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Cancer Immunology: Molecular Tools, New Therapeutic Targets, Challenges, and Opportunities
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Cancer Immunology: Molecular Tools, New Therapeutic Targets, Challenges, and Opportunities

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: 30 June 2026 | Viewed by 2743

Special Issue Editor

Dr. Pablo C. Ortiz-Lazareno

E-Mail Website
Guest Editor
Instituto Mexicano del Seguro Social, Mexico City, Mexico
Interests: immune iesponse; cancer immunlogy; immune checkpoints

Special Issue Information

Dear Colleagues,

We are pleased to announce the call for papers for a Special Issue entitled “Cancer Immunology: Molecular Tools, New Therapeutic Targets, Challenges, and Opportunities”. This Special Issue highlights the latest research and innovative approaches in cancer immunology. We welcome both original research articles and reviews, with topics of interest including the following:

- Mechanisms of tumor immune evasion;
- Drug repurposing to enhance the immune response;
- Immune checkpoints in cancer;
- Bioinformatics tools and flow cytometry to analyze the immune response in cancer;
- Cancer immunotherapy;
- Biomarkers of immunotherapy response;
- New therapeutic targets to modulate the immune response in cancer;
- Omics sciences in the study of immune responses;
- MicroRNA in the interactions between immune cells and tumor cells;
- Microbiome and its role in the immune response in cancer.

This Special Issue seeks to compile articles on advances in cancer immunology that highlight the most relevant findings and help improve the understanding of the interactions between immune cells and cancer cells.

Dr. Pablo C. Ortiz-Lazareno
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-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 immunology
  • immune response
  • immune evasion
  • immune checkpoints
  • immune response

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

Published Papers (3 papers)

