98%
921
2 minutes
20
Interferons (IFNs) are indispensable innate antiviral cytokines that orchestrate the vertebrate immune response against viral incursions. Nearly every cell possesses the remarkable ability to release IFNs upon detecting viral threats, triggering a robust signaling cascade that alerts neighboring cells and halts viral propagation via paracrine communication. The intricate influence of IFNs is mediated by an extensive network of proteins activated through the Jak-STAT pathways, facilitating the swift transcription of over 300 interferon-stimulated genes (ISGs) that fortify cellular defenses against replication. However, the cunning nature of viruses has led to the evolution of sophisticated evasion strategies, notably through the manipulation of host microRNAs (miRNAs) that disrupt vital components of the IFN signaling machinery. This review delves into the intricate interplay between viral infections and both host- and viral-derived miRNAs, exploring their potent roles in modulating RIG-I-like receptors, Toll-like receptors, IFN receptors, and the JAK/STAT pathway, ultimately shaping the landscape of antiviral immunity.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101089 | PMC |
http://dx.doi.org/10.3389/fimmu.2025.1567459 | DOI Listing |
Biomed J
September 2025
Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University. Electronic address:
Background: Lung cancer is the leading cause of cancer-related mortality worldwide. Although immune checkpoint inhibitors (ICIs), chemotherapy, and molecular targeted therapies have improved survival rates, therapeutic resistance remains a major barrier to curative outcomes. Recently, plasminogen activator inhibitor-1 (PAI-1) has been implicated in lung cancer progression and treatment resistance.
View Article and Find Full Text PDFJ Control Release
September 2025
Jiangsu Key Laboratory of Druggability of Biopharmaceuticals, Department of Pharmaceutics, China Pharmaceutical University, 639 Longmian Avenue, Nanjing 211198, PR China. Electronic address:
The tumor microenvironment (TME) is a complex and dynamic ecosystem that significantly influences tumor progression, immune modulation, and therapeutic response. A key component of the TME is the tumor-associated microbiota, which has emerged as an important player in cancer biology, affecting tumor metastasis, immune evasion, and resistance to treatments. The recent advent of high-throughput sequencing technologies has revolutionized our understanding of the microbiome, revealing distinct microbial communities across various tumor types.
View Article and Find Full Text PDFEur J Pharm Sci
September 2025
Department of Neurology, Massachusetts General Hospital, Boston, MA, 02129, USA; Neuroscience Program, Harvard Medical School, Boston, MA, 02129, USA. Electronic address:
Glioblastoma (GBM) is a highly malignant brain tumor with limited treatment options and poor prognosis. GBM exhibits resistance to conventional therapies, including temozolomide (TMZ), radiotherapy, and immunotherapy, partly due to immunosuppressive mechanisms such as programmed death-ligand 1 (PD-L1) overexpression. To address these challenges, we developed TMZ-loaded nanostructured lipid carriers (NLCs) conjugated with anti-PD-L1 single-chain variable fragments (scFv) for dual chemo-immunotherapy.
View Article and Find Full Text PDFBiochim Biophys Acta Rev Cancer
September 2025
Department of Neurosurgery, The First Hospital of China Medical University, Nanjing Street 155, Heping District, Shenyang 110001, PR China. Electronic address:
The complement system, a cornerstone of innate immunity, plays pivotal roles in both defense and pathology, particularly through its anaphylatoxins, C3a and C5a. These small peptides, generated during complement activation, not only mediate pro-inflammatory responses but also contribute to the progression of various cancers by modulating the tumor microenvironment (TME). Anaphylatoxins influence tumor cell proliferation, epithelial-mesenchymal transition, angiogenesis, immune suppression, and therapy resistance via key signaling pathways such as PI3K/AKT, MEK/ERK, and p38 MAPK.
View Article and Find Full Text PDFCancer Genet
August 2025
National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, India. Electronic address:
Cancer is a complex and heterogeneous disease characterized by the accumulation of genetic and epigenetic alterations that drive uncontrolled cellular proliferation and survival. This review provides a comprehensive overview of key cancer driver genes, including oncogenes such as KRAS and PIK3CA, as well as tumor suppressor genes like TP53, PTEN, and CDKN2A, highlighting their molecular mechanisms and roles across various types of cancer. Leveraging insights from large-scale cancer genome initiatives and whole-genome sequencing, we examine the landscape of somatic mutations and their association with hallmark cancer pathways, including cell cycle regulation, apoptosis, metabolic reprogramming, and immune evasion.
View Article and Find Full Text PDF