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Cancers
Special Issues
Cancer Cell Motility
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Cancer Cell Motility

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".

Deadline for manuscript submissions: closed (31 March 2025) | Viewed by 2950

Special Issue Editors

Dr. Gianluca Aguiari

E-Mail Website
Guest Editor
Department of Neuroscience and Rehabilitation, Section of Biochemistry, Molecular Biology and Genetics, University of Ferrara, 44121 Ferrara, Italy
Interests: analysis of EMT; tumor invasion; autophagy; apoptosis and signaling related to tumor cell migration in kidney; prostate and breast cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Nicoletta Bianchi

E-Mail Website
Guest Editor
Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy
Interests: transglutaminase type 2; non-coding RNAs; cancer cell migration and invasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

The motility of cancer cells is an important field of study that is strongly associated with migration and invasion and also represents a crucial step for addressing therapy. Understanding cell modifications and the mechanisms by which cancer cells move to new destinations could improve the identification of new therapeutic targets to prevent or reduce metastatisation, increasing the survival of patients. These biological processes are connected with energy metabolism, changes of cytoplasmic structures, loss of cell adhesion, and revision of relations with the microenvironment, supported by genetic and epigenetic modifications, also trigged by drug-resistance. Epithelial-to-mesenchymal transition may affect DNA damage response, leading to genomic instability and dysregulated expression that further promotes cancer progression. The investigation of DNA repair gene networks, as well as the signaling connected with cell reprogramming (including Cadherins, Vimentin and Fibronectin) and the interference of non-coding RNAs might enhance the knowledge on the ability of cell to move.

Dear Colleagues,

Cancer progression and metastasis is the main cause of death in patients suffering of cancer diseases. Mechanisms associated with epithelial–mesenchymal transition (EMT), cell invasion and metastasis are not fully understood. We have studied these oncogenic processes for several years, in particular for kidney and breast cancers. Our expertise area includes the research in the field of signaling pathways linked to cell cycle, cell growth, autophagy, apoptosis, EMT, drug resistance, targeted therapy and gene expression regulation. 

The investigation of these processes is essential to discover new therapeutic targets able to enhance the life of cancer patients.

We are pleased to invite you to contribute an article to the Special Issue “Cancer Cell Motility”.

This Special Issue aims to investigate networks involved in cancer cell invasion and migration in order to discover new therapeutic targets and drug resistance mechanisms.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: Cell Biology, Cell Biochemistry, Molecular Biology, Cell Signaling, Cell Cycle/proliferation, Apoptosis, DNA repair, Gene Expression Regulation and Targeted Therapy.

We look forward to receiving your contributions.

Dr. Gianluca Aguiari
Prof. Dr. Nicoletta Bianchi
Guest Editors

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 communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Cancers 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 2900 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

  • cancer
  • EMT
  • invasion
  • metastasis
  • p53-related signaling
  • apoptosis
  • autophagy
  • cell cycle
  • anticancer drugs

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Published Papers (2 papers)

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25 pages, 5089 KiB  
Article
LKB1 and STRADα Promote Epithelial Ovarian Cancer Spheroid Cell Invasion
by Charles B. Trelford, Adrian Buensuceso, Emily Tomas, Yudith Ramos Valdes, Owen Hovey, Shawn Shun-Cheng Li and Trevor G. Shepherd
Cancers 2024, 16(22), 3726; https://doi.org/10.3390/cancers16223726 - 5 Nov 2024
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Abstract
Late-stage epithelial ovarian cancer (EOC) involves the widespread dissemination of malignant disease throughout the peritoneal cavity, often accompanied by ascites. EOC metastasis relies on the formation of multicellular aggregates, called spheroids. Given that Liver Kinase B1 (LKB1) is required for EOC spheroid viability [...] Read more.
Late-stage epithelial ovarian cancer (EOC) involves the widespread dissemination of malignant disease throughout the peritoneal cavity, often accompanied by ascites. EOC metastasis relies on the formation of multicellular aggregates, called spheroids. Given that Liver Kinase B1 (LKB1) is required for EOC spheroid viability and LKB1 loss in EOC cells decreases tumor burden in mice, we investigated whether the LKB1 complex controls the invasive properties of human EOC spheroids. LKB1 signalling was antagonized through the CRISPR/Cas9 genetic knockout of LKB1 and/or the RNAi-dependent targeting of STE20-related kinase adaptor protein (STRAD, an LKB1 activator). EOC spheroids expressing nuclear GFP (green) or mKate2 (red) constructs were embedded in Matrigel for real-time live-cell invasion monitoring. Migration and invasion were also assessed in spheroid culture using Transwell chambers, spheroid reattachment, and mesothelial clearance assays. The loss of LKB1 and STRAD signalling decreased cell invasion through Matrigel and Transwell membranes, as well as mesothelial cell clearance. In the absence of LKB1, zymographic assays identified a loss of matrix metalloproteinase (MMP) activity, whereas spheroid reattachment assays found that coating plates with fibronectin restored their invasive potential. A three-dimensional EOC organoid model demonstrated that organoid area was greatly reduced by LKB1 loss. Overall, our data indicated that LKB1 and STRAD facilitated EOC metastasis by promoting MMP activity and fibronectin expression. Given that LKB1 and STRAD are crucial for EOC metastasis, targeting LKB1 and/or STRAD could disrupt the dissemination of EOC, making inhibitors of the LKB1 pathway an alternative therapeutic strategy for EOC patients. Full article
(This article belongs to the Special Issue Cancer Cell Motility)
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Review

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45 pages, 4817 KiB  
Review
Reciprocal Modulation of Tumour and Immune Cell Motility: Uncovering Dynamic Interplays and Therapeutic Approaches
by Angelo Aquino and Ornella Franzese
Cancers 2025, 17(9), 1547; https://doi.org/10.3390/cancers17091547 - 1 May 2025
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Abstract
Dysregulated cell movement is a hallmark of cancer progression and metastasis, the leading cause of cancer-related mortality. The metastatic cascade involves tumour cell migration, invasion, intravasation, dissemination, and colonisation of distant organs. These processes are influenced by reciprocal interactions between cancer cells and [...] Read more.
Dysregulated cell movement is a hallmark of cancer progression and metastasis, the leading cause of cancer-related mortality. The metastatic cascade involves tumour cell migration, invasion, intravasation, dissemination, and colonisation of distant organs. These processes are influenced by reciprocal interactions between cancer cells and the tumour microenvironment (TME), including immune cells, stromal components, and extracellular matrix proteins. The epithelial–mesenchymal transition (EMT) plays a crucial role in providing cancer cells with invasive and stem-like properties, promoting dissemination and resistance to apoptosis. Conversely, the mesenchymal–epithelial transition (MET) facilitates metastatic colonisation and tumour re-initiation. Immune cells within the TME contribute to either anti-tumour response or immune evasion. These cells secrete cytokines, chemokines, and growth factors that shape the immune landscape and influence responses to immunotherapy. Notably, immune checkpoint blockade (ICB) has transformed cancer treatment, yet its efficacy is often dictated by the immune composition of the tumour site. Elucidating the molecular cross-talk between immune and cancer cells, identifying predictive biomarkers for ICB response, and developing strategies to convert cold tumours into immune-active environments is critical to overcoming resistance to immunotherapy and improving patient survival. Full article
(This article belongs to the Special Issue Cancer Cell Motility)
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