Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 August 2025 | Viewed by 4845

Special Issue Editors


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Guest Editor
Department of Medical and Surgical Sciences -DIMEC, Alma Mater Studiorum, University of Bologna, Via San Giacomo 14, 40126 Bologna, Italy
Interests: immunotoxin; immunoconjugate; immunotargeting; plant toxins; ribosome-inactivating proteins
Special Issues, Collections and Topics in MDPI journals
Department of Cell Biology and Immunology, Centre of Postgraduate Medical Education, Marymoncka 99/103, 01-813 Warsaw, Poland
Interests: cancer cell biology; biomarkers; micro-RNAs; multidrug resistance; experimental anticancer therapies

Special Issue Information

Dear Colleagues,

Currently, chemotherapy, surgery, and radiotherapy are the most commonly available cancer treatments. However, despite their demonstrated anti-tumour efficacy, the use of radiotherapy and chemotherapeutic agents has shown many limitations, such as the lack of selectivity for tumour cells, the development of drug resistance, and the appearance of secondary malignancies. As a result, the study and development of alternative targeted therapies, such as immunotherapy and nanotherapy, have been extensively researched in order to find therapies with greater specificity for transformed cells and a lower non-specific toxicity. Therefore, it is essential that we intensify our studies on the molecular mechanisms of carcinogenesis and develop new tactics to diagnose and fight tumours.

In this Special Issue, we aim to provide an update on the most promising anticancer therapeutic strategies and current studies on the molecular factors that influence cancer biology.

Dr. Letizia Polito
Dr. Ewa Gajda
Guest Editors

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Keywords

  • cancer biology
  • experimental anticancer therapies
  • immunotherapy
  • immunotoxins
  • signalling pathways
  • targeted therapies

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Related Special Issue

Published Papers (5 papers)

