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Molecular Mechanisms Driving Cancer Progression and Metastasis
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Molecular Mechanisms Driving Cancer Progression and Metastasis

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 20 September 2026 | Viewed by 2252

Editor

Dr. Karolina Bajdak-Rusinek

E-Mail Website
Guest Editor
Department of Medical Genetics, Faculty of Medical Sciences in Katowice, Medical University of Silesia, Katowice, Medykow 18 Street, 40-752 Katowice, Poland
Interests: molecular mechanisms; cell therapy; mesenchymal stem cells; tissue regeneration; drug delivery; epithelial-to-mesenchymal transition; microRNA; molecular cancer biology; metastasis; personalized medicine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Cancer progression and metastasis remain the leading causes of cancer-related mortality worldwide. Elucidating the molecular mechanisms that govern tumor growth, invasion, and dissemination is crucial for improving diagnostics and therapeutic strategies. This Special Issue will focus on recent advances in our understanding of cancer progression, with particular emphasis on epithelial–mesenchymal transition, tumor plasticity, epigenetic and transcriptional regulation, signaling pathways, angiogenesis, and mechanisms of therapy resistance. We welcome original research articles, reviews, and short communications that provide novel insights into the biology of metastasis and its clinical implications. By integrating diverse perspectives, this Special Issue will expand our knowledge of tumor biology and promote innovative approaches to limit the spread of cancer.  

Best regards,
Dr. Karolina Bajdak-Rusinek
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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly 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 2400 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 progression
  • metastasis
  • epithelial–mesenchymal transition (EMT)
  • tumor plasticity
  • tumor microenvironment
  • signaling pathways
  • therapy resistance

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Published Papers (2 papers)

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Research

18 pages, 1301 KB  
Article
Role of Ki-67 and Annexin V in the Biological Behavior of Salivary Gland Tumors: Insights into Proliferation and Apoptosis
by Balkees Taha Garib and Dalya Ali Abdulla
Curr. Issues Mol. Biol. 2026, 48(4), 387; https://doi.org/10.3390/cimb48040387 - 10 Apr 2026
Viewed by 812
Abstract
Salivary gland tumors have diverse biological behaviors, and the exact molecular factors underlying their pathogenesis remain unclear. The expression of Annexin V and its potential association with Ki-67 in these tumors has not been explored. Therefore, this study aimed to evaluate the immunohistochemical [...] Read more.
Salivary gland tumors have diverse biological behaviors, and the exact molecular factors underlying their pathogenesis remain unclear. The expression of Annexin V and its potential association with Ki-67 in these tumors has not been explored. Therefore, this study aimed to evaluate the immunohistochemical expression of Ki-67 and Annexin V and to assess their relationship in salivary gland tumors. This study included 45 formalin-fixed, paraffin-embedded blocks (5 normal salivary gland tissues, 10 pleomorphic adenomas, 10 Warthin tumors, 10 mucoepidermoid carcinomas, and 10 adenoid cystic carcinomas). Immunohistochemical staining for Ki-67 and Annexin V was performed and evaluated semi-quantitatively. Depending on the results of the normality test, one-way ANOVA or the Kruskal-Wallis H test was used for group comparisons. Spearman’s rho test was used to assess correlations among the markers under study. A p-value < 0.05 was considered statistically significant. Both markers and their ratio showed statistically significant differences among the groups (p-value < 0.001). Normal salivary gland tissue and pleomorphic adenoma showed negative Ki-67 expression, whereas Warthin tumor, mucoepidermoid carcinoma, and adenoid cystic carcinoma showed weak proliferation indices. Annexin V expression was highest in the normal salivary gland tissue. Within individual tumor types, Ki-67 and Annexin V exhibited no significant correlation. The combined evaluation of Ki-67 and Annexin V expression, along with their relationship, may provide preliminary insights into the biological behavior of salivary gland tumors and warrant further clinicopathological investigation. Full article
(This article belongs to the Special Issue Molecular Mechanisms Driving Cancer Progression and Metastasis)
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13 pages, 1209 KB  
Article
ESRP1-Associated CD44 Alternative Splicing Stratifies Epithelial–Mesenchymal Identity States in a Non-Transformed Human Cell System
by Karolina Bajdak-Rusinek, Natalia Diak, Anna Trybus, Agnieszka Fus-Kujawa, Marcelina Salamon, Jan Olszewski, Weronika Wójtowicz and Patrycja Rozwadowska-Kunecka
Curr. Issues Mol. Biol. 2026, 48(2), 130; https://doi.org/10.3390/cimb48020130 - 24 Jan 2026
Viewed by 966
Abstract
Epithelial–mesenchymal plasticity encompasses a spectrum of epithelial and mesenchymal identity states that enable cells to adapt to changing biological contexts. While CD44 isoform usage and epithelial splicing regulators ESRP1/2 are well-characterized in cancer-associated epithelial–mesenchymal transition (EMT), their regulation across physiological, non-transformed identity states [...] Read more.
Epithelial–mesenchymal plasticity encompasses a spectrum of epithelial and mesenchymal identity states that enable cells to adapt to changing biological contexts. While CD44 isoform usage and epithelial splicing regulators ESRP1/2 are well-characterized in cancer-associated epithelial–mesenchymal transition (EMT), their regulation across physiological, non-transformed identity states remains less well defined. Here, we employed a non-malignant human cellular system comprising primary dermal fibroblasts, induced pluripotent stem (iPS) cells, and iPS-derived mesenchymal stem cells (iPS-MSCs) to define discrete epithelial, intermediate epithelial/mesenchymal, and mesenchymal identity states positioned along an epithelial–mesenchymal identity axis. Morphological assessment, lineage marker profiling, and RT-qPCR analyses revealed reproducible population-level stratification of these states. CD44 expression and alternative splicing followed this hierarchy, with CD44s predominating in fibroblasts, broad variant exon inclusion in iPS cells, and intermediate patterns in iPS-MSCs. ESRP1 expression mirrored CD44 splicing architecture, and ESRP1 silencing in iPS cells induced a shift toward CD44s, confirming its functional contribution to epithelial-associated CD44 splicing. In contrast, Notch-related transcriptional readouts displayed distinct, context-dependent profiles across the examined identity states. Together, this study establishes a tractable non-transformed human model that captures selected molecular features associated with epithelial–mesenchymal plasticity beyond malignant contexts. Full article
(This article belongs to the Special Issue Molecular Mechanisms Driving Cancer Progression and Metastasis)
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