ArticleJournal of cellular and molecular medicine2025
SNHG26 Promotes Colorectal Cancer Progression via CDKN2A-Dependent Regulation of Cuproptosis and CD8+ T Cell-Mediated Immunity.
Article in Journal of cellular and molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- SNHG26 Promotes Colorectal Cancer Progression via CDKN2A-Dependent Regulation of Cuproptosis and CD8+ T Cell-Mediated Immunity.Journal of cellular and molecular medicine · 2025Article
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2 authors.
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Abstract
Long non-coding RNAs (lncRNAs) play important roles in colorectal cancer (CRC) progression. However, the biological function and regulatory mechanism of small nucleolar RNA host gene 26 (SNHG26) in CRC remain largely unexplored. SNHG26 expression was analysed in CRC tissues and cell lines using quantitative real-time PCR (qRT-PCR). The biological functions of SNHG26 were investigated through loss- and gain-of-function approaches. Interaction between SNHG26 and CDKN2A was examined by RNA immunoprecipitation, RNA pull-down and RNA stability assays. The effects of the SNHG26-CDKN2A axis on Cu + ELES(copper plus elesclomol)-induced cuproptosis and CD8+ T cell-mediated anti-tumour immunity were evaluated through cell viability, apoptosis, co-culture cytotoxicity and migration assays. SNHG26 was significantly upregulated in CRC tissues and cell lines, with high expression showing trends toward poor prognosis. SNHG26 knockdown suppressed CRC cell proliferation and enhanced apoptosis. Additionally, it increased sensitivity to Cu + ELES-induced cuproptosis. Mechanistically, SNHG26 directly interacted with CDKN2A mRNA, promoting its degradation. CDKN2A, which exhibits context-dependent effects in CRC, was post-transcriptionally regulated by SNHG26. Rescue experiments demonstrated that CDKN2A knockdown partially reversed the oncogenic effects of SNHG26 overexpression, including enhanced proliferation, reduced apoptosis and increased resistance to cuproptosis. Furthermore, the SNHG26-CDKN2A axis modulated the tumour immune microenvironment by regulating CD8+ T cell cytotoxicity and chemokine expression, specifically downregulating CXCL9 and CXCL10, which are critical for T cell recruitment. Our findings reveal a novel regulatory axis whereby SNHG26 promotes CRC progression by destabilising CDKN2A mRNA, resulting in enhanced cell proliferation, cuproptosis and immune evasion. This study provides new insights into the molecular mechanisms underlying CRC development.
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