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Advances in Molecular Pathogenesis Regulation in Cancer 2025
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Advances in Molecular Pathogenesis Regulation in Cancer 2025

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: closed (31 March 2025) | Viewed by 11668

Special Issue Editor

Dr. Guido Giordano

E-Mail Website
Guest Editor
Unit of Medical Oncology and Biomolecular Therapy, Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy
Interests: oncology; molecular biology; cell biology; pancreatic cancer; colorectal cancer; gastric cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Genetic and epigenetic alterations, as well as the crosstalk between tumor cells and their surrounding microenvironment, have been widely investigated in order to understand the basis of cancer proliferation, invasiveness, metastasis and therapeutic resistance. Despite this enhanced knowledge, the molecular mechanisms underlying the pathogenesis of each tumor remain unclear. Therefore, there remains the need for the following:

  • A deeper definition of the genetic and epigenetic changes that occur in various tumors;
  • The enhanced detection of tumor microenvironment components.

This information could lead to the introduction of novel biomarkers that will facilitate the timely diagnosis of cancer or tailored therapeutic approaches (target therapies).

The aim of this Special Issue is to collect and publish papers (original articles and full reviews) addressing the following topics:

  • Cancer biology;
  • Cancer genetics and epigenetics;
  • Molecular mechanisms or pathways involved in cancer;
  • Tumor microenvironment;
  • Role of the immune system in cancer;
  • Biomarkers for cancer detections;
  • Biomarkers for therapeutic approaches.

We especially thank Dr. Parcesepe for his contributions and support to this Special Issue.

Dr. Guido Giordano
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 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. 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 2200 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
  • cancer biology
  • genetic
  • epigenetic
  • tumor microenvironment
  • molecular biology
  • immune system
  • biomarkers
  • cancer diagnosis
  • target therapy

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Published Papers (8 papers)

