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Cancer Biology: From Genetic Aspects to Treatment, 2nd Edition

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 June 2026 | Viewed by 4528

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Dr. Silvia Cantara

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Department of Medical, Surgical and Neurological Sciences, University of Siena, 53100 Siena, Italy
Interests: cancer biology; endocrinology; molecular biology; genetics; cellular biology
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Dear Colleagues,

Cancer is a complex disease characterized by the uncontrolled proliferation and dissemination of aberrant cells throughout the human body. This pathological condition stems from alterations in the fundamental genetic code encoded within our DNA. Predominantly, these alterations manifest within specific DNA segments referred to as genes.

The expanding frontiers of scientific knowledge have led to molecular biology playing a pivotal role in contemporary oncological research. This prominence arises from its capacity to identify mechanisms underpinning cellular growth and differentiation, novel diagnostic indicators, and therapeutic focal points. Thus, molecular biology has emerged as the fulcrum of progressive advancements in the field of oncology, offering possibilities for developing efficacious therapeutic interventions.

This Special Issue of IJMS, ‘Cancer Biology: From Genetic Aspects to Treatment, 2nd Edition’, led by Dr. Silvia Cantara, will focus on new insights, novel developments and discoveries, current challenges, and future perspectives in the field of cancer biology.

Therefore, we invite you to submit your papers to this Special Issue.

Dr. Silvia Cantara
Guest Editor

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Keywords

cancer biology
cancer biomarker
cancer progression
cancer metastasis
genetic of cancer

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Published Papers (4 papers)

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Research

22 pages, 17796 KB

Open AccessArticle

Suppression of Glucosylceramide Synthase Reverses Drug Resistance in Cancer Cells Harboring Homozygous p53 Mutants

by Md Saqline Mostaq, Mohammad N. Amin, Amanda Raphael, Celine Asbury, Anish Gupta, Xin Gu, Xianlin Han, Davorka Sekulic, Pawel Michalak, Lin Kang and Yong-Yu Liu

Int. J. Mol. Sci. 2026, 27(7), 3237; https://doi.org/10.3390/ijms27073237 - 2 Apr 2026

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Abstract

Glucosylceramide synthase (GCS) catalyzes ceramide glycosylation in response to cell stress that produces glucosylceramide and other glycosphingolipids. GCS overexpression is a cause of drug resistance and enriches cancer stem cells (CSCs) during cancer chemotherapy. Previous studies showed that GCS modulates the expression of p53 mutants and oncogenic gain-of-function (GOF) in heterozygous knock-in cell models (TP53 R273H^−/+). However, it is unclear whether GCS can modulate the effects of homozygous p53 mutations, which are common in many cancer cases. We report herewith that inhibition of GCS, via UGCG knockout and using an inhibitor (Genz-161), effectively re-sensitizes drug resistance and diminishes CSCs in colon cancer cells carrying the homozygous p53 R273H mutation. In aggressive WiDr cells carrying TP53 R273H mutation, knockout of UGCG gene using CRISPR/Cas9 editing or inhibition of GCS with Genz-161 sensitized cancer cells to oxaliplatin, irinotecan and paclitaxel. With decreased ceramide glycosylation in lipidomic profiling, both UGCG knockout and Genz-161 treatments substantially decreased wound healing, and diminished CSCs and tumor growth under chemotherapy. Interestingly, inhibition of RNA m⁶A methylation by neplanocin A markedly increased p53 function and reversed drug resistance. Mechanistic investigation revealed that GCS inhibition downregulated methyltransferase-like 3 (METTL3) expression and decreased RNA-m⁶A modification on mutant p53 R273H effects. Altogether, our findings demonstrate that ceramide glycosylation promotes METTL3 expression and RNA m⁶A methylation in response to drug-induced stress, thereby promoting mutant p53 expression and associated GOF. Conversely, inhibition of GCS can diminish CSCs and drug resistance via reduction in m⁶A modification and advance of p53-assocaited tumor suppressive function. GCS inhibition is an achievable approach for mutant cancer treatment. Full article

(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment, 2nd Edition)

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13 pages, 4979 KB

Open AccessArticle

Tissue-Specific Expression of the EWSR1::FLI1 Fusion Protein Identifies col2a1a-Positive Cells as a Source of Ewing Sarcoma-like Tumors in Zebrafish

by Rebecca A. Anderson, Xin Chen, Usua Oyarbide, Nicolas J. Alvarez, Aidan Sievers, Gary K. Schwartz and Seth J. Corey

Int. J. Mol. Sci. 2026, 27(7), 3131; https://doi.org/10.3390/ijms27073131 - 30 Mar 2026

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Abstract

Ewing sarcoma (ES) is the second most common primary bone malignancy in children and adolescents and remains one of the most lethal pediatric cancers. Found in more than 85% of patients with ES, EWSR1::FLI1 results from the t(11;22)(q24;q12) chromosomal translocation. This fusion encodes an aberrant transcription factor that dysregulates gene expression and drives oncogenic transformation. Although this oncogene was identified over three decades ago, therapeutic progress has been limited, in part due to the lack of robust and permissive animal models. Prior efforts to generate transgenic mouse models have been unsuccessful, and while zebrafish have emerged as a promising system, a tissue context capable of supporting EWSR1::FLI1-driven tumorigenesis has not been defined. Here, we report that tissue-specific expression of EWSR1::FLI1 in zebrafish induces tumor formation that recapitulates the histologic and molecular hallmarks of human ES, including small round blue cell morphology and characteristic biomarker expression. Tumors were driven by the col2a1a promoter and resulted in ~70% incidence of notochord tumors within the first 72–96 h. Of the surviving fish, ~5% developed CD99-positive small round blue cell tumors at ~9 months post-fertilization. This work establishes a stable tissue-specific transgenic model of ES, providing a powerful in vivo platform to investigate disease pathogenesis and evaluate novel therapeutic strategies. Full article

