Elza Khusnutdinova

This review summarizes current data on the role of small nucleolar RNAs (snoRNAs) and their host genes (SNHGs) in the development of bladder cancer (BC). It examines snoRNA biogenesis, classical functions (rRNA modification), and non-canonical oncogenic mechanisms, including microRNA sponging, sdRNA production, and protein interactions (EZH2, DNMT3A, hnRNPK). The factors involved in the deregulation of snoRNA/SNHG expression during tumour transformation are described, such as amplifications, epigenetic changes, and transcriptional control (c-Myc, p53). Studies have shown that in BC, the majority of snoRNAs/SNHGs (SNHG1, SNHG3, SNHG6, SNHG13, SCARNA12) act as oncogenes, activating the PI3K/AKT, Wnt/β-catenin, NF-κB, and c-Myc pathways, thereby enhancing proliferation, EMT, invasion, and metastasis. Suppressor molecules (SNHG2/GAS5) are also discussed. The clinical potential of snoRNAs as prognostic signatures (SNORS), diagnostic biomarkers (SNHG1 in urine), and therapeutic targets (e.g., SNHG3) is analyzed. Thus, snoRNAs and SNHGs represent a promising class of molecules for the development of new diagnostic and therapeutic approaches for BC, although further investigation in prospective studies is required.

Prostate cancer (PrC) is one of the most common malignancies among men worldwide. However, the contribution of genetic variation in microRNA (miRNA) biogenesis pathway genes to PrC susceptibility remains poorly characterized in many ethnically diverse populations. We conducted a case–control study involving 532 PrC patients and 550 controls from the Volga-Ural region of Eurasia to evaluate the association of twenty-one single nucleotide polymorphisms (SNPs) with PrC risk using single-variant and polygenic approaches. Association analyses identified rs595055 in the AGO1 gene as significantly associated with PrC risk after correction for multiple testing. To evaluate the cumulative effect of genetic variation, weighted and unweighted polygenic risk scores (PRSs) were constructed. The weighted PRS was significantly associated with PrC risk (odds ratio per standard deviation increase = 1.63, 95% CI [1.43–1.85], P = 1.37 × 10⁻¹³), and demonstrated moderate discriminatory performance (AUC = 63.1%), outperforming the unweighted model. Individuals in the highest PRS quartile had approximately threefold higher odds of PrC than those in the lowest quartile. Combining the weighted PRS with prostate-specific antigen improved discrimination (AUC = 68.1%). These findings support the contribution of miRNA biogenesis pathway genes to PrC susceptibility and highlight the potential value of pathway-based polygenic risk stratification in understudied populations.

Renal cell carcinoma (RCC) remains a major challenge in modern oncological urology, owing to its high heterogeneity, latent clinical course, and intrinsic resistance to chemotherapy and radiotherapy. In recent decades, the paradigm of carcinogenesis research has shifted from a primary focus on protein-coding genes alone to a broader investigation of the non-coding part of the transcriptome. Within this framework, long non-coding RNAs (lncRNAs) have emerged as fundamental regulators of cellular homeostasis. Accumulating evidence indicates that lncRNAs are not merely ‘transcriptional noise’ but components of intricate regulatory networks governing epigenetic, transcriptional, and post-transcriptional processes. Here, we present a comprehensive systematic review of the current literature addressing the role of lncRNA in the molecular pathogenesis of RCC. We discuss the roles of these molecules in key oncogenic signaling pathways, including PI3K/AKT/mTOR, Wnt/β-catenin, and Notch, and their contributions to tumor metabolic plasticity. The paper summarizes data on the link between lncRNAs and novel forms of regulated cell death—ferroptosis, cuproptosis, and disulphidosis. Particular attention is paid to their role in mediating resistance to tyrosine kinase inhibitors and their potential utility as highly specific biomarkers. Collectively, this review provides an updated perspective on the contribution of lncRNAs to RCC pathogenesis and outlines strategic directions for future research to support the development of more precise approaches in personalized oncology.