The Mechanisms Underlying the Aberrant Expression and Oncogenic Role of SNHG1 in Cancer
TL;DR
A mechanism-driven approach is adopted to systematically examine SNHG1 dysregulation and its roles in cancer, which complements existing literature and provides a clear framework for future SNHG1 research.
Abstract
: Small nucleolar RNA host genes (SNHGs) generate both long non-coding RNAs and small nucleolar RNAs from the same primary transcripts. Among the 32 identified members, SNHG1 is the most extensively studied and primarily acts as an oncogene. This review adopts a mechanism-driven approach to systematically examine SNHG1 dysregulation and its roles in cancer. Specifically, we address: (1) how SNHG1 is transcriptionally and post-transcriptionally dysregulated in tumors; (2) the molecular mechanisms by which it regulates gene expression, including epigenetic mechanisms (histone modifications, DNA methylation), transcriptional regulation, post-transcriptional regulation (mRNA stability, microRNA sponging), and protein-level regulation; and (3) how these mechanisms collectively drive cancer behaviors such as proliferation, migration, epithelial-to-mesenchymal transition, apoptosis, and ferroptosis. We also discuss potential crosstalk among SNHG1, circadian rhythm, and the nervous system, and identify major knowledge gaps, including isoform-specific functions, tumor-suppressive contexts, and challenges in clinical translation. Experimental roadmaps are proposed to address these open questions. This mechanism-focused synthesis complements existing literature and provides a clear framework for future SNHG1 research.