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The **Stem cell inhibitory RNA transcript (SCIRT)** is a long noncoding RNA (lncRNA) that serves as an important regulator of cancer cell fate, stemness, and cell cycle dynamics[1][2][7]. SCIRT is upregulated in tumorspheres and counteracts tumorigenesis by balancing the transcriptional programs of cell-cycle activation and stem-cell self-renewal, primarily via direct antagonism of chromatin-modifying and stem-cell-associated transcription factors such as EZH2 and SOX2[1][7]. In breast cancer, SCIRT inhibits self-renewal and activates cell-cycle gene expression by partnering with EZH2, modulating EZH2's affinity for other proteins such as FOXM1, and binding to promoters and enhancers across the genome[1]. In epithelial ovarian cancer, its alias DATOC-1 is highly expressed and is associated with greater cell proliferation, invasion, and poorer patient prognosis; knockdown leads to reduced tumor progression, suggesting it as a potential therapeutic target[2][3][5]. Additionally, SCIRT acts as a molecular sponge for microRNAs (such as miR-146a) in non-cancer contexts, such as atherosclerosis, where it suppresses smooth muscle cell proliferation[3]. No pharmacological agents currently target SCIRT directly. Its role as a biomarker and target in cancer is of emerging interest due to its regulatory functions at the chromatin level, influence on cell fate, and impact on disease outcomes[2][7].
Antagonism of EZH2-mediated gene repression (modulates chromatin state); Activation of cell-cycle-promoting gene transcription; Suppression of stemness-associated gene expression.
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