Jan 2026· BioMed Research International· Vol 2026· 0 citations· 76 references
Medicine
TL;DR
An overview of studies on SNHG18 is presented, emphasizing its biological functions and its potential as a promising biomarker for the diagnosis and treatment of diverse cancer types.
Abstract
Numerous recent studies have shown that long noncoding RNAs (lncRNAs) play a crucial role in the development of diverse cancers. Small nucleolar RNA host gene 18 (SNHG18) is a cancer‐related lncRNA in the SNHG family, whose expression is dysregulated in various tumors and acts as either an oncogenic or tumor‐suppressive factor. Several studies have demonstrated that SNHG18 exhibits dual effects in various cancers. The role of this molecule is context‐dependent, acting as a tumor suppressor in certain cancers while exhibiting oncogenic properties in others. The expression of SNHG18 is cancer‐type specific: it is upregulated in glioma, multiple myeloma, and lung cancer, but downregulated in bladder and hepatocellular cancer. Clinical studies have also found a correlation between SNHG18 expression and prognosis in different cancers. We present an overview of studies on SNHG18, emphasizing its biological functions and its potential as a promising biomarker for the diagnosis and treatment of diverse cancer types.
Long noncoding RNAs (lncRNAs) are emerging as critical regulators of tumor initiation and progression through transcriptional and posttranscriptional mechanisms. UPK1A antisense RNA 1 (UPK1A-AS1), a cancer‐associated lncRNA, has been reported to participate in oncogenic processes; however, its overall landscape across human malignancies and its biological role in therapy resistance remain poorly understood. Given the increasing importance of identifying functional lncRNAs with prognostic and therapeutic potential, this study presents a comprehensive multiomics characterization of UPK1A-AS1 and its experimental validation in hepatocellular carcinoma (HCC). We integrated datasets from The Cancer Genome Atlas (TCGA), the Genotype‐Tissue Expression Project (GTEx), the cancer immunology data engine (CIDE), and the cBioPortal for cancer genomics (cBioPortal) to systematically assess its expression pattern, genomic alterations, clinical significance, and immunological associations. Our analyses revealed that UPK1A-AS1 is significantly upregulated in multiple tumor types, with copy‐number amplification as the predominant genomic alteration driving its overexpression. Elevated UPK1A-AS1 expression was correlated with advanced disease stage, poor differentiation, immune exclusion, and unfavorable prognosis, supporting its potential as a cancer type‐dependent biomarker. In parallel, functional studies demonstrated that hypoxia transcriptionally induces UPK1A-AS1 in HCC, where it promotes sorafenib resistance by suppressing apoptosis. Silencing UPK1A-AS1 restored apoptotic and enhanced sorafenib efficacy both in vitro and in vivo. Collectively, our findings suggest that UPK1A-AS1 is a hypoxia‐inducible oncogenic lncRNA that plays dual roles in cancer, with cancer type‐dependent associations with progression and immune modulation across malignancies and mechanistically mediating hypoxia‐associated drug resistance in HCC.
Ze-Kai Li, Min Luo, Shu-Sen Fang et al.· Analytical Cellular Patholog...· 0 citations
A mechanism-driven approach is adopted to systematically examine SNHG1 dysregulation and its roles in cancer, which complements existing literature and provides a clear framework for future SNHG1 research.
Hao Zhou, Jian-Lin Zhou, Lin Zhou· Biocell (Mendoza)· 0 citations
Brain cancers are among the most aggressive malignancies associated with significant global morbidity and mortality. Cancer immunotherapy has emerged as a promising novel approach for the treatment of brain cancer through regulating the PD-1/PD-L1 signaling and disrupting tumor immune escape. Several targeted therapies have been developed to inhibit the PD-1/PD‑L1 route, but reduced therapeutic responses and drug resistance remain a major challenge that needs to be addressed. Notably, non-coding RNAs (ncRNAs), which include microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs), exert crucial effects on cell proliferation, invasion, and immune escape in the tumor microenvironment (TME). It has been shown that ncRNAs reduce tumor formation and progression by regulating the PD-1/PD-L1 pathway and by down-regulating key transcription factors, including NF-κB, JAK, and STAT. Therefore, identifying novel regulatory ncRNAs and their associated target genes offers promising opportunities for developing therapeutic interventions against brain cancer. This review highlights recent advances in understanding the regulatory role of ncRNAs on the PD-1/ PD-L1 pathway in brain cancer tumorigenesis.