(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment, 2nd Edition)

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14 pages, 1255 KB

Open AccessArticle

KRAS Copy Number Gain in Cell-Free DNA Analysis-Based Liquid Biopsy of Plasma and Bile in Patients with Various Pancreatic Neoplasms

by Mark Jain, David Atayan, Tagir Rakhmatullin, Tatiana Dakhtler, Victoria Inokenteva, Pavel Popov, Aleksandr Farmanov, Mikhail Viborniy, Iuliia Gontareva, Larisa Samokhodskaya and Vyacheslav Egorov

Int. J. Mol. Sci. 2025, 26(18), 8763; https://doi.org/10.3390/ijms26188763 - 9 Sep 2025

Cited by 2 | Viewed by 1779

Abstract

Cell-free DNA (cfDNA) analysis-based liquid biopsy is a rapidly emerging diagnostic and prognostic tool in pancreatic ductal adenocarcinoma (PDAC). KRAS point mutations are the main biomarkers used for the detection of tumor cfDNA. However, there is another less studied yet frequent genetic alteration in this gene, namely copy number gain (CNG). The aim of this study was to evaluate the diagnostic and prognostic potential of KRAS CNG analysis in plasma and bile of patients with PDAC using ddPCR. This study included healthy volunteers (n = 69), patients with PDAC (n = 94), and other pancreatic neoplasms (OPN) (n = 17). The sensitivity and specificity of KRAS CNG compared to the control group were 16% and 100% (AUC-ROC—0.580), and compared to the OPN group, 16% and 94% (AUC-ROC—0.554), respectively. Addition of KRAS point mutations to the analysis increased the sensitivity to 65% (AUC-ROC—0.824 and 0.801, respectively). Bile exhibited an equal KRAS CNG detection rate compared to plasma (20% vs. 16%). KRAS CNG was not associated with clinical parameters, except prognosis. The probability of survival was worse in patients with KRAS CNG (HR—3.54; 95% CI: 1.55–8.12; p = 0.001). KRAS CNG in cfDNA might be a promising biomarker for both diagnostic and prognostic purposes in PDAC. Full article

(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment, 2nd Edition)

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23 pages, 1226 KB

Open AccessArticle

Multi-Layered Analysis of TGF-β Signaling and Regulation via DNA Methylation and microRNAs in Astrocytic Tumors

by Klaudia Skóra, Damian Strojny, Dawid Sobański, Rafał Staszkiewicz, Paweł Gogol, Mateusz Miller, Przemysław Rogoziński, Nikola Zmarzły and Beniamin Oskar Grabarek

Int. J. Mol. Sci. 2025, 26(16), 7798; https://doi.org/10.3390/ijms26167798 - 12 Aug 2025

Viewed by 1208

Abstract

Astrocytic tumors are a heterogeneous group of glial neoplasms characterized by marked differences in biological behavior and patient prognosis. Transforming growth factor-beta (TGF-β) signaling plays a pivotal role in astrocytoma pathogenesis; however, the extent and mechanisms of its epigenetic regulation remain poorly understood. This study aimed to investigate how promoter methylation and microRNA-mediated mechanisms regulate key genes within the TGF-β signaling pathway across various astrocytoma grades. Tumor tissue samples from 65 patients with WHO grade II–IV astrocytomas were analyzed using Affymetrix gene expression and microRNA microarrays. Promoter methylation of TGF-β signaling genes was assessed using methylation-specific polymerase chain reaction (MSP). Gene expression was validated by reverse transcription quantitative polymerase chain reaction (RT-qPCR), and protein levels were quantified using enzyme-linked immunosorbent assay (ELISA). MicroRNA targets were predicted using bioinformatic tools, and survival analyses were conducted using Kaplan–Meier and Cox regression models. Six genes—SMAD1, SMAD3, SKIL, BMP2, SMAD4, and MAPK1—showed significant upregulation in high-grade tumors (fold change > 5.0, p < 0.05), supported by RT-qPCR and protein-level data. Promoter hypomethylation and reduced expression of regulatory microRNAs (e.g., hsa-miR-145-5p targeting SMAD3) were more common in higher-grade tumors. Protein–protein interaction analysis indicated strong functional interconnectivity among the overexpressed genes. High protein levels of SMAD1, SMAD3, and SKIL were significantly associated with shorter overall survival (p < 0.001). This multi-level analysis reveals that astrocytic tumor progression involves epigenetic derepression and microRNA-mediated dysregulation of TGF-β signaling. Elevated expression of SMAD1, SMAD3, and SKIL emerged as strong prognostic indicators, underscoring their potential as biomarkers and therapeutic targets in astrocytic tumors. Full article

(This article belongs to the Special Issue Cancer Biology: From Genetic Aspects to Treatment, 2nd Edition)

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