Small nucleolar RNA host gene 16 (non-protein coding) (SNHG16)

Small nucleolar RNA host gene 16 (SNHG16) is a long non-coding RNA (lncRNA), originally identified in neuroblastoma, that functions as a competing endogenous RNA (ceRNA) and plays a crucial oncogenic role in many cancer types[1][2][3]. SNHG16 is frequently overexpressed in tumors, with elevated expression correlating with increased cell proliferation, enhanced migration and invasion, reduced apoptosis, and poor clinical prognosis[1][2][3]. Mechanistically, SNHG16 exerts its effects by sponging tumor-suppressive microRNAs (miRNAs), thereby modulating the expression of key genes involved in tumor progression, cell cycle regulation, and metastasis (such as ROCK1, BCL9, E2F5, and MMP9)[1][3]. SNHG16 also participates in epigenetic regulation by interacting with chromatin modifiers like EZH2 to suppress tumor suppressor genes (e.g., p21)[1][2]. The regulatory roles of SNHG16 extend to several biological processes associated with RNA metabolism and processing, possibly mediated through its binding to various RNA-binding proteins[2]. These functional attributes make SNHG16 a candidate biomarker for prognosis and a potential, albeit currently untargeted, therapeutic target in oncology[1][2][3].

Other names

ncRANNbla12061Nbla10727ELNAT1non-coding RNA expressed in aggressive neuroblastomaEV-mediated LN-associated transcript 1

miRNA sponging (acting as a ceRNA to regulate gene expression); Epigenetic regulation (interaction with EZH2, suppression of p21); Activation of oncogenic signaling pathways (e.g., PI3K/Akt, AKT phosphorylation); Promotion of metastasis via upregulation of genes like ZEB1, E2F5, ROCK1, BCL9, MMP9