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Cells
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Cell Migration and Invasion
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Cell Migration and Invasion

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 30 June 2026 | Viewed by 12313

Special Issue Editor

Dr. Veronika Miskolci

E-Mail Website1 Website2
Guest Editor
1. Department of Microbiology, Biochemistry and Molecular Genetics, New Jersey Medical School, Rutgers Health, Rutgers University, Newark, NJ, USA
2. Center for Cell Signaling, Rutgers Health, Rutgers University, Newark, NJ, USA
3. Center for Immunity and Inflammation, Rutgers Health, Rutgers University, Newark, NJ, USA
Interests: innate immunity; immunometabolism; cell migration; biosensors; FLIM

Special Issue Information

Dear Colleagues,

This Special Issue, "Cell Migration and Invasion", aims to explore the intricate mechanisms and regulatory pathways that govern these critical cellular processes within the broader context of cell biology. Cell migration and invasion play pivotal roles in various physiological and pathological conditions, including embryonic development, wound healing, and cancer metastasis. This issue will feature cutting-edge research on the molecular and cellular factors that drive cell motility, the role of the extracellular matrix and microenvironment, and the interplay between different signaling pathways.

Contributions will cover a wide range of topics, including the role of the cytoskeleton, cell adhesion, and innovative imaging techniques. Additionally, this issue will highlight novel therapeutic strategies and diagnostic tools for targeting cell migration and invasion in various diseases. By bringing together a diverse range of studies, this Special Issue will provide a comprehensive overview of the current state of knowledge and future directions in the field.

Dr. Veronika Miskolci
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cell migration
  • cell invasion
  • cancer metastasis
  • molecular mechanisms
  • therapeutic strategies
  • signaling pathways

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Published Papers (7 papers)

