Snhg8, short for Small nucleolar RNA host gene 8, is a long non-coding RNA. It has physiological roles in epithelial and muscle satellite cells. Snhg8 can act as a molecular sponge for multiple miRNAs, regulating various target genes, and is involved in diverse biological processes and signaling pathways. Its dysregulation is associated with many human disorders, making it an important gene for understanding disease mechanisms [1].

In tauopathies, Snhg8 was significantly reduced in a mouse model and in affected human brains. Overexpression of mutant tau reduced Snhg8 expression and induced stress granule formation, while rescuing Snhg8 expression decreased stress granule formation, suggesting Snhg8 dysregulation drives stress granule formation via TIA1 in tauopathies [2].

In multiple cancer types like gastric, breast, and nasopharyngeal carcinomas, Snhg8 knockdown inhibited tumor cell proliferation, migration, and invasion. For example, in EBV-associated gastric cancer, Snhg8 promoted tumorigenesis and invasion by sponging miR-512-5p and upregulating TRIM28 [3]. In breast cancer, it functioned through the miR-634/ZBTB20 axis [4], and in nasopharyngeal carcinoma, via the miR-588/HMGA2 axis [5].

In osteogenic differentiation of periodontal ligament stem cells (PDLSCs), mechanical force decreased Snhg8 expression, which promoted osteogenic differentiation. Knockdown of Snhg8 in PDLSCs increased osteogenic-related gene expression [6].

In cerebral ischemia-reperfusion injury in mice, LncRNA Snhg8 improved the injury by inhibiting miR-494-3p expression, suppressing microglia inflammatory reactions and apoptosis [7].

In high-glucose-induced endothelial cell injury, silencing lncRNA Snhg8 reversed the decrease in eNOS activation, NO production, migration, and angiogenesis of primary human umbilical vein endothelial cells (pHUVECs) [8].

In diffuse large B-cell lymphoma, knockdown of Snhg8 inhibited cell proliferation and colony formation while promoting apoptosis by targeting miR-335-5p [9].

In nasopharyngeal carcinoma, Snhg8 promoted aggressive behaviors via regulating the miR-656-3p/SATB1 axis [10].

In conclusion, Snhg8 is a crucial long non-coding RNA involved in various biological processes and disease conditions. Studies using gene-knockout or knockdown models in different tissues and disease models have revealed its role in cancer progression, neurodegenerative diseases, osteogenic differentiation, and ischemia-reperfusion injury. These findings contribute to a better understanding of the molecular mechanisms underlying these diseases and may provide potential therapeutic targets.