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Research

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14 pages, 13308 KiB  
Article
Analysis of ROMO1 Expression Levels and Its Oncogenic Role in Gastrointestinal Tract Cancers
by Selçuk Yaman, Osman Akidan, Mehmet Vatansever, Sema Misir and Serap Ozer Yaman
Curr. Issues Mol. Biol. 2024, 46(12), 14394-14407; https://doi.org/10.3390/cimb46120863 - 20 Dec 2024
Viewed by 895
Abstract
Gastrointestinal tract cancers account for approximately one-third of cancer-related deaths. Early diagnosis and effective treatment are the most important ways to prevent cancer-related morbidity and mortality. ROMO1 has been shown to play an important role in many types of cancer. However, the biological [...] Read more.
Gastrointestinal tract cancers account for approximately one-third of cancer-related deaths. Early diagnosis and effective treatment are the most important ways to prevent cancer-related morbidity and mortality. ROMO1 has been shown to play an important role in many types of cancer. However, the biological function of ROMO1 is still poorly understood in gastrointestinal system cancers. The aim of this study is to reveal the expression change and oncogenic role of ROMO in gastrointestinal system cancers. Gene Expression Profiling Interactive Analysis (GEPIA), UALCAN, TIMER, GeneMANIA, TISIDB, and STRING were applied to assess the biological function of ROMO1 in gastrointestinal cancers (colon adenocarcinoma (COAD), esophageal carcinoma (ESCA), liver hepatocellular carcinoma (LIHC), pancreatic adenocarcinoma (PAAD), and stomach adenocarcinoma (STAD)). ROMO1 is significantly increased in COAD, ESCA, LUHC, and PAAD, and the overexpression of ROMO1 is associated with clinicopathological features. In addition, ROMO1 has been found to be closely associated with tumor-infiltrating immune cells in gastrointestinal cancers. ROMO1 is closely related to the inner mitochondrial membrane proteins (TIMM) family. The study revealed that ROMO1 is of significant clinical importance for gastrointestinal cancers and may have potential clinical utility in treatment and prognosis. Functional tests on cell lines derived from these particular gastrointestinal cancers can also be performed in vitro to evaluate the impact of the ROMO1 gene and other factors, like potential drugs, on the expression of these genes and the development and progression of the cancer. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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30 pages, 3725 KiB  
Article
Association of SIGLEC9 Expression with Cytokine Expression, Tumor Grading, KRAS, NRAS, BRAF, PIK3CA, AKT Gene Mutations, and MSI Status in Colorectal Cancer
by Błażej Ochman, Anna Kot, Sylwia Mielcarska, Agnieszka Kula, Miriam Dawidowicz, Dominika Koszewska, Dorota Hudy, Monika Szrot, Jerzy Piecuch, Dariusz Waniczek, Zenon Czuba and Elżbieta Świętochowska
Curr. Issues Mol. Biol. 2024, 46(12), 13617-13646; https://doi.org/10.3390/cimb46120814 - 29 Nov 2024
Viewed by 1080
Abstract
SIGLEC9 (sialic acid-binding Ig-like lectin 9) is a molecule thought to have a significant influence on the immune properties of the colorectal cancer (CRC) tumor microenvironment (TME). In our study, we assessed the expression of the SIGLEC9 protein in CRC tissue and the [...] Read more.
SIGLEC9 (sialic acid-binding Ig-like lectin 9) is a molecule thought to have a significant influence on the immune properties of the colorectal cancer (CRC) tumor microenvironment (TME). In our study, we assessed the expression of the SIGLEC9 protein in CRC tissue and the surgical margin tissue. Using RT-PCR, we analyzed mutations in the KRAS, NRAS, BRAF, PIK3CA, and AKT genes. We observed a significantly elevated expression of the SIGLEC9 protein in CRC tissue compared to the control group. No significant differences were observed in SIGLEC9 protein expression depending on mutations in the KRAS, NRAS, BRAF, PIK3CA, and AKT genes or microsatellite instability (MSI) status. However, we found a significantly higher expression of the SIGLEC9 protein in high-grade tumors compared to the low-grade tumors group. SIGLEC9 expression was significantly associated with the expression of multiple cytokines, chemokines, and growth factors in the CRC TME. These associations suggest the significant potential of SIGLEC9 as a molecule that plays a crucial role in shaping the immune properties of the CRC TME, as well as its potential therapeutic relevance, particularly in the group of high-grade CRC tumors. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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17 pages, 2561 KiB  