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Research

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20 pages, 5056 KB  
Article
A New Single-Chain, Genetically Encoded Biosensor for RhoB GTPase Based on FRET, Useful for Live-Cell Imaging
by Sandra Pagano and Louis Hodgson
Cells 2026, 15(4), 347; https://doi.org/10.3390/cells15040347 - 14 Feb 2026
Viewed by 738
Abstract
RhoB is an atypical Rho GTPase whose function is tightly linked to its subcellular localization and membrane trafficking, reflecting its unique post-translational modifications and association with endosomal membranes in addition to the plasma membrane. Despite its implication in membrane trafficking and cytoskeletal regulation, [...] Read more.
RhoB is an atypical Rho GTPase whose function is tightly linked to its subcellular localization and membrane trafficking, reflecting its unique post-translational modifications and association with endosomal membranes in addition to the plasma membrane. Despite its implication in membrane trafficking and cytoskeletal regulation, tools to directly monitor RhoB activity in space and time have been lacking. Here, we describe the development and validation of a single-chain, genetically encoded Förster resonance energy transfer (FRET) biosensor that enables direct visualization of RhoB activity in living cells while preserving its native membrane-targeting determinants. The biosensor exhibits a large dynamic range and resolves spatially heterogeneous RhoB activity during leading-edge protrusion–retraction cycles in migrating mouse embryonic fibroblasts. To demonstrate the utility of this tool, we performed multiplex live-cell imaging with a previously developed near-infrared FRET biosensor for the exocytic Rho GTPase TC10. Quantitative morphodynamic and cross-correlation analyses reveal coordinated yet antagonistic spatiotemporal patterns of RhoB and TC10 activities at the leading edge and show that perturbation of TC10 regulation reorganizes their spatial coupling. Together, this work introduces a robust biosensor for RhoB and establishes a multiplex imaging framework to study the coordination of trafficking and signaling during cell migration. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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20 pages, 10775 KB  
Article
Targeting Lung Cancer Cell Motility Using Microbeam Radiation Therapy
by Ömer Dağkazanlı, Aleksandra Čolić, Rainer Lindner, Stefan Bartzsch, Stephanie E. Combs, Thomas E. Schmid and Marina Santiago Franco
Cells 2026, 15(2), 107; https://doi.org/10.3390/cells15020107 - 7 Jan 2026
Viewed by 958
Abstract
Radiotherapy (RT) is currently among the standard treatments for lung cancer. However, in vitro studies have revealed that irradiation can increase lung cancer cell motility. This way, RT could potentially enhance the malignancy of solid tumors post-treatment, promoting metastasis. Therefore, there is a [...] Read more.
Radiotherapy (RT) is currently among the standard treatments for lung cancer. However, in vitro studies have revealed that irradiation can increase lung cancer cell motility. This way, RT could potentially enhance the malignancy of solid tumors post-treatment, promoting metastasis. Therefore, there is a continued need to continue evolving RT modalities into safer and more effective treatments. The present study compares the impact of the broad beam (BB) and the spatially fractionated modality of microbeam radiation therapy (MRT) on the motility of A549 lung cancer cells. Our data corroborates previous findings that showed BB irradiation is a promoter of cell motility. For MRT, however, we observed a prevention of cellular migration. A significant reduction in NF-κB expression was observed only when A549 cells were irradiated with MRT, indicating a potential mechanism behind these findings. Finally, our data supports potential issues regarding MRT irradiation of key components of the tumor microenvironment, such as fibroblasts. Co-culturing A549 cells with MRT-irradiated MRC-5 lung fibroblasts led to increased tumor cell invasion, not observed when the fibroblasts received BB irradiation. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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23 pages, 2409 KB  
Article
Multi-Omic Characterization of Epithelial–Mesenchymal Transition: Lipidomic and Metabolomic Profiles as Key Markers of TGF-β-Induced Transition in Huh7 Hepatocellular Carcinoma
by Agnese Bertoldi, Gaia Cusumano, Eleonora Calzoni, Husam B. R. Alabed, Roberto Maria Pellegrino, Sandra Buratta, Lorena Urbanelli and Carla Emiliani
Cells 2025, 14(16), 1233; https://doi.org/10.3390/cells14161233 - 10 Aug 2025
Cited by 2 | Viewed by 2662
Abstract
Epithelial–mesenchymal transition (EMT) is a key process in cancer progression and fibrogenesis. In this study, EMT was induced in Huh7 hepatocellular carcinoma cells via TGF-β1 treatment, and the resulting lipidomic and metabolomic alterations were characterized. Morphological changes and protein marker analyses confirmed the [...] Read more.
Epithelial–mesenchymal transition (EMT) is a key process in cancer progression and fibrogenesis. In this study, EMT was induced in Huh7 hepatocellular carcinoma cells via TGF-β1 treatment, and the resulting lipidomic and metabolomic alterations were characterized. Morphological changes and protein marker analyses confirmed the transition to a mesenchymal phenotype, with reduced E-cadherin and increased vimentin and N-cadherin expression. Lipidomic profiling revealed a dose-dependent reorganization of membrane lipids, with a pronounced increase in the levels of ceramides, cholesteryl esters, and lysophospholipids, consistent with alterations in membrane structure, potential cellular stress, and modulation of inflammatory pathways. Changes in the content of phospholipid classes, including phosphatidylethanolamines and phosphatidylserines, indicate possible variations in membrane dynamics and potentially point to modifications in mitochondrial function, cellular stress responses, and redox balance. Metabolomic analysis further indicates an alteration of choline and phosphatidylcholine metabolism, consistent with a shift from de novo membrane synthesis toward lipid turnover. Reduced glycolytic capacity and modified acylcarnitine levels indicated impaired metabolic flexibility and mitochondrial efficiency. The integration of phenotypic, lipidomic, and metabolomic data suggests that TGF-β1 induces EMT and drives a coordinated metabolic reprogramming. These findings highlight the involvement of lipid and energy metabolism in sustaining EMT and suggest that specific metabolic reprogramming events characterize the mesenchymal shift in hepatocellular carcinoma. By exploring this process in a tumor-specific context, we aim to deepen our understanding of EMT complexity and its implications for tumor progression and therapeutic vulnerability. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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Review

