Plasticity of cancer cell invasion: Patterns and mechanisms

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Abstract

Cancer cell migration and invasion are integral components of metastatic disease, which is the major cause of death in cancer patients. Cancer cells can disseminate and migrate via several alternative mechanisms including amoeboid cell migration, mesenchymal cell migration, and collective cell migration. These diverse movement strategies display certain specific and distinct hallmarks in cell-cell junctions, actin cytoskeleton, matrix adhesion, and protease activity. During tumor progression, cells pass through complex microenvironments and adapt their migration strategies by reversible mesenchymal-amoeboid and individual-collective transitions. This plasticity in motility patterns enables cancer cells disseminate further and thus limit the efficiency of anti-metastasis therapies. In this review, we discuss the modes and mechanisms of cancer cell migration and focus on the plasticity of tumor cell movement as well as potential emerging therapeutic options for reducing cancer cell invasion.

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Highlights

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Cancer cells can disseminate via amoeboid cell migration, mesenchymal cell migration or collective cell migration.
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Tumor microenvironment and certain therapeutic challenge can trigger the transitions of migration patterns.
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Plasticity of cancer cells migration limit efficiency of anti-metastasis therapies.
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Combination therapy targeting different migration is a promising anti-metastasis therapy.

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Most cited references 91

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Initial steps of metastasis: Cell invasion and endothelial transmigration

Franziska van Zijl, Georg Krupitza, Wolfgang Mikulits (2011)

Metastasis is the leading cause of cancer mortality. The metastatic cascade represents a multi-step process which includes local tumor cell invasion, entry into the vasculature followed by the exit of carcinoma cells from the circulation and colonization at the distal sites. At the earliest stage of successful cancer cell dissemination, the primary cancer adapts the secondary site of tumor colonization involving the tumor–stroma crosstalk. The migration and plasticity of cancer cells as well as the surrounding environment such as stromal and endothelial cells are mandatory. Consequently, the mechanisms of cell movement are of utmost relevance for targeted intervention of which three different types have been reported. Tumor cells can migrate either collectively, in a mesenchymal or in an amoeboid type of movement and intravasate the blood or lymph vasculature. Intravasation by the interaction of tumor cells with the vascular endothelium is mechanistically poorly understood. Changes in the epithelial plasticity enable carcinoma cells to switch between these types of motility. The types of migration may change depending on the intervention thereby increasing the velocity and aggressiveness of invading cancer cells. Interference with collective or mesenchymal cell invasion by targeting integrin expression or metalloproteinase activity, respectively, resulted in an amoeboid cell phenotype as the ultimate exit strategy of cancer cells. There are little mechanistic details reported in vivo showing that the amoeboid behavior can be either reversed or efficiently inhibited. Future concepts of metastasis intervention must simultaneously address the collective, mesenchymal and amoeboid mechanisms of cell invasion in order to advance in anti-metastatic strategies as these different types of movement can coexist and cooperate. Beyond the targeting of cell movements, the adhesion of cancer cells to the stroma in heterotypic circulating tumor cell emboli is of paramount relevance for anti-metastatic therapy.

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Cancer invasion and the microenvironment: plasticity and reciprocity.

Peter Friedl, Stephanie Alexander (2011)

Cancer invasion is a cell- and tissue-driven process for which the physical, cellular, and molecular determinants adapt and react throughout the progression of the disease. Cancer invasion is initiated and maintained by signaling pathways that control cytoskeletal dynamics in tumor cells and the turnover of cell-matrix and cell-cell junctions, followed by cell migration into the adjacent tissue. Here, we describe the cell-matrix and cell-cell adhesion, protease, and cytokine systems that underlie tissue invasion by cancer cells. We explain how the reciprocal reprogramming of both the tumor cells and the surrounding tissue structures not only guides invasion, but also generates diverse modes of dissemination. The resulting "plasticity" contributes to the generation of diverse cancer invasion routes and programs, enhanced tumor heterogeneity, and ultimately sustained metastatic dissemination. Copyright © 2011 Elsevier Inc. All rights reserved.

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Fibroblast-led collective invasion of carcinoma cells with differing roles for RhoGTPases in leading and following cells.

Cédric Gaggioli, Steven Hooper, Cristina Hidalgo-Carcedo … (2007)

Imaging of collectively invading cocultures of carcinoma cells and stromal fibroblasts reveals that the leading cell is always a fibroblast and that carcinoma cells move within tracks in the extracellular matrix behind the fibroblast. The generation of these tracks by fibroblasts is sufficient to enable the collective invasion of the squamous cell carcinoma (SCC) cells and requires both protease- and force-mediated matrix remodelling. Force-mediated matrix remodelling depends on integrins alpha3 and alpha5, and Rho-mediated regulation of myosin light chain (MLC) activity in fibroblasts, but these factors are not required in carcinoma cells. Instead, carcinoma cells use Cdc42 and MRCK (myotonic dystrophy kinase-related CDC42-binding protein kinases) mediated regulation of MLC to follow the tracks generated by fibroblasts.

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Author and article information

Contributors

Ya-ling Tang

Xin-hua Liang

Journal

Journal ID (nlm-ta): Transl Oncol

Journal ID (iso-abbrev): Transl Oncol

Title: Translational Oncology

Publisher: Neoplasia Press

ISSN (Electronic): 1936-5233

Publication date PMC-release: 17 October 2020

Publication date Collection: January 2021

Publication date (Electronic): 17 October 2020

Volume: 14

Issue: 1

Electronic Location Identifier: 100899

Affiliations

[a ]State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China

[b ]Department of Head and Neck Surgery, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan, China

Author notes

[* ]Corresponding authors at: State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology (Sichuan University), Chengdu, Sichuan 610041, China. tangyaling@ 123456scu.edu.cn lxh88866@ 123456scu.edu.cn

[1]

These authors contributed equally to this work.

[2]

Post address: State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology (Sichuan University), Chengdu Sichuan 610041, China.

[3]

Post address: Department of Head and Neck Surgery, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610041, China.

Article

Publisher Item ID: S1936-5233(20)30391-0 Publisher ID: 100899

DOI: 10.1016/j.tranon.2020.100899

PMC ID: 7573380

PubMed ID: 33080522

SO-VID: 48361c48-6726-450c-85b6-75852e51e321

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

Plasticity of cancer cell invasion: Patterns and mechanisms

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Abstract

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Cancer Immunotherapy

Most cited references 91

Initial steps of metastasis: Cell invasion and endothelial transmigration

Cancer invasion and the microenvironment: plasticity and reciprocity.

Fibroblast-led collective invasion of carcinoma cells with differing roles for RhoGTPases in leading and following cells.

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