Role of tight junctions in the epithelial-to-mesenchymal transition of cancer cells.


Journal

Biochimica et biophysica acta. Biomembranes
ISSN: 1879-2642
Titre abrégé: Biochim Biophys Acta Biomembr
Pays: Netherlands
ID NLM: 101731713

Informations de publication

Date de publication:
01 03 2021
Historique:
received: 28 05 2020
revised: 20 10 2020
accepted: 21 10 2020
pubmed: 16 11 2020
medline: 30 6 2021
entrez: 15 11 2020
Statut: ppublish

Résumé

The epithelial-mesenchymal transition (EMT) is an essential step in cancer progression. Epithelial cells possess several types of cell-cell junctions, and tight junctions are known to play important roles in maintaining the epithelial program. EMT is characterized by a loss of epithelial markers, including E-cadherin and tight junction proteins. Somewhat surprisingly, the evidence is accumulating that upregulated expression of tight junction proteins plays an important role in the EMT of cancer cells. Tight junctions have distinct tissue-specific and cancer-specific regulatory mechanisms, enabling them to play different roles in EMT. Tight junctions and related signaling pathways are attractive targets for cancer treatments; signal transduction inhibitors and monoclonal antibodies for tight junction proteins may be used to suppress EMT, invasion, and metastasis. Here we review the role of bicellular and tricellular tight junction proteins during EMT. Further investigation of regulatory mechanisms of tight junctions during EMT in cancer cells will inform the development of biomarkers for predicting prognosis as well as novel therapies.

Identifiants

pubmed: 33189716
pii: S0005-2736(20)30346-1
doi: 10.1016/j.bbamem.2020.183503
pii:
doi:

Substances chimiques

Biomarkers, Tumor 0

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

183503

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Daisuke Kyuno (D)

Department of Pathology, Sapporo Medical University, Sapporo, Japan; Department of Surgery, Surgical Oncology and Science, Sapporo Medical University, Sapporo, Japan. Electronic address: kyuno@sapmed.ac.jp.

Akira Takasawa (A)

Department of Pathology, Sapporo Medical University, Sapporo, Japan.

Shin Kikuchi (S)

Department of Anatomy, Sapporo Medical University, Sapporo, Japan.

Ichiro Takemasa (I)

Department of Surgery, Surgical Oncology and Science, Sapporo Medical University, Sapporo, Japan.

Makoto Osanai (M)

Department of Pathology, Sapporo Medical University, Sapporo, Japan.

Takashi Kojima (T)

Department of Cell Science, Research Institute for Frontier Medicine, Sapporo Medical University, Sapporo, Japan.

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Classifications MeSH