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37 pages, 1405 KB  
Review
Interplay Between TLR4 and Gelatinases in Tumour Growth and Metastasis
by Abdulfattah Al-Kadash, Peter Michael Moyle and Marie-Odile Parat
Cells 2026, 15(9), 822; https://doi.org/10.3390/cells15090822 - 30 Apr 2026
Viewed by 411
Abstract
The modulation of the tumour microenvironment represents a pivotal step in tumorigenesis and metastasis and results from direct and paracrine cellular interactions. The innate immune Toll-like receptor 4 (TLR4) controls immune and inflammatory signalling in the tumour microenvironment. A growing body of evidence [...] Read more.
The modulation of the tumour microenvironment represents a pivotal step in tumorigenesis and metastasis and results from direct and paracrine cellular interactions. The innate immune Toll-like receptor 4 (TLR4) controls immune and inflammatory signalling in the tumour microenvironment. A growing body of evidence shows that TLR4 activation in cancer, immune and stromal cells upregulate gelatinase expression and activity, linking innate immune responses to extracellular matrix (ECM) remodelling. Gelatinases, or matrix metalloproteinases (MMP2) and (MMP9) play a pivotal role in tumour matrix degradation, thereby facilitating invasion, angiogenesis and metastasis. Interestingly, although TLR4 signalling in cancer cells and tumour-associated macrophages leads to different activation outputs, they can both induce gelatinases through NF-κB, MAPK, and Akt pathways. Evidence from clinical tumour tissues, co-culture models, in vivo and in vitro studies supports the crucial interplay between TLR4 signalling and gelatinases production in tumour growth and metastasis. An in-depth understanding of this crosstalk may reveal new therapeutic opportunities in targeted strategies. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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43 pages, 1480 KB  
Review
Signaling Networks Regulating Metastatic Progression in Triple-Negative Breast Cancer
by Zuzanna Senkowska, Katarzyna Owczarek, Karolina Niewinna and Urszula Lewandowska
Cells 2026, 15(9), 809; https://doi.org/10.3390/cells15090809 - 29 Apr 2026
Viewed by 763
Abstract
Triple-negative breast cancer (TNBC) is one of the most aggressive and clinically challenging subtypes of breast cancer, defined by the absence of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 expression. The lack of actionable molecular targets contributes to limited [...] Read more.
Triple-negative breast cancer (TNBC) is one of the most aggressive and clinically challenging subtypes of breast cancer, defined by the absence of estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2 expression. The lack of actionable molecular targets contributes to limited therapeutic options, frequent recurrence, and a high propensity for distant metastasis. Metastatic dissemination remains the principal cause of mortality in patients with TNBC and is driven by complex molecular mechanisms involving multiple interconnected signaling networks. This review summarizes current knowledge of the molecular mechanisms underlying metastatic progression in TNBC, with particular emphasis on signaling pathways that regulate tumor invasion, migration, and colonization of distant organs. We discuss the roles of key pathways, including PI3K/Akt, TGF-β, Wnt/β-catenin, NF-κB, and Rho/ROCK signaling, in the regulation of epithelial–mesenchymal transition, cytoskeletal remodeling, cancer stem cell phenotypes, and tumor–microenvironment interactions. A deeper understanding of these signaling networks may facilitate the identification of novel therapeutic targets and support the development of more effective strategies to limit metastatic disease in TNBC. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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23 pages, 2240 KB  
Review
Crosstalk Between Inflammasome Signalling and Epithelial-Mesenchymal Transition in Cancer and Benign Disease: Mechanistic Insights, Context-Dependence, and Therapeutic Opportunities
