Submit to Special Issue Submit Abstract to Special Issue Review for CIMB Propose a Special Issue

Journal Menu

Journal Browser

Cancer-Associated Remodeling of Functional Molecular Pathways

Print Special Issue Flyer
Editor
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 2748

Share This Special Issue

Editor

Prof. Dr. Dumitru Iacobas

E-Mail Website
Guest Editor

Personalized Genomics Laboratory, Undergraduate Medical Academy, Prairie View A&M University, Prairie View, TX 77446, USA
Interests: cancer therapy; cancer biomarker; neurogenomics; systems biology; intercellular communication; neurotransmission
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancerization has dramatic consequences for the life of affected cells and their integration in multi-cellular tissue. Compared to their normal counterparts, cancer cells exhibit an enlarged and spherically imperfect nuclear shape with prominent nucleoli and coarse chromatin, reduced and basophilic cytoplasm, poorly developed Golgi apparatus, smaller mitochondria, reduced programmed death, and uncontrolled proliferation. Their increased ability to invade surrounding tissues comes from changes in the composition and organization of microfilaments, intermediate filaments, and microtubules. There is increasing evidence of substantial cancer-related alterations to metabolism, genetic and environmental information processing, most of the major cellular processes, and the physiology of several organismal systems. However, despite decades of research and innumerable publications, both the dynamic remodeling of the functional pathways and the molecular mechanisms responsible for cancer development are still not completely understood.

This Special Issue welcomes both experimental and review papers of the remodeling of major cellular and organismal functional pathways at the transcriptomic and proteomic levels.

Prof. Dr. Dumitru A. Iacobas
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

metabolism alteration
alteration of genetic information processing
alteration of environmental information processing
alterations of cellular processes
alterations of organismal systems

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (5 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

23 pages, 5121 KB

Open AccessArticle

Multiscale Transcriptomic and Molecular Modeling Analyses Suggest DCPMU-Associated Epithelial Remodeling and Tumor Microenvironment Perturbation in Prostate Cancer

by Jianhao Lin, Dajun Fang, Li Ding and Deqi Su

Curr. Issues Mol. Biol. 2026, 48(9), 935; https://doi.org/10.3390/cimb48090935 - 13 Sep 2026

Viewed by 133

Abstract

DCPMU, a major demethylated metabolite of diuron, is an environmentally persistent contaminant with potential endocrine-disrupting and carcinogenic relevance, yet its mechanistic association with prostate cancer remains unclear. This study investigated DCPMU-related mechanisms in prostate cancer by integrating network toxicology, molecular modeling, bulk transcriptomics, single-cell and spatial transcriptomics, and virtual perturbation analysis. Differentially expressed genes from TCGA-PRAD were intersected with DCPMU-associated and prostate cancer-related targets. Functional enrichment, machine learning screening, and external GEO validation identified seven candidate hub genes: APOBEC3G, SCGB1A1, PTGS1, CA12, CES1, FOLH1, and NOS1. Molecular docking showed favorable DCPMU binding to these proteins, and molecular dynamics simulations further supported stable interactions with PTGS1, CA12, CES1, and FOLH1. Single-cell analysis of GSE141445 revealed cell-type-specific expression, with FOLH1 and CA12 enriched in epithelial cells, CES1 in fibroblasts, and PTGS1 in mast cells. Spatial transcriptomics from GSE181294 showed tumor-enriched FOLH1 expression and increased Core4 module activity in malignant regions. Virtual knockout analysis suggested that FOLH1 perturbation was associated with predicted downstream transcriptional changes, with PTGS1 showing marked perturbation responsiveness. Overall, our integrative analyses suggest that DCPMU exposure is associated with epithelial malignancy, inflammatory metabolism, xenobiotic handling, and tumor-microenvironment remodeling, particularly within malignant epithelial niches. These hypothesis-generating findings require experimental validation to establish any causal role in prostate cancer progression. Full article

(This article belongs to the Special Issue Cancer-Associated Remodeling of Functional Molecular Pathways)

► Show Figures

Figure 1

22 pages, 7650 KB

Open AccessArticle

The Oncogenic Role of Prostate Stem Cell Antigen (PSCA) in Colorectal Cancer: Implications for Targeted Therapy

by Jinyue Duan, Yi Wang, Qisen Li, Yujue Wang, Jinrui Liu, Yi Qi, Yichi Zhang, Changhao Fu, Zhongyi Cong, Can Wang and Manman Su

Curr. Issues Mol. Biol. 2026, 48(7), 737; https://doi.org/10.3390/cimb48070737 - 20 Jul 2026