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Research

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11 pages, 1327 KiB  
Article
Diminishing Hepcidin via Reducing IL-6/STAT3 Pathway by Utilizing Ferulic Acid: An In Vitro Study
by Ola M. Al-Sanabra, Luay F. Abu-Qatouseh, Mohammad I. A. Ahmad, Mutaz Jamal Al-Khreisat and Majd M. Alsaleh
Biomedicines 2025, 13(4), 923; https://doi.org/10.3390/biomedicines13040923 - 9 Apr 2025
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Abstract
Background/Objectives: Hepcidin is a negative regulator of iron absorption that is released by hepatocytes. It is one of the main contributors to hypoferremia and anemia in inflammatory and oncological disorders that are mediated by the proinflammatory cytokine IL-6/STAT3 pathway. Ferulic acid [...] Read more.
Background/Objectives: Hepcidin is a negative regulator of iron absorption that is released by hepatocytes. It is one of the main contributors to hypoferremia and anemia in inflammatory and oncological disorders that are mediated by the proinflammatory cytokine IL-6/STAT3 pathway. Ferulic acid (FA) is a phenolic compound with pleiotropic biological activities, including anti-inflammatory activity. However, its effect on hepcidin secretion is still unknown. Thus, this study aimed to explore the impact of FA on hepcidin levels and the underlying mechanism. Methods: HepG2 cells were treated with different log percentages of FA, and their viability was determined via the MTT assay. The relative expression of IL-6 and HAMP in treated and untreated cells was measured via qRT-PCR, and the protein levels of hepcidin, IL-6 and STAT3 were measured using ELISA. Results: The MTT test showed an inverse relationship between FA concentrations and HepG2 cell proliferation; FA’s IC50 value was 0.07669%. The expression levels of IL-6 and HAMP were significantly increased in HepG2 cells following 24 h of culture with 4 μg/mL LPS. Meanwhile, the addition of FA significantly decreased the relative expression levels of these two genes and the secretion levels of IL-6, STAT3 and hepcidin compared to the cells treated with LPS alone. Conclusions: Overall, these findings show that FA modifies inflammatory pathways, affecting hepcidin levels via the IL-6/STAT3 pathway. Thus, this suggests FA as a potential therapeutic agent against the hypoferremia and anemia developed due to dysregulated hepcidin levels in diseases such as inflammatory and oncological disorders. Full article
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28 pages, 39795 KiB  
Article
Therapeutic Target Discovery for Multiple Myeloma: Identifying Druggable Genes via Mendelian Randomization
by Shijun Jiang, Fengjuan Fan, Qun Li, Liping Zuo, Aoshuang Xu and Chunyan Sun
Biomedicines 2025, 13(4), 885; https://doi.org/10.3390/biomedicines13040885 - 5 Apr 2025
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Abstract
Background: Multiple myeloma (MM) is a hematological malignancy originating from the plasma cells present in the bone marrow. Despite significant therapeutic advancements, relapse and drug resistance remain major clinical challenges, highlighting the urgent need for novel therapeutic targets. Methods: To identify [...] Read more.
Background: Multiple myeloma (MM) is a hematological malignancy originating from the plasma cells present in the bone marrow. Despite significant therapeutic advancements, relapse and drug resistance remain major clinical challenges, highlighting the urgent need for novel therapeutic targets. Methods: To identify potential druggable genes associated with MM, we performed Mendelian randomization (MR) analysis. Causal candidates were further validated using a single-tissue transcriptome-wide association study (TWAS), and colocalization analysis was conducted to assess shared genetic signals between gene expression and disease risk. Potential off-target effects were assessed through an MR phenome-wide association study (MR-PheWAS). Additionally, molecular docking and functional assays were used to evaluate candidate drug efficacy. Results: The MR analysis identified nine druggable genes (FDR < 0.05), among which Orosomucoid 1 (ORM1) and Oviductal Glycoprotein 1 (OVGP1) were supported by both TWAS and colocalization evidence (PPH4 > 0.75). Experimental validation demonstrated the significant downregulation of ORM1 and OVGP1 in MM cells (p < 0.05). Pregnenolone and irinotecan, identified as agonists of ORM1 and OVGP1, respectively, significantly inhibited MM cell viability, while upregulating their expression (p < 0.05). Conclusions: Our study highlights ORM1 and OVGP1 as novel therapeutic targets for MM. The efficacy of pregnenolone and irinotecan in suppressing MM cell growth suggests their potential for clinical application. These findings provide insights into MM pathogenesis and offer a promising strategy for overcoming drug resistance. Full article
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14 pages, 2138 KiB  
Article
Natural Compounds and Histone Deacetylase Inhibitors: A Combined Approach Against mCRPC Cells
by Janiah Alimudin, Zeynep Betts and Asuman Deveci Ozkan
Biomedicines 2025, 13(2), 296; https://doi.org/10.3390/biomedicines13020296 - 25 Jan 2025
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Abstract
Background: Sodium butyrate (NaBu), a short-chain fatty acid, modulates global gene expression through histone deacetylase (HDAC) inhibition, suppressing proliferation and inducing apoptosis in various cancers. Rutin (RUT), a polyphenolic flavonoid found in many plants, exhibits notable anticancer properties. Combining chemotherapeutic agents with [...] Read more.
Background: Sodium butyrate (NaBu), a short-chain fatty acid, modulates global gene expression through histone deacetylase (HDAC) inhibition, suppressing proliferation and inducing apoptosis in various cancers. Rutin (RUT), a polyphenolic flavonoid found in many plants, exhibits notable anticancer properties. Combining chemotherapeutic agents with natural polyphenols represents a promising strategy for cancer therapy. This study aims to evaluate, for the first time, the potential effects of NaBu and RUT combination therapy on metastatic castration-resistant prostate cancer (mCRPC) cells. Methods: PC-3 cells were treated with varying concentrations of NaBu, RUT, and their combinations. Cell viability was assessed using the WST-1 assay. Based on combination index values, selected treatments were further analyzed for apoptosis (Annexin V assay), intracellular reactive oxygen species (ROS) production, mRNA expression levels, and changes in cell and nuclear morphology. Results: The combined treatment of NaBu and RUT significantly reduced cell viability compared to individual treatments. Enhanced apoptotic induction and elevated ROS levels were observed in combination-treated cells, alongside notable changes in cellular and nuclear morphology and mRNA expression levels. Conclusions: NaBu and RUT combination therapy exhibits a synergistic anticancer effect in mCRPC cells by inhibiting cell viability, inducing apoptosis, and increasing ROS production. These findings suggest a promising therapeutic approach that warrants further investigation to elucidate the underlying molecular mechanisms and assess its potential in preclinical and clinical settings. Full article
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19 pages, 5333 KiB  
Article
Identifying MTHFD1 and LGALS4 as Potential Therapeutic Targets in Prostate Cancer Through Multi-Omics Mendelian Randomization Analysis
by Huan Han, Hanwen Su, Zhihua Lv, Chengliang Zhu and Jingtao Huang
Biomedicines 2025, 13(1), 185; https://doi.org/10.3390/biomedicines13010185 - 13 Jan 2025
Cited by 1 | Viewed by 1368
Abstract
Background: Prostate cancer remains one of the leading causes of cancer-related mortality in men worldwide. The treatment of it is currently based on surgical removal, radiotherapy, and hormone therapy. It is crucial to improve therapeutic prospects for the diagnosis and treatment of prostate [...] Read more.
Background: Prostate cancer remains one of the leading causes of cancer-related mortality in men worldwide. The treatment of it is currently based on surgical removal, radiotherapy, and hormone therapy. It is crucial to improve therapeutic prospects for the diagnosis and treatment of prostate cancer via drug target screening. Methods: We integrated eQTL data from the eQTLGen Consortium and pQTL data from UK Biobank Proteome Plasma Proteins (UKB-PPP) and deCODE health datasets. MR analyses (SMR, heterogeneity in dependent instruments (HEIDI), IVW, Wald ratio, weighted median, and MR-Egger) were used to screen candidate genes associated with prostate adenocarcinoma (PRAD) risk. Candidate genes were further verified through TCGA-based gene expression profile, survival analysis, and immune microenvironment evaluations. TIDE analysis was utilized to investigate gene immunotherapy response. Single-cell RNA sequencing data from the GSE176031 dataset were used to investigate the gene expression patterns. The Drug Bank, Therapeutic Target Database and Drug Signatures Database were utilized to predict targeted drugs for candidate genes. Results: MTHFD1 and LGALS4 were identified as promising therapeutic targets for PRAD, with evidence provided at multi-omics levels. LGALS4 was predominantly expressed in malignant cells and was correlated with enhanced immune checkpoint pathways, increased TIDE scores, and immunotherapy resistance. In contrast, MTHFD1was expressed in both tumor and microenvironmental cells and was associated with poor survival. Drug target prediction suggested that there are no currently approved drugs specifically targeting MTHFD1 and LGALS4. Conclusions: Our study identified MTHFD1 and LGALS4 as potential preventive targets for PRAD. However, future experiments are warranted to assess the utility and effectiveness of these candidate proteins. Full article
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Review

