Small nucleolar RNA host gene 3 (SNHG3)

Small nucleolar RNA host gene 3 (SNHG3) is a long non-coding RNA primarily known for its role as a molecular scaffold and competing endogenous RNA (ceRNA), sequestering multiple tumor-suppressor microRNAs and thereby derepressing oncogenic pathways and gene products such as c-MYC and BMI1[1][3][4]. SNHG3 is frequently overexpressed in a broad array of cancers, where it drives cell proliferation, cell cycle progression, migration, invasion, apoptosis resistance, and drug resistance[1][3][4][5][7]. Epigenetically, SNHG3 exerts effects by binding and recruiting chromatin-modifying proteins like EZH2 to silence tumor suppressor loci via DNA methylation and histone modification[3][4]. In normal physiology, SNHG3 is essential for embryonic stem cell pluripotency, partly via interaction with core stemness regulators Nanog and Oct4, and participates in metabolic regulation[2][6]. Given its widespread oncogenic functions and ability to modulate key regulatory networks, SNHG3 is a focus of ongoing research as both a potential therapeutic target and cancer biomarker, though concerns regarding biological specificity and safety remain[2][4][6][7].

Other names

U17HGU17HG-ANCRNA00014non-protein coding RNA 14RNU17CRNU17DU17HG-ABU17 small nucleolar RNA hostsmall nucleolar RNA host gene (non-protein coding) 3small nucleolar RNA host gene 3 (non-protein coding)SNHG3

ceRNA activity (sponging tumor-suppressor miRNAs which leads to upregulation of oncogenic targets such as c-MYC, Rab22a, BMI1, etc.)[1][3][4]; Epigenetic silencing (recruitment of EZH2 to silence tumor suppressor gene promoters including KLF2, p21, MED18)[3][4]; Modulating transcription factor activity (interactions with E2F1, Nanog, Oct4, among others)[2][4]; Regulation of protein stability (via ubiquitination, e.g., SND1 in lipid metabolism models)[6]