Article
Microgravity as a Tool to Investigate Cancer Induction in Pleura Mesothelial Cells
by Valentina Bonetto, Corinna Anais Pagano, Maurizio Sabbatini, Valeria Magnelli, Massimo Donadelli, Emilio Marengo and Maria Angela Masini
Curr. Issues Mol. Biol. 2024, 46(10), 10896-10912; https://doi.org/10.3390/cimb46100647 - 27 Sep 2024
Viewed by 1558
Abstract
The present work shows that the exposure of mesothelial cells to simulated microgravity changes their cytoskeleton and adhesion proteins, leading to a cell switch from normal towards tumoral cells. Immunohistochemical and molecular data were obtained from both MeT-5A exposed to simulated microgravity and [...] Read more.
The present work shows that the exposure of mesothelial cells to simulated microgravity changes their cytoskeleton and adhesion proteins, leading to a cell switch from normal towards tumoral cells. Immunohistochemical and molecular data were obtained from both MeT-5A exposed to simulated microgravity and BR95 mesothelioma cell lines. Simulated microgravity was found to affect the expression of actin, vinculin, and connexin-43, altering their quantitative and spatial distribution pattern inside the cell. The analysis of the tumoral markers p27, CD44, Fibulin-3, and NANOG and the expression of genes related to cancer transformation such as NANOG, CDH-1, and Zeb-1 showed that the simulated microgravity environment led to expression patterns in MeT-5A cells similar to those observed in BR95 cells. The alteration in both quantitative expression and structural organization of the cytoskeleton and adhesion/communication proteins can thus be considered a pivotal mechanism involved in the cellular shift towards tumoral progression. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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25 pages, 5756 KiB  
Article
Impacts of DROSHA (rs10719) and DICER (rs3742330) Variants on Breast Cancer Risk and Their Distribution in Blood and Tissue Samples of Egyptian Patients
by Aly A. M. Shaalan, Essam Al Ageeli, Shahad W. Kattan, Amany I. Almars, Nouf A. Babteen, Abdulmajeed A. A. Sindi, Eman A. Toraih, Manal S. Fawzy and Marwa Hussein Mohamed
Curr. Issues Mol. Biol. 2024, 46(9), 10087-10111; https://doi.org/10.3390/cimb46090602 - 12 Sep 2024
Viewed by 1762
Abstract
MicroRNAs (miRNAs) are small, noncoding RNAs that regulate gene expression and play critical roles in tumorigenesis. Genetic variants in miRNA processing genes, DROSHA and DICER, have been implicated in cancer susceptibility and progression in various populations. However, their role in Egyptian patients [...] Read more.
MicroRNAs (miRNAs) are small, noncoding RNAs that regulate gene expression and play critical roles in tumorigenesis. Genetic variants in miRNA processing genes, DROSHA and DICER, have been implicated in cancer susceptibility and progression in various populations. However, their role in Egyptian patients with breast cancer (BC) remains unexplored. This study aims to investigate the association of DROSHA rs10719 and DICER rs3742330 polymorphisms with BC risk and clinical outcomes. This case–control study included 209 BC patients and 106 healthy controls. Genotyping was performed using TaqMan assays in blood, tumor tissue, and adjacent non-cancerous tissue samples. Associations were analyzed using logistic regression and Fisher’s exact test. The DROSHA rs10719 AA genotype was associated with a 3.2-fold increased risk (95%CI = 1.23–9.36, p < 0.001), and the DICER rs3742330 GG genotype was associated with a 3.51-fold increased risk (95%CI = 1.5–8.25, p = 0.001) of BC. Minor allele frequencies were 0.42 for rs10719 A and 0.37 for rs3742330 G alleles. The risk alleles were significantly more prevalent in tumor tissue than adjacent normal tissue (rs10719 A: 40.8% vs. 0%; rs3742330 G: 42.7% vs. 0%; p < 0.001). However, no significant associations were observed with clinicopathological features or survival outcomes over a median follow-up of 17 months. In conclusion, DROSHA rs10719 and DICER rs3742330 polymorphisms are associated with increased BC risk and more prevalent in tumor tissue among our cohort, suggesting a potential role in miRNA dysregulation during breast tumorigenesis. These findings highlight the importance of miRNA processing gene variants in BC susceptibility and warrant further validation in larger cohorts and different ethnic populations. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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Review

