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Small nucleolar RNA host gene 25 (SNHG25) is a long non-coding RNA that acts as a host for specific small nucleolar RNAs and regulates gene expression primarily by functioning as a competing endogenous RNA (ceRNA), sponging microRNAs such as miR-497-5p and miR-296-3p[1][2][6]. It is predominantly localized in either the nucleus or cytoplasm depending on cell type, and is documented to facilitate tumor cell proliferation, migration, and invasion, while suppressing apoptosis, across several human cancers including neuroblastoma, colorectal cancer, endometrial cancer, and prostate cancer[1][2][3][4][6]. SNHG25 enhances oncogenic pathways and contributes to tumor progression by upregulating targets such as FASN and MMP2, activating the PI3K/AKT and MAPK pathways, and stabilizing proteins like histone deacetylase 1 (HDAC1)[1][2][4][6]. Its expression is associated with worse clinical outcomes and represents a promising molecular target and biomarker for cancer diagnosis and prognosis[3][4][6]. At present, there are no drugs known to directly target SNHG25.
SNHG25's mechanism of action involves miRNA sponging (e.g., sequestering miR-497-5p, miR-296-3p), positive regulation of target gene expression (e.g., FASN, MMP2), indirect activation of oncogenic signaling pathways (e.g., MAPK pathway, PI3K/AKT pathway), and RNA-protein interactions (e.g., recruitment of DKC1).
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