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<p>Long non-coding RNAs (lncRNAs) have been evidenced to function as pivotal modulators in tumorigenesis. LncRNA SNHG25 is highly expressed in colorectal cancer (CRC), but its specific function in CRC has not been elucidated yet. The expression of SNHG25, miR-329-3p, and PPP2R2D was determined using qRT-PCR analysis and western blot analysis. The influence of the SNHG25/miR-329-3p/PPP2R2D axis on CRC progression was explored through in vitro assays including CCK-8, colony formation, wound healing, Transwell assays and in vivo orthotopic xenografts assay. The interaction between miR-329-3p and SNHG25 or PPP2R2D was examined by RNA pull-down, RIP, and luciferase reporter assays. SNHG25 presented high expression in CRC cell lines. Silencing of SNHG25 suppressed the malignant phenotypes of CRC cells in vitro and tumor growth in vivo. MiR-329-3p, which displayed low expression in CRC cells, was sponged by SNHG25. Downregulation of miR-329-3p reversed the inhibitory effects of SNHG25 silencing on CRC cell malignant behaviors. Additionally, PPP2R2D served as a miR-329-3p downstream target, whose expression was downregulated by overexpressing miR-329-3p. Importantly, overexpression of PPP2R2D rescued SNHG25 silencing-induced repression on CRC cell malignancy. SNHG25 plays a carcinogenic role&#xa0;in CRC via regulation of the miR-329-3p/PPP2R2D axis.</p>

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LncRNA SNHG25 facilitates colorectal cancer progression by upregulating PPP2R2D expression through sponging miR-329-3p

  • 期刊论文

  • 发表日期：

    2025年4月18日

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  • Yuanqiang Li,
  • Weipeng Liu,
  • Chao Liu,
  • Guangsheng Wang,
  • Xin Zhou

摘要

Long non-coding RNAs (lncRNAs) have been evidenced to function as pivotal modulators in tumorigenesis. LncRNA SNHG25 is highly expressed in colorectal cancer (CRC), but its specific function in CRC has not been elucidated yet. The expression of SNHG25, miR-329-3p, and PPP2R2D was determined using qRT-PCR analysis and western blot analysis. The influence of the SNHG25/miR-329-3p/PPP2R2D axis on CRC progression was explored through in vitro assays including CCK-8, colony formation, wound healing, Transwell assays and in vivo orthotopic xenografts assay. The interaction between miR-329-3p and SNHG25 or PPP2R2D was examined by RNA pull-down, RIP, and luciferase reporter assays. SNHG25 presented high expression in CRC cell lines. Silencing of SNHG25 suppressed the malignant phenotypes of CRC cells in vitro and tumor growth in vivo. MiR-329-3p, which displayed low expression in CRC cells, was sponged by SNHG25. Downregulation of miR-329-3p reversed the inhibitory effects of SNHG25 silencing on CRC cell malignant behaviors. Additionally, PPP2R2D served as a miR-329-3p downstream target, whose expression was downregulated by overexpressing miR-329-3p. Importantly, overexpression of PPP2R2D rescued SNHG25 silencing-induced repression on CRC cell malignancy. SNHG25 plays a carcinogenic role in CRC via regulation of the miR-329-3p/PPP2R2D axis.