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Research

13 pages, 2522 KB  
Article
Nivolumab Enhances the Cytotoxicity of Chemotherapeutic Agents in A549 Lung Adenocarcinoma Cell Lines
by Nilgün Okşak and Oğur Karhan
Curr. Issues Mol. Biol. 2026, 48(5), 443; https://doi.org/10.3390/cimb48050443 (registering DOI) - 24 Apr 2026
Viewed by 61
Abstract
Background and Objectives: The integration of chemotherapy (ChT) and immune checkpoint inhibitors (ICIs) has become a standard approach in oncology. Although the addition of ICIs to double-agent ChT regimens has demonstrated clinical benefit in multiple studies, other trials have reported no significant improvement. [...] Read more.
Background and Objectives: The integration of chemotherapy (ChT) and immune checkpoint inhibitors (ICIs) has become a standard approach in oncology. Although the addition of ICIs to double-agent ChT regimens has demonstrated clinical benefit in multiple studies, other trials have reported no significant improvement. ChT is hypothesized to potentiate the effects of ICIs through multiple mechanisms, including tumor antigen release and modulation of the tumor microenvironment. This study aimed to evaluate whether nivolumab enhances the cytotoxic effects of cisplatin or paclitaxel in lung adenocarcinoma (A549) cell lines under immune-independent conditions. Materials and Methods: A549 lung alveolar carcinoma cell lines were treated with varying concentrations of nivolumab, cisplatin, and paclitaxel, individually and in combinations. Cytotoxicity and apoptosis were assessed using mitochondrial membrane potential analysis, cell viability assays, and morphological evaluation of cellular and nuclear alterations characteristic of apoptotic cell death. Results: Nivolumab alone exhibited no cytotoxic activity. The combination of cisplatin at its IC50 (half-maximal inhibitory concentration) (3 µg/mL) with 13 µg/mL nivolumab yielded the most pronounced cytotoxicity (89%) compared to cisplatin alone (49%, p < 0.001). Paclitaxel combined with nivolumab increased cytotoxicity to 69% versus 51% for paclitaxel alone (p < 0.05). The enhancement effect was greater with cisplatin than with paclitaxel. Notably, adding nivolumab to the cisplatin–paclitaxel combination reduced cytotoxicity from 73% to 64%. Mechanistic analysis revealed a significant reduction in Rhodamine 123 fluorescence intensity in drug-treated groups versus controls (p < 0.001), indicating loss of mitochondrial membrane potential, a hallmark of intrinsic apoptotic activation, suggesting apoptotic priming. Conclusions: Nivolumab potentiates the cytotoxic effects of cisplatin and paclitaxel in A549 lung adenocarcinoma cells, with a more pronounced effect observed in combination with cisplatin. This enhancement is associated with mitochondrial membrane potential loss, supporting mitochondrial apoptotic priming as a potential underlying mechanism of drug synergy. Full article
(This article belongs to the Special Issue Cancer Immunology: Molecular Tools, New Therapeutic Targets, Challenges, and Opportunities)
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24 pages, 4295 KB  
Article
Construction of a Prognostic Model for Lung Adenocarcinoma Based on Necrosis by Sodium Overload-Related Genes and Identification of DENND1C as a New Prognostic Marker
by Huijun Tan, Yang Zhang, Maoting Tan and Depeng Jiang
Curr. Issues Mol. Biol. 2026, 48(2), 146; https://doi.org/10.3390/cimb48020146 - 28 Jan 2026
Cited by 1 | Viewed by 604
Abstract
Background: Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality. The prognostic significance and functional role of sodium overload-induced necrosis (a novel form of regulated cell death driven by disrupted sodium homeostasis, hereafter abbreviated as NECSO) in LUAD are largely unexplored. Methods: [...] Read more.
Background: Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality. The prognostic significance and functional role of sodium overload-induced necrosis (a novel form of regulated cell death driven by disrupted sodium homeostasis, hereafter abbreviated as NECSO) in LUAD are largely unexplored. Methods: A prognostic model was constructed utilizing the NECSO key gene TRPM4 and analyzed through Cox, LASSO, and multivariate Cox regression analyses. LUAD patients were stratified into high- and low-risk groups. The model’s predictive performance was evaluated using time-dependent ROC curves and nomograms. Functional enrichment analysis elucidated underlying biological disparities. The tumor immune microenvironment was characterized using ESTIMATE, ssGSEA, CIBERSORTx, and TIDE algorithms, with results corrected for multiple testing. Drug sensitivity to chemotherapeutic and targeted agents was predicted. The functional role of a key gene, DENND1C, was validated in vitro. Its association with immunotherapy survival outcomes was assessed in a real-world cohort. Results: The NECSO-based prognostic signature demonstrated robust performance in risk stratification across training and independent validation cohorts. Patients in the high-risk group exhibited significantly shorter overall survival. Functional enrichment revealed associations with processes related to plasma membrane integrity, cell death, metabolism, and immune response. Multi-algorithm immunogenomic analyses consistently identified an immunosuppressive microenvironment in high-risk patients. The risk score was predictive of differential sensitivity to therapeutics, including taxanes and EGFR inhibitors. In vitro experiments confirmed DENND1C as a tumor suppressor, inhibiting LUAD cell proliferation, invasion, and migration. Furthermore, high DENND1C expression was associated with improved survival in patients receiving immunotherapy. Conclusions: This study establishes and validates a novel NECSO-based prognostic model for LUAD. DENND1C is identified as a key tumor suppressor and a potential biomarker for immunotherapy, offering insights for personalized treatment strategies in LUAD. Full article
(This article belongs to the Special Issue Cancer Immunology: Molecular Tools, New Therapeutic Targets, Challenges, and Opportunities)
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23 pages, 10293 KB  
Article
The SMIM25-COX-2 Axis Modulates the Immunosuppressive Tumor Microenvironment and Predicts Immunotherapy Response in Hepatocellular Carcinoma
by Zhenxing Wang, Xia Li, Shiyi Zhang, Jiamin Sun, Qinchen Lu, Yuting Tao, Shuang Liang, Xiuwan Lan, Jianhong Zhong and Qiuyan Wang
Curr. Issues Mol. Biol. 2025, 47(9), 693; https://doi.org/10.3390/cimb47090693 - 27 Aug 2025
Cited by 1 | Viewed by 1634
Abstract
Hepatocellular carcinoma (HCC) is a malignancy that is notorious for its dismal prognosis. Dysregulation of the tumor microenvironment (TME) in HCC has emerged as a key hallmark in determining disease progression and the response to immunotherapy. The aim of this study was to [...] Read more.
Hepatocellular carcinoma (HCC) is a malignancy that is notorious for its dismal prognosis. Dysregulation of the tumor microenvironment (TME) in HCC has emerged as a key hallmark in determining disease progression and the response to immunotherapy. The aim of this study was to identify novel TME regulators that contribute to therapeutic resistance, thus providing mechanistic insights for targeted interventions. The expression of SMIM25 was evaluated in the the Cancer Genome Atlas-Liver Hepatocellular Carcinoma(TCGA-LIHC) and Guangxi HCC cohorts, and its clinicopathological significance was assessed. RNA sequencing and bioinformatics analyses were performed to elucidate the potential impact of elevated SMIM25 levels. Immunohistochemistry (IHC) and single-cell mass cytometry (CyTOF) were employed to examine the cellular composition of the tumor microenvironment. The biological effects of SMIM25 on cell proliferation and migration were studied in vitro using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium Bromide(MTT) and wound healing assays, while its impact on tumor growth was evaluated in vivo in a nude mouse model. Transcriptomic and single-cell proteomic analyses were integrated to explore the mechanism by which SMIM25 affects the progression of HCC. The expression of SMIM25 was significantly up-regulated in both HCC tissues and cell lines (p < 0.05). RNA sequencing analyses revealed a significant positive correlation between SMIM25 expression and immunosuppression, and between SMIM25 expression and extracellular matrix(ECM)-related molecular features. Single-cell mass cytometry revealed two immunosuppressive cell clusters that were enriched in HCC patients with high SMIM25 expression. Moreover, SMIM25 was associated with immune exclusion and ECM remodeling signals in the TME of HCC. SMIM25 overexpression was associated with the expression of the tumor inflammatory marker cyclooxygenase-2(COX-2), and a COX-2 inhibitor could partially reverse the biological phenotype associated with SMIM25 expression in HCC cells (p < 0.05). Further transcriptome analysis in immunotherapy cohorts suggested the SMIM25-COX-2 axis might have predictive value for the response to immunotherapy. Our results suggest that SMIM25 may serve as a biomarker for the prognosis of HCC patients and may also be a predictive biomarker for the response to immunotherapy, enabling more precise and personalized HCC treatment. Full article
(This article belongs to the Special Issue Cancer Immunology: Molecular Tools, New Therapeutic Targets, Challenges, and Opportunities)
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