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Cancer Cell Motility (2nd Edition)
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Cancer Cell Motility (2nd Edition)

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

Deadline for manuscript submissions: 2 April 2026 | Viewed by 1114

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

Dear Colleagues,

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 metastasis, increasing the survival of patients. These biological processes are connected with energy metabolism, changes in cytoplasmic structures, loss of cell adhesion, and revision of relations with the microenvironment, supported by genetic and epigenetic modifications, also triggered by drug resistance. The epithelial-to-mesenchymal transition may affect the 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 cells to move.

Cancer progression and metastasis are the main causes of death in patients suffering from 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 research in the field of signaling pathways linked to the 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 lives 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
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 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. 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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Research

21 pages, 3645 KB  
Article
Dual Role of Diallyl Disulfide (DADS) on Invasive Potential and β-Catenin Dynamics in HER2-Positive Breast Cancer Cells
by Marcello Dell’Aira, Silvia Grassilli, Marina Pierantoni, Valeria Bertagnolo and Federica Brugnoli
Cancers 2025, 17(21), 3572; https://doi.org/10.3390/cancers17213572 - 5 Nov 2025
Viewed by 457
Abstract
Background/Objectives: Natural compounds are being increasingly explored as potential adjuvants to conventional drugs in oncological treatments. Regarding breast tumors, several studies indicate that garlic (Allium sativum) may protect against onset, counteracts aggressiveness, and prevents malignant progression of cells from non-invasive tumors. [...] Read more.
Background/Objectives: Natural compounds are being increasingly explored as potential adjuvants to conventional drugs in oncological treatments. Regarding breast tumors, several studies indicate that garlic (Allium sativum) may protect against onset, counteracts aggressiveness, and prevents malignant progression of cells from non-invasive tumors. It has been widely demonstrated that garlic derivatives induce apoptosis and reduce invasive potential in ER-positive and triple-negative breast tumor cells. However, the current literature lacks studies investigating their effects on HER2-positive (HER2+) breast cancers. This study therefore aimed to explore the effects of a garlic extract and diallyl disulfide (DADS), one of its most bioactive organosulfur compounds, on HER2+ phenotype breast tumor cells. Methods: The effects of a garlic extract and diallyl disulfide (DADS) were investigated on MDA-MB-453 and SKBR3 breast tumor cell lines. Cell growth, invasive potential, and Akt-related signaling were assessed after 4–72 h of garlic derivatives administration. The intracellular localization of β-catenin was examined with immunofluorescent confocal microscopy. Results: A dual role of DADS, dependent on the duration of treatment, was revealed. Acute administration induced a significant decrease in invasive potential, while prolonged treatment promoted HER2+ cell invasiveness. These effects were directly correlated with the activation of Akt and the nuclear accumulation of β-catenin, known to induce expression of genes associated with tumor malignancy. Conclusions: Although further investigations are needed to establish the exact mechanism and to assess the in vivo reproducibility of these phenomena, our results highlight the heterogeneous response to natural compounds of complex diseases like cancer. Full article
(This article belongs to the Special Issue Cancer Cell Motility (2nd Edition))
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17 pages, 4125 KB  
Article
Assessing the Tumor Suppressive Impact and Regulatory Mechanisms of SPDEF Expression in Breast Cancer
by Maansi Solanky, Maninder Khosla and Suresh K. Alahari
Cancers 2025, 17(21), 3556; https://doi.org/10.3390/cancers17213556 - 2 Nov 2025
Viewed by 481
Abstract
Background/Objectives: Breast cancer is a heterogeneous disease, and the role of the transcription factor SPDEF remains controversial. We aimed to clarify the prognostic value of SPDEF, explore demographic and molecular correlates of its expression, and investigate potential regulatory mechanisms underlying its dysregulation. Methods: [...] Read more.
Background/Objectives: Breast cancer is a heterogeneous disease, and the role of the transcription factor SPDEF remains controversial. We aimed to clarify the prognostic value of SPDEF, explore demographic and molecular correlates of its expression, and investigate potential regulatory mechanisms underlying its dysregulation. Methods: Genomic and clinical data for 1218 breast cancer tumors were obtained from The Cancer Genome Atlas (TCGA). SPDEF mRNA expression was compared across intrinsic subtypes, age, and race, and prognostic significance was evaluated by Kaplan–Meier analysis. Promoter methylation patterns and DNA methyltransferase (DNMT) expression were examined as potential regulatory drivers. Co-expression analysis was performed using gene panels representing luminal differentiation, basal identity, EMT, proliferation, DNA repair, and immune signaling. Results: Low SPDEF expression was significantly associated with worse overall, relapse-free, and metastasis-free survival across all breast cancers. Expression was lowest in Basal tumors, as well as among younger and Black or African American patients. Promoter methylation at six CpG islands correlated with both reduced SPDEF expression and inferior survival, and DNMT1, DNMT3A, and DNMT3B overexpression also aligned with poor prognosis and Basal enrichment. Co-expression analysis revealed that SPDEF downregulation coincided with loss of luminal markers and increased EMT, proliferation, DNA repair, and immune pathways. Conclusions: SPDEF functions as a tumor suppressor in breast cancer, with reduced expression linked to poor outcomes, aggressive molecular features, and epigenetic regulation. These findings highlight SPDEF and DNMT-driven methylation as potential prognostic biomarkers for enhanced risk stratification and targets for novel therapies, particularly in Basal breast cancers. Full article
(This article belongs to the Special Issue Cancer Cell Motility (2nd Edition))
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