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37 pages, 4013 KiB  
Review
Demystifying the Role of Histone Demethylases in Colorectal Cancer: Mechanisms and Therapeutic Opportunities
by Yuanbin Liu, Min Huang, Xia Tian and Xiaodong Huang
Curr. Issues Mol. Biol. 2025, 47(4), 267; https://doi.org/10.3390/cimb47040267 - 9 Apr 2025
Viewed by 483
Abstract
Histone demethylases (HDMs) play a pivotal role in colorectal cancer (CRC) progression through dynamic epigenetic regulation. This review summarizes the role and therapeutic potential of HDM in CRC. HDMs primarily target lysine (K) for demethylation (lysine demethylase, KDM). The KDM family is divided [...] Read more.
Histone demethylases (HDMs) play a pivotal role in colorectal cancer (CRC) progression through dynamic epigenetic regulation. This review summarizes the role and therapeutic potential of HDM in CRC. HDMs primarily target lysine (K) for demethylation (lysine demethylase, KDM). The KDM family is divided into the lysine-specific demethylase family and the Jumonji C domain-containing family. HDMs play complex roles in CRC cell proliferation, invasion, migration, stemness, epithelial–mesenchymal transition, immune response, and chemoresistance through epigenetic regulation of different histone demethylation sites. Increasing evidence suggests that KDM may interact with certain factors and regulate CRC tumorigenesis by modulating multiple signaling pathways and affecting the transcription of target genes. These processes may be regulated by upstream genes and thus form a complex epigenetic regulatory network. However, the potential roles and regulatory mechanisms of some HDMs in CRC remain understudied. Preclinical studies have revealed that small-molecule inhibitors targeting HDM impact the activity of specific genes and pathways by inhibiting specific HDM expression, thereby reshaping the tumorigenic landscape of CRC. However, the clinical translational potential of these inhibitors remains unexplored. In conclusion, HDMs play a complex and critical role in CRC progression by dynamically regulating histone methylation patterns. These HDMs shape the malignant behavior of CRC by influencing the activity of key pathways and target genes through epigenetic reprogramming. Targeting HDM may be a promising direction for CRC treatment. Further exploration of the role of specific HDMs in CRC and the therapeutic potential of HDM-specific inhibitors is needed in the future. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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14 pages, 608 KiB  
Review
Integration of Genomic Tests in Prostate Cancer Care: Implications for Clinical Practice and Patient Outcomes
by Christos Roidos, Anastasios Anastasiadis, Stavros Tsiakaras, Charalampos Loutradis, Panagiotis Baniotis, Dimitrios Memmos, Georgios Dimitriadis and Maria Papaioannou
Curr. Issues Mol. Biol. 2024, 46(12), 14408-14421; https://doi.org/10.3390/cimb46120864 - 20 Dec 2024
Cited by 1 | Viewed by 1095
Abstract
Prostate cancer (PCa) is a common malignancy in men and is among the leading causes of cancer-related death worldwide. Genomic tests assess disease aggressiveness and guide treatment, particularly in low- and intermediate-risk PCa. We reviewed the literature on the use of four genomic [...] Read more.
Prostate cancer (PCa) is a common malignancy in men and is among the leading causes of cancer-related death worldwide. Genomic tests assess disease aggressiveness and guide treatment, particularly in low- and intermediate-risk PCa. We reviewed the literature on the use of four genomic tests (Prolaris®, Promark®, Oncotype DX®, and Decipher®) in assessing the prognosis of PCa and their use in treatment decision-making. Most of the studies showed that Prolaris® has a strong correlation with biochemical recurrence, metastasis risk, PCa-specific mortality (PCSM), and pathological features. Similarly, three studies on Promark® indicated a connection between results and pathological features in the subsequent prostatectomy, time to metastasis, and biochemical recurrence. Fourteen studies on Oncotype DX® showed a clear correlation between high scores, death, and PCSM. One study found that routine biopsy pathology reports, combined with serum PSA levels, provide a risk assessment comparable to Oncotype DX® testing. Results from 22 studies on Decipher® were controversial. The test was associated with conservative management, suggesting that patients with a high GC score are more likely to need radiation after surgery. Comparative studies indicated that Oncotype DX® is preferable for assessing PCSM, Decipher® for predicting metastasis, and Prolaris® for predicting recurrence. With the incidence rate of PCa dramatically increasing, genomic tests appear to be useful adjunctive precision medicine tools with significant potential in improving prognostic discrimination, facilitating better risk stratification, and guiding personalized treatment, especially in the intermediate-risk patient group. Large-scale, prospective, multi-sectional studies are required to validate the utility of these tests prior to their integration into clinical practice. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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35 pages, 3440 KiB  