Viewed by 663

Abstract

Prostate stem cell antigen (PSCA), a pivotal member of the lymphocyte antigen-6 (Ly6) protein family, has been implicated in the tumorigenesis and neoplastic progression of diverse cancer types. In this study, we conducted a thorough investigation into the role of PSCA in the development of colorectal cancer (CRC). Survival analysis based on The Cancer Genome Atlas (TCGA) dataset demonstrated that elevated expression of PSCA was tightly correlated with unfavorable overall survival, inferior relapse-free survival, and worse post-progression survival among CRC patients. Additionally, PSCA exhibited significantly higher expression levels in colorectal cancer stem cell (CRC-SCs) relative to CRC cell lines. Loss-of-function assays using small interfering RNA (siRNA)-mediated silencing were performed to evaluate the effects of PSCA downregulation on the stemness properties of CRC-SCs, including proliferative capacity, invasive potential, and apoptotic rate, which were assessed by MTS assay, transwell invasion assay, and flow cytometry analysis, respectively. The results showed that silencing PSCA markedly suppressed the proliferation and invasion of CRC-SCs, while significantly promoting cellular apoptosis. RNA sequencing was performed to identify differentially expressed genes (DEGs) in the PSCA knockdown group compared to the negative control group. Follow-up analyses using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) indicated that these DEGs were significantly enriched in the cell-substrate adherens junction term and the mitogen-activated protein kinase 9MAPK signaling pathway. Moreover, PSCA silencing substantially reduced the phosphorylation levels of the core MAPK signaling constituents, pBRAF and pERK1/2; conversely, PSCA overexpression prominently upregulated the expression of pBRAF and pERK1/2. In nude mice with CRC-SCs cancer xenograft tumors, treatment with PSCA siRNA significantly decreased tumor volume and weight, while also notably extending the survival time of the tumor-bearing mice compared to the control group. Collectively, these findings confirm that PSCA plays a critical oncogenic role in CRC cancer growth and malignant progression, suggesting its potential as a novel and promising therapeutic target for CRC. Full article

(This article belongs to the Special Issue Cancer-Associated Remodeling of Functional Molecular Pathways)

► Show Figures

Figure 1

18 pages, 6371 KB

Open AccessArticle

IGF2BP2 Promotes Esophageal Squamous-Cell Carcinoma Progression with Potential Involvement of PI3K/AKT Signaling

by Xiaohang Gao, Minghui Yang, Jing Yang, Yunpeng Zhong, Chao Ma, Guoliang Xu, Lin Zhang and Rong Zhang

Curr. Issues Mol. Biol. 2026, 48(7), 726; https://doi.org/10.3390/cimb48070726 - 16 Jul 2026

Viewed by 535

Abstract

Esophageal squamous-cell carcinoma (ESCC) remains a highly lethal malignancy, with long-term survival still unsatisfactory and an urgent need for clinically relevant molecular targets. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is an RNA-binding protein with oncogenic activity in several tumor types, but the signaling events associated with its role in ESCC have not been fully defined. IGF2BP2 expression was examined in paired ESCC and adjacent non-tumor tissues by immunohistochemistry (10 paired samples) and qRT-PCR (16 paired samples). Associations with clinicopathological variables were evaluated in 108 TCGA ESCC cases. Stable lentiviral shRNA-mediated knockdown was established in KYSE30 and ECA109 cells. CCK-8, colony formation, Transwell, EdU, and flow cytometry assays were used to assess proliferation, clonogenic growth, migration, invasion, apoptosis, and cell-cycle distribution. EMT-associated markers were measured by Western blotting and qRT-PCR. RNA sequencing, KEGG enrichment analysis, and rescue experiments using the AKT activator SC79 were performed to explore downstream signaling. IGF2BP2 was upregulated in ESCC tissues at both the transcript and protein levels, and higher expression was associated with unfavorable clinicopathological characteristics. Silencing IGF2BP2 reduced proliferation, colony formation, migration, and invasion, promoted G0/G1 cell-cycle arrest, and increased apoptosis. EMT-associated marker analysis showed decreased Snail and increased Slug expression, indicating that these changes require cautious interpretation. RNA sequencing and KEGG analysis suggested enrichment of PI3K/AKT-related signaling after IGF2BP2 knockdown. IGF2BP2 silencing decreased PI3K and p-PI3K levels, whereas SC79 partly restored migratory and invasive capacities. IGF2BP2 contributes to malignant phenotypes in ESCC and may be associated with PI3K/AKT-related signaling. These findings indicate that IGF2BP2 is a candidate biomarker and potential therapeutic target, although further mechanistic and pharmacologic validation is required. Full article

(This article belongs to the Special Issue Cancer-Associated Remodeling of Functional Molecular Pathways)

► Show Figures

Figure 1

18 pages, 5370 KB

Open AccessArticle

5-ALA Photodynamic Therapy Induces Competing Death and Survival Pathways in Glioblastoma Cells

by Julia Inglot, Dorota Bartusik-Aebisher, Joanna Katarzyna Strzelczyk, Angelika Myśliwiec, Klaudia Dynarowicz, Dorota Hudy, Oliwia Trzaskoś, Jacek Tabarkiewicz, Aleksandra Kawczyk-Krupka, Magdalena Moś and David Aebisher

