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Genetic mutations accumulated overtime could generate many growth and survival advantages for cancer cells, but these mutations also mark cancer cells as targets to be eliminated by the immune system. To evade immune surveillance, cancer cells adopted different intrinsic molecules to suppress immune response. PD-L1 is frequently overexpressed in many cancer cells, and its engagement with PD-1 on T cells diminishes the extent of cytotoxicity from the immune system. To resume immunity for fighting cancer, several therapeutic antibodies disrupting the PD-1/PD-L1 interaction have been introduced in clinical practice. However, their immunogenicity, low tissue penetrance, and high production costs rendered these antibodies beneficial to only a limited number of patients. PD-L1 dimer formation shields the interaction interface for PD-1 binding; hence, screening for small molecule compounds stabilizing the PD-L1 dimer may make immune therapy more effective and widely affordable. In the current study, 111 candidates were selected from over 180,000 natural compound structures through virtual screening, contact fingerprint analysis, and pharmacological property prediction. Twenty-two representative candidates were further evaluated in vitro. Two compounds were found capable of inhibiting the PD-1/PD-L1 interaction and promoting PD-L1 dimer formation. Further structure optimization and clinical development of these lead inhibitors will eventually lead to more effective and affordable immunotherapeutic drugs for cancer patients.
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http://dx.doi.org/10.3390/molecules25225293 | DOI Listing |
Biomaterials
September 2025
Key Laboratory of Biopharmaceutical Preparation and Delivery, Institute of Process Engineering, Chinese Academy of Sciences, Beijing, 100190, PR China; University of Chinese Academy of Sciences, Beijing, 100049, PR China. Electronic address:
The stimulator of interferon genes (STING) pathway represents a promising target in cancer immunotherapy. However, the clinical translation of cyclic dinucleotide (CDN)-based STING agonists remains hindered by insufficient formation of functional CDN-STING complexes. This critical bottleneck arises from two interdependent barriers: inefficient cytosolic CDN delivery and tumor-specific STING silencing via DNA methyltransferase-mediated promoter hypermethylation.
View Article and Find Full Text PDFJMIR Res Protoc
September 2025
Department of Medical Oncology, Early Phase Unit, Georges-François Leclerc Centre, Dijon, France.
Background: Sarcomas are rare cancer with a heterogeneous group of tumors. They affect both genders across all age groups and present significant heterogeneity, with more than 70 histological subtypes. Despite tailored treatments, the high metastatic potential of sarcomas remains a major factor in poor patient survival, as metastasis is often the leading cause of death.
View Article and Find Full Text PDFBlood Adv
September 2025
BC Cancer, Vancouver, British Columbia, Canada.
Classical Hodgkin Lymphoma (CHL) is characterized by a complex tumor microenvironment (TME) that supports disease progression. While immune cell recruitment by Hodgkin and Reed-Sternberg (HRS) cells is well-documented, the role of non-malignant B cells in relapse remains unclear. Using single-cell RNA sequencing (scRNA-seq) on paired diagnostic and relapsed CHL samples, we identified distinct shifts in B-cell populations, particularly an enrichment of naïve B cells and a reduction of memory B cells in early-relapse compared to late-relapse and newly diagnosed CHL.
View Article and Find Full Text PDFPLoS Comput Biol
September 2025
Department of Evolutionary Biology and Environmental Studies, University of Zurich, Zurich, Switzerland.
Ubiquity of cancer across the tree of life yields opportunities to understand variation in cancer defences across species. Peto's paradox, the finding that large-bodied species do not suffer from more cancer despite having more cells at risk of oncogenic mutations compared to small species, can be explained if large size selects for better cancer defences. Since birds live longer than non-flying mammals of equivalent size, and are descendants of moderate-sized dinosaurs, we ask whether ancestral cancer defences are retained if body size shrinks in a lineage.
View Article and Find Full Text PDFPLoS One
September 2025
Institute of Computational Science and Technology, Guangzhou University, Guangzhou, China.
MicroRNAs (miRNAs) are critical regulators of gene expression in cancer biology, yet their spatial dynamics within tumor microenvironments (TMEs) remain underexplored due to technical limitations in current spatial transcriptomics (ST) technologies. To address this gap, we present STmiR, a novel XGBoost-based framework for spatially resolved miRNA activity prediction. STmiR integrates bulk RNA-seq data (TCGA and CCLE) with spatial transcriptomics profiles to model nonlinear miRNA-mRNA interactions, achieving high predictive accuracy (Spearman's ρ > 0.
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