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Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition)
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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 7357

Special Issue Editors

Dr. Letizia Polito

E-Mail Website
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
Dr. Ewa Gajda

E-Mail Website
Guest Editor
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

Manuscript Submission Information

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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. Biomedicines 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 2600 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 biology
  • experimental anticancer therapies
  • immunotherapy
  • immunotoxins
  • signalling pathways
  • targeted therapies

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Related Special Issue

Published Papers (7 papers)

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Research

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22 pages, 6165 KiB  
Article
Single-Cell Transcriptomic Analysis Unveils Key Regulators and Signaling Pathways in Lung Adenocarcinoma Progression
by Jialu Ma, Caleb McQuay, John Talburt, Amit K. Tiwari and Mary Qu Yang
Biomedicines 2025, 13(7), 1606; https://doi.org/10.3390/biomedicines13071606 - 30 Jun 2025
Viewed by 233
Abstract
Background: Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality despite advances in treatments, necessitating more effective therapeutic strategies. Single-cell RNA sequencing (scRNA-seq) technology has revolutionized our ability to dissect the cellular complexity of cancers, which is often obscured in conventional bulk [...] Read more.
Background: Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality despite advances in treatments, necessitating more effective therapeutic strategies. Single-cell RNA sequencing (scRNA-seq) technology has revolutionized our ability to dissect the cellular complexity of cancers, which is often obscured in conventional bulk transcriptomic experiments. Methods: In this study, we performed an integrative analysis of scRNA-seq data from multiple LUAD patient cohorts to investigate cell-type-specific transcriptomic changes across disease stages. Clustering, lineage trajectory analysis, and transcriptional regulatory network reconstruction were employed to identify stage-specific gene markers and their upstream regulators. Additionally, we constructed intercellular communication networks to evaluate signaling changes within the tumor microenvironment (TME) during LUAD progression. Results: Our analysis revealed that epithelial cells from stage IV tumors exhibited a distinct transcriptional profile compared to earlier stages, a separation not observed in immune or stromal cell populations. We identified a panel of gene markers that differentiated epithelial cells across disease stages and effectively stratified patients into subgroups with distinct survival outcomes and TME compositions. Regulatory network analysis uncovered key transcription factors, including ATF3, ATF4, HSF1, KLF4, and NFIC, as potential upstream regulators of these stage-specific genes. Moreover, cell–cell communication analysis revealed a significant increase in signaling originating from epithelial cells and a concomitant decrease in immune-derived signals in late-stage LUAD. We identified several signaling pathways enriched in stage-specific crosstalk, including Wnt, PTN, and PDGF pathways, which may play critical roles in LUAD progression. Conclusions: This study provides a comprehensive single-cell resolution map of LUAD progression, highlighting epithelial-driven regulatory programs and dynamic intercellular communication within the TME. Our findings uncover novel molecular markers and regulatory mechanisms with potential prognostic and therapeutic value for more precise treatment. Full article
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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15 pages, 1631 KiB  
Article
Altered Expression of NK Receptors in Racially/Ethnically Diverse and Risk-of-Relapse Pediatric Acute Lymphoblastic Leukemia Patients
by Stephen Mathew, Roslin Jose George, Alexsis Garcia, Sheila Powers, Subhash Aryal and W. Paul Bowman
Biomedicines 2025, 13(6), 1412; https://doi.org/10.3390/biomedicines13061412 - 9 Jun 2025
Viewed by 443
Abstract
Background/Objectives: Acute Lymphoblastic Leukemia (ALL) is a cancer that predominantly affects white blood cells within the blood and bone marrow of adults and children. Currently, ALL is one of the most prevalent malignancies in pediatric patients and is most seen among Caucasian and [...] Read more.
Background/Objectives: Acute Lymphoblastic Leukemia (ALL) is a cancer that predominantly affects white blood cells within the blood and bone marrow of adults and children. Currently, ALL is one of the most prevalent malignancies in pediatric patients and is most seen among Caucasian and Hispanic descent, with lower incidence in African American children. The goal of the study was to investigate the expression of immune cell receptors in racial/ethnic populations and risk factors for relapse that could potentially influence the pediatric ALL outcomes. Methods: Twenty healthy subjects and forty-two pediatric ALL subjects were enrolled in the study and whole-blood was collected at diagnosis and post-chemotherapy, and the cell surface expression of various immune receptors, including 2B4, CS1, LLT1, Nkp30, and NKp46, was determined by flow cytometry. Results: Very high-risk and high-risk of relapse ALL subjects showed increased expression of LLT1 on NK cells, T cells, and monocytes at diagnosis compared to healthy subjects. CS1 was also significantly overexpressed on monocytes of very-high risk ALL subjects both at diagnosis and after the end of chemotherapy as compared to healthy subjects. Also, there was a significantly increased expression of NKp30 on T cells of Caucasians as compared to Hispanics and African Americans at diagnosis, and downregulation of CS1 and LLT1 on T cells of Caucasians post-induction chemotherapy. Conclusions: The altered expression of immune receptors in racial/ethnic and risk stratified groups may provide insights into the immune surveillance mediated by T cells and NK cells against pediatric ALL. Full article
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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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
Viewed by 689
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
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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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
Viewed by 691
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
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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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
Viewed by 1429
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
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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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 3 | Viewed by 1814
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
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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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
Viewed by 1164
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
(This article belongs to the Special Issue Advances in Cancer Biology and Experimental Anticancer Therapies (2nd Edition))
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