ArticleOncology letters2026
LINC00184 promotes esophageal squamous cell carcinoma progression via DNMT1-mediated methylation of the NDRG2 promoter and PI3K/AKT pathway activation.
Article in Oncology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Esophageal squamous cell carcinoma (ESCC) is a highly aggressive cancer with poor clinical outcomes, highlighting the need for enhanced understanding of its molecular drivers. The present study investigated the functional role of long non-coding RNA LINC00184 in ESCC progression. Using overexpression experiments in KYSE-150 and TE-1 cell lines, the present study demonstrated that LINC00184 significantly enhances ESCC cell proliferation and migration while inhibiting apoptosis. Mechanistic studies revealed that LINC00184 recruits DNA methyltransferase 1 (DNMT1) to the promoter of the tumor suppressor gene N-Myc downstream regulated gene 2 (NDRG2), thereby catalyzing CpG island hypermethylation and transcriptional silencing of NDRG2. The subsequent downregulation of NDRG2 results in activation of the oncogenic PI3K/AKT signaling pathway. Notably, treatment with the DNMT1 inhibitor 5-azacytidine reverses LINC00184-induced NDRG2 promoter methylation, restores NDRG2 expression and attenuates PI3K/AKT pathway activation. The present study findings identified a novel LINC00184/DNMT1/NDRG2/PI3K-AKT regulatory axis in ESCC and suggested that targeting this epigenetic pathway may represent a promising therapeutic strategy in the future.
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