Small nucleolar RNA host gene 26 (SNHG26)

Small nucleolar RNA host gene 26 (SNHG26) is a long non-coding RNA (lncRNA) encoded in the human genome at chromosome 7q22.1, spanning approximately 3100 nucleotides according to Ensembl transcript ENST00000415611.9[2][5]. SNHG26 is part of the SNHG family, which are lncRNAs often transcribed from loci containing small nucleolar RNAs (snoRNAs)[7]. SNHG26 does not encode a protein and is localized primarily in the nucleus and cytoplasm, with expression upregulated in certain physiological contexts such as wound-edge keratinocytes and pathologically in various cancers (e.g., gastric cancer, tongue squamous cell carcinoma, head and neck cancer)[2][4][1]. Mechanistically, SNHG26 regulates oncogenic processes by modulating translation and stabilization of key proteins—including c-Myc and PGK1—through direct binding, influencing cancer cell proliferation, invasion, EMT, drug resistance, and metabolic reprogramming via the Akt/mTOR and c-Myc/hexokinase 2 (HK2) signaling pathways[1][4]. In wound healing, SNHG26 promotes basal keratinocyte proliferation and migration by interacting with ILF2 and regulating the transition from inflammatory to proliferative states[2][6]. High SNHG26 expression is associated with aggressive disease, poor prognosis, and chemotherapy resistance in several cancers, suggesting its utility as a prognostic biomarker and potential therapeutic target[4].

Other names

AC005682.5SNHG26

Modulation of protein translation (e.g., c-Myc); Interaction with proteins (e.g., stabilization of PGK1 by inhibiting ubiquitination, relocation of transcription factor ILF2); Activation of signaling pathways (e.g., Akt/mTOR via PGK1 stabilization); Regulation of glycolytic metabolism (via HK2 and c-Myc feedback loop)