchymal transition, metastasis, tumor stemness, circulating tumor cells

The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis

Read this article at

Abstract

Related collections

Karger: Oncology

Most cited references 310

Epithelial-mesenchymal transitions in development and disease.

Molecular mechanisms of epithelial-mesenchymal transition.

The basics of epithelial-mesenchymal transition.

Author and article information

Contributors

Journal

Affiliations

Article

History

Funding

Categories

Custom metadata

Comments

Comment on this article

Similar content 301

Cited by 138

Most referenced authors 4,261