Current Molecular Medicine - Volume 25, Issue 6, 2025

MicroRNAs (miRNAs) have emerged as crucial regulators of gene expression, playing pivotal roles in various biological processes, including cancer development and progression. Among them, miR-125b has garnered significant attention due to its multifaceted functional roles in human hepatocellular carcinoma (HCC). Extensive research has revealed that miR-125b plays a dual role in HCC, acting as both a tumor suppressor and an oncogene, depending on the context. As a tumor suppressor, miR-125b inhibits HCC by targeting key oncogenic pathways and genes involved in cell proliferation, migration, invasion, and angiogenesis. Its downregulation in HCC is frequently observed and correlates with aggressive tumor characteristics and poor prognosis. Conversely, miR-125b can also function as an oncogene in specific HCC subtypes or under certain conditions. It has been shown to promote HCC growth, metastasis, and therapeutic resistance by targeting tumor suppressor genes, modulating the epithelial-mesenchymal transition (EMT) process, and enhancing cancer stem cell-like properties. The upregulation of miR-125b in HCC has been associated with advanced disease stages and unfavorable clinical outcomes. Furthermore, a complex network of regulatory mechanisms influences the dysregulation of miR-125b expression in HCC. Understanding these regulatory mechanisms is crucial for deciphering the precise functional roles of miR-125b in HCC and exploring its potential as a diagnostic biomarker or therapeutic target. In the current review study, we comprehensively elucidated the diverse functional roles of miR-125b in HCC, providing a comprehensive overview of its regulatory mechanisms and impact on key cellular processes involved in HCC progression.

The human leukocyte antigen (HLA, also known as the major histocompatibility complex or MHC) system, is responsible for immune monitoring of the intracellular proteome of all nucleated cells. The presentation of antigen peptides separates malignant or infected cells from their healthy counterparts and forms aberrant cells tagged as the foundation for identification. Therefore, peptide-MHC molecules can give potential diagnostic targets for cancer or infection. TCR-like antibodies recognize specific peptides that bind to MHC molecules, allowing them to target Such inaccessible cytoplasmic or nuclear tumors or virus-associated antigens. It binds to MHC, presenting peptides found on the surface of target cells. These antibodies have shown promising clinical applications in diagnosing and imaging cancer and infected cells. This review presents the current situation of TCR-like antibodies and its prospects for application in the field of intracellular antigen diagnostics. It also lists the potential application targets of TCR, like antibodies in various disease diagnoses, providing valuable information for developing diagnostic reagents and selecting targets in the future.

As lncRNAs have increasingly been investigated, they are no longer simply defined as RNAs with no transcription capability. Studies have identified significant associations between the abnormal expression of lncRNAs and human diseases, particularly the mechanisms by which lncRNAs play a part in cancers, which are of considerable attention to researchers. As a result of the complex spatial structure, the mechanisms of interaction of lncRNAs in cancer cells are also complicated and diversified. Among a series of lncRNAs, TUG1, which is now considered to be a very high-value lncRNA, has recently been identified to express abnormally in some malignancies, leading to different alterations in cancer cells proliferation, migration, invasion, apoptosis, and drug resistance, and hence promoting or inhibiting cancer progression. Current studies have implicitly indicated that TUG1 can be used as a therapeutic target for human cancers. However, the biological functions of TUG1 have been studied for a short period of time, and the complete molecular mechanism still needs to be clarified. Accordingly, this review focuses on the principal molecular mechanisms of TUG1 in human cancers and the specific mechanisms of action in different cancer development processes based on existing studies.

miRNA-21 is regarded as both an abundant and highly conserved member of the microRNA (miRNA) family. It is expressed in virtually every cell and is responsible for critical regulatory actions that are important in health and disease. This microRNA has been shown to potentially have a role in the pathogenesis of several immune-related disorders, including autoimmune diseases, such as Multiple sclerosis and systemic lupus erythematosus, as two prominent examples of diseases that might be involved. In the current research, we looked at the role of miRNA-21, regarded as one of the most significant pathogenic miRNAs with a role in the development of autoimmune illness.

Glioblastoma multiforme [GBM] is a highly aggressive grade IV central nervous system tumor with a dismal prognosis. Factors such as late detection, treatment limitations due to its aggressive nature, and, notably, drug resistance significantly affect clinical outcomes. Despite the effectiveness of Temozolomide [TMZ], a potent chemotherapy agent, the development of drug resistance remains a major challenge. Given the poor survival rates and chemoresistance, there is an urgent need for novel treatment strategies. Non-coding RNAs, particularly microRNAs [miRNAs], offer a promising approach to GBM diagnosis and treatment. These small non-coding RNAs play crucial roles in tumor progression, either suppressing or promoting oncogenic characteristics. The phosphoinositide-3 kinase [PI3K]/AKT/ mTOR pathway, which regulates essential biological processes like proliferation and survival, is a key target of miRNAs in cancer. Studies have underscored the significance of PI3K/AKT/mTOR signaling in drug resistance development and its interplay with non-coding RNAs as mediators of tumorigenesis. This review aims to outline the involvement of PI3K/AKT/mTOR signaling in miRNA modulation and strategies to overcome chemoresistance in GBM.

Interferon epsilon (IFN-ε) belongs to the type I IFN group and exhibits various biological properties. IFN-ε exhibits different regulation mechanisms and expression via other type I IFNs. Its hormonal regulation suggests that this INF can have different functions and pathways from other type I IFNs. Although IFN-ε exhibits lower antiproliferative, anti-tumor, and antiviral activities compared to IFN-α, it has been identified to contribute to mucosal immunity, combat bacterial infections, and aid in the prevention of specific sexually transmitted diseases, such as HIV, Zika virus, etc. IFN-α and IFN-β with their well-established properties have been a research hotspot for many years; nevertheless, IFN-ε, whose unique roles are only now beginning to emerge, may be an intriguing subject for future study. This review focuses on the known activity of IFN-ε in certain cancers, pregnancy, autoimmune diseases, bacterial infections, and viruses. The aim of this paper is to enhance the understanding of the potential efficacy of IFN-ε treatment in the future.

Subarachnoid hemorrhage is a serious subtype of stroke with high mortality and disability. The rupture of intracranial aneurysms is the main cause. However, in recent years, with the popularization of CT, MRI, and cerebral angiography, the detection rate of unruptured aneurysms has increased, and the incidence of aneurysm rupture and hemorrhage has gradually decreased. However, there are still some patients who fail to detect aneurysms in time and receive treatment, resulting in the occurrence of aneurysm rupture and bleeding, and these patients usually have a poor prognosis and leave a lasting disability. Therefore, exploring the causes of aneurysm formation and the mechanism of brain injury caused by aneurysm rupture is of great significance for preventing aneurysm formation and improving the prognosis of patients. MicroRNAs (miRNAs) are highly conserved non-coding RNAs that can bind to the 3'UTR of target mRNAs to regulate gene expression. Studies have shown that miRNAs can affect the formation and rupture of intracranial aneurysms by participating in apoptosis, inflammation, phagocyte migration, and vascular smooth muscle cells (VSMCs) regulation, and regulate the damage of brain tissue after aneurysm rupture. They play a role in multiple pathophysiological processes of aneurysmal subarachnoid hemorrhage. This article reviews the role of miRNAs in different pathophysiological stages of aneurysmal subarachnoid hemorrhage (aSAH). We further described the research progress of miRNAs as biomarkers for the diagnosis and prognosis of aSAH and discussed their application prospects in the prevention and treatment of aSAH.