Curr. Issues Mol. Biol. 2026, 48(7), 689; https://doi.org/10.3390/cimb48070689 - 3 Jul 2026

Viewed by 522

Abstract

Glioblastoma multiforme (GBM), isocitrate dehydrogenase (IDH)-wildtype, is the most aggressive primary malignant tumor of the central nervous system, characterized by poor prognosis and high recurrence rates despite standard multimodal treatment. This study investigates the molecular response of glioblastoma cells to 5-aminolevulinic acid (5-ALA)-based photodynamic therapy (PDT), focusing on gene expression changes associated with apoptosis, ferroptosis, and oxidative stress. Human glioblastoma T98G cells were treated with 5-ALA followed by light irradiation, and gene expression was analyzed using RT-qPCR. PDT induced moderate upregulation of pro-apoptotic genes (BAX, CASP3, FAS) alongside increased expression of the anti-apoptotic gene BCL2, indicating simultaneous activation of cell death and survival pathways. Ferroptosis-related genes showed mixed responses, with slight upregulation of ACSL4 and downregulation of GPX4, suggesting increased susceptibility to lipid peroxidation. The most significant change was observed in GCH1 expression, reflecting activation of oxidative stress response mechanisms. However, none of the observed changes reached statistical significance, likely due to the limited sample size. These findings demonstrate that PDT induces a complex and dual biological response in glioblastoma cells, involving both cytotoxic and adaptive mechanisms. This may limit therapeutic efficacy and contribute to treatment resistance. The results support the rationale for combining PDT with targeted molecular therapies aimed at inhibiting antioxidant defenses and anti-apoptotic pathways. Additionally, personalized therapeutic strategies based on tumor molecular profiles may enhance treatment outcomes. Further studies with larger sample sizes and functional validation are required to confirm these preliminary observations. Full article

(This article belongs to the Special Issue Cancer-Associated Remodeling of Functional Molecular Pathways)

► Show Figures

Figure 1

20 pages, 3778 KB

Open AccessArticle

Oxidative DNA Damage as an Integrative Marker of Redox Dysfunction Associated with Doxorubicin-Induced Cardiotoxicity in Pediatric Leukemia

by Jesús Alonso Gándara-Mireles, Elio Aarón Reyes Espinoza, Verónica Loera-Castañeda, Lourdes Patricia Córdova Hurtado, Antonio Emilio González Font, Julio Cesar Grijalva Ávila, Ignacio Villanueva Fierro, Ismael Lares-Asseff, Cynthia Mora Muñoz, Gabriela Velasco Villa, Hugo Payán Gándara, Leslie Patrón-Romero and Horacio Almanza-Reyes

Curr. Issues Mol. Biol. 2026, 48(6), 577; https://doi.org/10.3390/cimb48060577 - 1 Jun 2026

Viewed by 512

Abstract

Doxorubicin (Dox) is a cornerstone in the treatment of pediatric acute lymphoblastic leukemia (ALL), but its use is limited by dose-dependent cardiotoxicity. Oxidative stress, arising from mitochondrial dysfunction, enzymatic generation of reactive oxygen species, and cardiotoxic metabolites, has been implicated as a central mechanism, with interindividual variability partly influenced by genetic factors. This study evaluated oxidative DNA damage 8-hydroxy-2′-deoxyguanosine (8-OHdG) as an integrative marker of redox-related pathways in Dox-induced cardiotoxicity. In a prospective case–control study, 93 pediatric patients with ALL treated with Dox and 63 controls were included. Cardiotoxicity was assessed by serial echocardiography, and 8-OHdG levels were measured by ELISA. Genotyping of ABCC1 rs3743527, NCF4 rs1883112, and CBR3 rs1056892 was performed, and multivariable analyses were conducted. Dox-treated patients showed higher 8-OHdG levels than controls, and patients with cardiotoxicity (n = 11) had higher levels than those without. A higher frequency and severity of cardiotoxicity was observed in female patients, although this finding should be interpreted cautiously. Although allele frequencies did not reach statistical significance, distinct distribution patterns were observed between groups. These findings suggest that 8-OHdG may function as an integrative marker of redox dysfunction associated with Dox-induced cardiotoxicity. Full article

(This article belongs to the Special Issue Cancer-Associated Remodeling of Functional Molecular Pathways)

► Show Figures

Journal Menu

Journal Browser

Cancer-Associated Remodeling of Functional Molecular Pathways

Share This Special Issue

Editor

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (5 papers)

Research

Further Information

Guidelines

MDPI Initiatives

Follow MDPI