Review
Clinical Potential of Misshapen/NIKs-Related Kinase (MINK) 1—A Many-Sided Element of Cell Physiology and Pathology
by Anna Kot, Dominika Koszewska, Błażej Ochman and Elżbieta Świętochowska
Curr. Issues Mol. Biol. 2024, 46(12), 13811-13845; https://doi.org/10.3390/cimb46120826 - 5 Dec 2024
Cited by 2 | Viewed by 1975
Abstract
Misshapen/NIKs-related kinase (MINK) 1 belongs to the mammalian germinal center kinase (GCK) family. It contains the N-terminal, conserved kinase domain, a coiled-coil region, a proline-rich region, and a GCK, C-terminal domain with the Citron-NIK-Homology (CNH) domain. The kinase is an essential component of [...] Read more.
Misshapen/NIKs-related kinase (MINK) 1 belongs to the mammalian germinal center kinase (GCK) family. It contains the N-terminal, conserved kinase domain, a coiled-coil region, a proline-rich region, and a GCK, C-terminal domain with the Citron-NIK-Homology (CNH) domain. The kinase is an essential component of cellular signaling pathways, which include Wnt signaling, JNK signaling, pathways engaging Ras proteins, the Hippo pathway, and STRIPAK complexes. It thus contributes to regulating the cell cycle, apoptosis, cytoskeleton organization, cell migration, embryogenesis, or tissue homeostasis. MINK1 plays an important role in immunological responses, inhibiting Th17 and Th1 cell differentiation and regulating NLRP3 inflammasome function. It may be considered a link between ROS and the immunological system, and a potential antiviral target for human enteroviruses. The kinase has been implicated in the pathogenesis of sepsis, rheumatoid arthritis, asthma, SLE, and more. It is also involved in tumorigenesis and drug resistance in cancer. Silencing MINK1 reduces cancer cell migration, suggesting potential for new therapeutic approaches. Targeting MINK1 could be a promising treatment strategy for patients insensitive to current chemotherapies, and could improve their prognosis. Moreover, MINK1 plays an important role in the nervous system and the cardiovascular system development and function. The modulation of MINK1 activity could influence the course of neurodegenerative diseases, including Alzheimer’s disease. Further exploration of the activity of the kinase could also help in gaining more insight into factors involved in thrombosis or congenital heart disease. This review aims to summarize the current knowledge on MINK1, highlight its therapeutic and prognostic potential, and encourage more studies in this area. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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14 pages, 299 KiB  
Review
Genetics and Molecular Pathogenesis of the Chondrosarcoma: A Review of the Literature
by Georgian-Longin Iacobescu, Antonio-Daniel Corlatescu, Bogdan Serban, Razvan Spiridonica, Horia Petre Costin and Catalin Cirstoiu
Curr. Issues Mol. Biol. 2024, 46(11), 12658-12671; https://doi.org/10.3390/cimb46110751 - 8 Nov 2024
Viewed by 1981
Abstract
The chondrosarcoma, a cartilage-forming bone tumor, presents significant clinical challenges due to its resistance to chemotherapy and radiotherapy. Surgical excision remains the primary treatment, but high-grade chondrosarcomas are prone to recurrence and metastasis, necessitating the identification of reliable biomarkers for diagnosis and prognosis. [...] Read more.
The chondrosarcoma, a cartilage-forming bone tumor, presents significant clinical challenges due to its resistance to chemotherapy and radiotherapy. Surgical excision remains the primary treatment, but high-grade chondrosarcomas are prone to recurrence and metastasis, necessitating the identification of reliable biomarkers for diagnosis and prognosis. This review explores the genetic alterations and molecular pathways involved in chondrosarcoma pathogenesis. These markers show promise in distinguishing between benign enchondromas and malignant chondrosarcomas, assessing tumor aggressiveness, and guiding treatment. While these advancements offer hope for more personalized and targeted therapeutic strategies, further clinical validation of these biomarkers is essential to improve prognostic accuracy and patient outcomes in chondrosarcoma management. Full article
(This article belongs to the Special Issue Advances in Molecular Pathogenesis Regulation in Cancer 2025)
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