by Abdul L. Shakerdi, Emma Finnegan, Yin-Yin Sheng, Karlo Vidovic, Jessica M. Logan, Mark P. Ward, Sharon A. O’Toole, Cara Martin, Stavros Selemidis, Doug Brooks, John J. O’Leary and Prerna Tewari
Cells 2025, 14(20), 1594; https://doi.org/10.3390/cells14201594 - 14 Oct 2025
Cited by 1 | Viewed by 1799
Abstract
Epithelial-mesenchymal transition (EMT) and inflammasome signalling are intercon-nected processes which underpin tumour progression, metastasis, and therapeutic re-sistance. Inflammasomes such as NLRP3 encourage pro-inflammatory states (IL-1β, IL-18, NF-κB) and the activation of signalling pathways like TGF-β that promote mes-enchymal traits crucial for EMT. EMT [...] Read more.
Epithelial-mesenchymal transition (EMT) and inflammasome signalling are intercon-nected processes which underpin tumour progression, metastasis, and therapeutic re-sistance. Inflammasomes such as NLRP3 encourage pro-inflammatory states (IL-1β, IL-18, NF-κB) and the activation of signalling pathways like TGF-β that promote mes-enchymal traits crucial for EMT. EMT transcriptional programmes can then in turn modulate the inflammasome via NF-κB/TGF-β signalling, creating self-perpetuating mechanisms of cellular plasticity and dysregulated therapeutic response. We have re-viewed the mechanistic evidence for EMT–inflammasome crosstalk in cancer and discussed the potential therapeutic implications. The function of the EMT-inflammasome axis is clearly context-dependent, with the cancer type, stage, and the complexity of the tumour microenvironment heavily contributing. The crosstalk between EMT and the inflammasome is an overlooked mechanism of tumour evolution, and targeting inflammasomes like NLRP3, or their downstream signalling pathways, offers a promising therapeutic avenue, with the objective of inhibiting metastasis and overcoming drug resistance. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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66 pages, 2939 KB  
Review
Mechanistic Insights and Clinical Implications of ELK1 in Solid Tumors: A Narrative Review
by Georgios Kalampounias, Theodosia Androutsopoulou and Panagiotis Katsoris
Cells 2025, 14(16), 1257; https://doi.org/10.3390/cells14161257 - 14 Aug 2025
Cited by 9 | Viewed by 4041
Abstract
ELK1 is a Transcription factor (TF) belonging to the ETS-domain TF family, mainly activated via RAS-RAF-MEK-ERK signaling. As a nethermost pathway molecule, ELK1 binds to Serum-response elements (SREs) and directly regulates the transcription of Immediate early genes (IEGs) including FOS and EGR1. [...] Read more.
ELK1 is a Transcription factor (TF) belonging to the ETS-domain TF family, mainly activated via RAS-RAF-MEK-ERK signaling. As a nethermost pathway molecule, ELK1 binds to Serum-response elements (SREs) and directly regulates the transcription of Immediate early genes (IEGs) including FOS and EGR1. Due to ELK1’s influence on key cellular processes such as proliferation, migration, apoptosis evasion, and Epithelial-to-mesenchymal transition (EMT), its role as a key contributor to tumorigenesis is emerging. In recent years, elevated expression and/or activation of ELK1 has been reported in various malignancies, including lung, breast, prostate, colorectal, blood, gastric, liver, cervical, thyroid and ovarian cancer. ELK1 acts primarily through direct DNA binding but also through interaction with other oncogenes, noncoding RNA molecules, TFs, and upstream kinases (other than ERK1/2), thus participating in diverse axes of transcriptional regulation. Its crucial role in IEG expression has been particularly implicated in cancer progression, metastasis, and drug resistance. Owing to its role in multiple cellular functions and its subsequent oncogenic potential, further elucidation of intracellular ELK1 interactions is of paramount importance. This review aims to summarize current evidence on ELK1’s involvement in solid tumors, dissect reported mechanistic roles, and highlight recent insights that could fuel future ventures of high translational interest. Full article
(This article belongs to the Special Issue Cell Migration and Invasion)
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