Snhg11, a small nucleolar RNA host gene, is a type of long non-coding RNA (lncRNA) that lacks protein-coding potential but plays critical regulatory roles in transcription, translation, and protein function. It is involved in various biological processes and is associated with multiple signaling pathways such as the Wnt/β -catenin pathway [2,4]. Snhg11 has been found to be of great biological importance in tumors and inflammatory diseases [1].

In a carbon tetrachloride-treated C57BL/6J mouse model, Snhg11 expression was highly up-regulated in fibrotic livers and activated primary hepatic stellate cells (HSCs). Knockdown of Snhg11 attenuated the accumulation of fibrotic markers in liver fibrosis tissues and activated HSCs, indicating its role in promoting liver fibrosis by reprogramming glutaminolysis in HSCs through the Wnt/β-catenin/GLS axis [2]. In lung adenocarcinoma cells, down-regulation of Snhg11 hindered cell viability, proliferation, migration, and tumor growth in vivo, as it activated the Notch pathway via regulating Notch3 and competitively bound with miR-193a-5p to up-regulate Notch3 [3]. In gastric cancer, Snhg11 is upregulated and its upregulation correlated with poor patient outcomes. It aggravated oncogenic autophagy and promoted cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition by activating the Wnt/β-catenin pathway and regulating autophagy-related genes through specific miRNAs [4].

In conclusion, Snhg11 is a crucial lncRNA that plays significant roles in various biological processes related to tumors and inflammatory diseases. Mouse models, especially those with Snhg11 knockdown, have revealed its pro-fibrotic role in liver fibrosis, its role in promoting the progression of lung adenocarcinoma and gastric cancer. Understanding the functions of Snhg11 through these models provides insights into the mechanisms of disease development, potentially leading to new therapeutic strategies for these diseases.