Reihane Behnam-Rassouli, Farzaneh Entezari, Majid Ghorbanzadeh et al.· Iranian Journal of Basic Med...· 0 citations
Background Aberrant expression of miR-326, a microRNA involved in tumor suppression, has been associated with a broad range of diseases, including cancer and autoimmune disorders. The NOB1 gene (NIN One Binding Protein 1 Homolog) is a critical component that plays a pivotal role in the biogenesis and proper functioning of the 26S proteasome. Researchers have found that miR-326 acts as a regulator of NOB1 expression by targeting its mRNA, ultimately leading to a decrease in NOB1 protein translation. Methods This study seeks to assess the expression levels of miR-326 and NOB1 genes within breast cancer (BC) tumor tissue, along with an examination of their potential correlation, in comparison to both normal‐adjacent (NATs) and healthy tissues. Forty‐one BC, NATs, and eight healthy breast tissues were used. To compare the expression profiles of miR-326 and NOB1 in different tissue groups, including BC, NATs, and healthy tissues, quantitative real‐time PCR (qRT‐PCR) was used. Results miR-326 expression was significantly decreased in BC tissues compared with NATs (p < 0.0001) and healthy tissues (p < 0.0001). The expression levels of NOB1 were increased significantly in BC tissue compared with NATs (p < 0.0001) and healthy tissues (p < 0.0001). A significant negative correlation was observed between miR-326 and NOB1 expression (p < 0.005). Receiver‐operating characteristic (ROC) curve analysis showed that AUC = 0.8349 and AUC = 0.7 are for miR-326 and NOB1, respectively. Conclusion Decreasing the expression of miR-326 in patients with BC may affect its target gene (NOB1) and probably lead to an increase in the expression of the NOB1 gene. This negative correlation suggests a potential regulatory role for miR-326 in controlling NOB1 expression. Our findings demonstrate that dysregulation of the miR-326 and NOB1 expression levels may contribute to BC development and progression, indicating the potential of these two genes as biomarkers for diagnostic and therapeutic approaches in BC.
Milad Noei, F. Forouzesh, F. Abbasvandi et al.· International Journal of Bre...· 0 citations
Abstract Lung cancer is currently the leading cause of cancer-related deaths worldwide. Approximately 85% of lung cancer patients have non-small cell lung cancer (NSCLC), and >50% of these patients present with metastasis at their initial diagnosis. Despite advances in our understanding of lung cancer oncogenesis, the mechanism by which lung cancer becomes aggressive and leads to patient death is still poorly characterized. We found that long noncoding RNA RNA-associated with metastasis 11 (RAMS11) (LINC01564) is significantly upregulated in lung cancer patients compared to healthy patients. Here, we demonstrate that RAMS11 is critical for NSCLC tumor progression by regulating expression of NOTCH3, a key driver of tumorigenic potential. Mechanistically, RAMS11 is essential for NRF2 chromatin binding and the associated deposition of the active enhancer mark, H3K27ac, at the NOTCH3 enhancer region. Functional analysis revealed RAMS11–NRF2-dependent activation of NOTCH3 signaling enforces a tumor-initiating capacity, characterized by enhanced self-renewal capabilities and tumor initiation ability, thereby supporting malignant proliferation. Moreover, disruption of RAMS11 signaling markedly suppressed tumorigenic growth and sensitized NSCLC cells to cisplatin-induced apoptosis, uncovering a potential therapeutic vulnerability to more effectively target NSCLC patients. Collectively, these findings reveal a previously unknown role of RAMS11 in NSCLC progression and chemotherapy resistance.
Gejae G. L. Jeffers, Y. Kim, Nicole M. White et al.· NAR Cancer· 0 citations
This computational study identifies several candidate lncRNAs associated with clinical outcomes in breast cancer, which should be interpreted as preliminary candidates, which require future validation and functional studies to determine their biological roles and evaluate their potential as prognostic biomarkers.
M. Acencio, Xin-Hui Wang, Flavia R. Rotea Mangone et al.· International Journal of Mol...· 0 citations
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