Long non-coding RNA SNHG11 regulates the Wnt/β-catenin signaling pathway through rho/ROCK in trabecular meshwork cells.
Trabecular meshwork (TM) cell dysfunction is the leading cause of elevated intraocular pressure (IOP) and glaucoma. The long non-coding RNA (lncRNA) small nucleolar RNA host gene 11 (SNHG11) is associated with cell proliferation and apoptosis, but its biological functions and role in glaucoma pathogenesis remain unclear. In the present study, we investigated the role of SNHG11 in TM cells using immortalized human TM and glaucomatous human TM (GTM3 ) cells and an acute ocular hypertension mouse model. SNHG11 expression was depleted using siRNA targeting SNHG11. Transwell assays, quantitative real-time PCR analysis (qRT-PCR), western blotting, and CCK-8 assay were used to evaluate cell migration, apoptosis, autophagy, and proliferation. Wnt/β-catenin pathway activity was inferred from qRT-PCR, western blotting, immunofluorescence, and luciferase reporter and TOPFlash reporter assays. The expression of Rho kinases (ROCKs) was detected using qRT-PCR and western blotting. SNHG11 was downregulated in GTM3 cells and mice with acute ocular hypertension. In TM cells, SNHG11 knockdown inhibited cell proliferation and migration, activated autophagy, and apoptosis, repressing the Wnt/β-catenin signaling pathway, and activated Rho/ROCK. Wnt/β-catenin signaling pathway activity increased in TM cells treated with ROCK inhibitor. SNHG11 regulated Wnt/β-catenin signaling through Rho/ROCK by increasing GSK-3β expression and β-catenin phosphorylation at Ser33/37/Thr41 while decreasing β-catenin phosphorylation at Ser675. We demonstrate that the lncRNA SNHG11 regulates Wnt/β-catenin signaling through Rho/ROCK via β-catenin phosphorylation at Ser675 or GSK-3β-mediated phosphorylation at Ser33/37/Thr41, affecting cell proliferation, migration, apoptosis, and autophagy. Through its effects on Wnt/β-catenin signaling, SNHG11 is implicated in glaucoma pathogenesis and is a potential therapeutic target.
Liu L
，Yang X
，Zhang J
，Jiang W
，Hou T
，Zong Y
，Bai H
，Yang K
，Yang X
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SNHG11: A New Budding Star in Tumors and Inflammatory Diseases.
Long non-coding RNAs (lncRNAs) are transcripts that are over 200 nucleotides in length and lack protein-coding potential. Despite their name, lncRNAs have important regulatory roles in transcription, translation, and protein function by interacting with DNA, RNA, and protein molecules. Small nucleolar RNAs (snoRNAs), found in various tumors, are encoded by lncRNAs and have gained attention in recent research. The lncRNAs, encoding snoRNAs are known as small nucleolar RNA host genes (SNHGs), a newly identified class of lncRNAs. SNHG11, a specific SNHG, is a critical regulatory factor involved in various biological processes. Accumulating evidence suggests that SNHG11 can impact tumor development and inflammatory diseases by modulating downstream gene expression through chromatin modification, transcription, or post-transcriptional mechanisms. The expression levels of SNHG11 vary significantly in different normal tissues, tumors, and stages of tumor development. Currently, treatment options for advanced cancers are mainly palliative and lack curative potential.
This review aims to explore the modifications and functions of lncRNA SNHG11 in various tumors and inflammatory diseases. Through a comprehensive analysis of relevant literature on SNHG11 in PubMed, the review aims to provide a comprehensive description of the roles of SNHG11 in known tumors and inflammatory diseases and elucidate the specific mechanism's underlying functions. The changes in SNHG11 expression in tumors and inflammatory diseases can serve as early biomarkers, therapeutic targets, and prognostic indicators. Improving the clinical detection, staging, treatment, and prognosis of tumors is of great value. Additionally, the structural modifications of SNHG11 can potentially enhance its function as a drug carrier to maximize the therapeutic potential of drugs. Furthermore, understanding the specific mechanisms of SNHG11 in tumors and inflammatory diseases may provide new ways for targeted therapy.
Relevant studies were retrieved and collected from the PubMed system. SNHG11 was identified as the research object, and research literature on SNHG11 in the past ten years was analyzed to determine its strong association with the onset and progression of various diseases. The precise mechanisms of SNHG11's mode of action were reviewed, and references were further determined based on their impact factors for comprehensive analysis.
Through review and analysis, it was found that SNHG11 is involved in a wide range of tumors and inflammatory diseases through its high expression, including lung cancer, colorectal cancer, prostate cancer, hepatocellular carcinoma, triple-negative breast cancer, gastric cancer, glioma, ovarian cancer, pancreatic cancer, acute pancreatitis, and ischemic stroke, but with lower expression in virus myocarditis. SNHG11 is abnormally expressed in cells of these tumors and inflammatory diseases mainly contributes to disease proliferation, metastasis, ceRNA activity, miRNA sponging, drug resistance, and tumor prognosis. However, the specific mechanisms of SNHG11 in tumors and inflammatory diseases require further detailed exploration. Understanding the known regulatory mechanisms can expand the scope of clinical applications and promote early clinical detection, monitoring, and treatment.
LncRNA SNHG11 can serve as an early diagnostic biomarker, therapeutic target, and prognostic indicator in various diseases, particularly tumors. SNHG11 plays a crucial role in the occurrence and development of tumors and inflammatory diseases through various mechanisms, which has significant implications for clinical diagnosis and treatment.
Wu Y
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Circulating lncRNA SNHG11 as a novel biomarker for early diagnosis and prognosis of colorectal cancer.
Colorectal cancer (CRC) is the third most common cancer and the second leading cause of cancer mortality worldwide. Emerging evidence indicates that tumour cells release substantial amounts of RNA into the bloodstream, in which RNA strongly resists RNases and is present at sufficient levels for quantitative analyses. Our study aimed to discover blood-based markers for the early detection of CRC and to ascertain their efficiency in discriminating healthy controls, patients with polyps and adenomas and cancer patients. We first analysed and screened ZFAS1, SNHG11, LINC00909 and LINC00654 in a bioinformatics database and then collected clinical plasma samples for preliminary small-scale analysis and further large-scale verification. We then explored the mechanism of dominant lncRNA SNHG11 expression in CRC by in vitro and in vivo assays. The combination of ZFAS1, SNHG11, LINC00909 and LINC00654 showed high diagnostic performance for CRC (AUC: 0.937), especially early-stage disease (AUC: 0.935). Plasma levels of the four candidate lncRNAs were significantly reduced in postoperative samples compared to preoperative samples. A panel including these four lncRNAs performed well in distinguishing patient groups with different stages of colon disease, and SNHG11 exhibited the greatest diagnostic ability to identify precancerous lesions and early-stage tumour formation. Mechanistically, high SNHG11 expression promotes proliferation and metastasis by targeting the Hippo pathway. Taken together, the data indicate that SNHG11 may be a novel therapeutic target for the treatment of CRC and a potential biomarker for the early detection of CRC.
Xu W
，Zhou G
，Wang H
，Liu Y
，Chen B
，Chen W
，Lin C
，Wu S
，Gong A
，Xu M
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