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12 pages, 561 KiB  
Review
Pharmacological Modulation of Mutant TP53 with Oncotargets Against Esophageal Cancer and Therapy Resistance
by Pei-I Lin, Yu-Cheng Lee, I-Hung Chen and Hsien-Hui Chung
Biomedicines 2025, 13(2), 450; https://doi.org/10.3390/biomedicines13020450 - 12 Feb 2025
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Abstract
The prevalence and deaths from esophageal cancer (EC) have recently increased. Although therapeutic strategies depend on the EC stage and recurrence, such as surgical intervention, chemotherapy, radiation therapy, chemoradiation therapy, targeted therapy, and immunotherapy, a more effective and novel treatment for EC is [...] Read more.
The prevalence and deaths from esophageal cancer (EC) have recently increased. Although therapeutic strategies depend on the EC stage and recurrence, such as surgical intervention, chemotherapy, radiation therapy, chemoradiation therapy, targeted therapy, and immunotherapy, a more effective and novel treatment for EC is still required. This review briefly describes and summarizes some insightful oncotargets involved in the metabolic modulation of EC, including (1) cancer stem cells (CSCs) for EC progression, poor prognosis, tumor recurrence, and therapy resistance; (2) retinoic acid receptors (RARs) for esophageal carcinogenesis and regeneration; (3) phosphofructokinase (PFK) for EC-reprogrammed glycolysis; (4) lactate dehydrogenase (LDH) as an EC peripheral blood biomarker; and (5) hypoxia-inducible factor-1 alpha (HIF-1α) for the tumor microenvironment under hypoxic conditions. Moreover, the aforementioned oncotargets can be modulated by mutant TP53 and have their own features in the carcinogenesis, differentiation, proliferation, and metastasis of EC. Thus, the clarification of pharmacological mechanisms regarding the interaction between mutant TP53 and the abovementioned oncotargets could provide precise and perspective opinions for minimizing prediction errors, reducing therapy resistance, and developing novel drugs against EC. Full article
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