Li Yuanqiang, Liu Weipeng, Liu Chao, Wang Guangsheng, Zhou Xin
Department of Gastrointestinal Surgery, The First College of Clinical Medical Science, China Three Gorges University, Yichang, China.
Yichang Central People's Hospital, No. 183 Yiling Road, Wujiagang District, Yichang City, Hubei Province China.
Cytotechnology. 2025 Jun;77(3):89. doi: 10.1007/s10616-025-00753-3. Epub 2025 Apr 18.
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.
The online version contains supplementary material available at 10.1007/s10616-025-00753-3.
长链非编码RNA(lncRNAs)已被证明在肿瘤发生过程中起关键调节作用。LncRNA SNHG25在结直肠癌(CRC)中高表达,但其在CRC中的具体功能尚未阐明。采用qRT-PCR分析和蛋白质印迹分析确定SNHG25、miR-329-3p和PPP2R2D的表达。通过CCK-8、集落形成、伤口愈合、Transwell实验等体外实验以及体内原位异种移植实验,探讨SNHG25/miR-329-3p/PPP2R2D轴对CRC进展的影响。通过RNA下拉实验、RIP实验和荧光素酶报告基因实验检测miR-329-3p与SNHG25或PPP2R2D之间的相互作用。SNHG25在CRC细胞系中高表达。沉默SNHG25可抑制CRC细胞的体外恶性表型和体内肿瘤生长。在CRC细胞中低表达的miR-329-3p被SNHG25吸附。下调miR-329-3p可逆转SNHG25沉默对CRC细胞恶性行为的抑制作用。此外,PPP2R2D是miR-329-3p的下游靶点,过表达miR-329-3p可下调其表达。重要的是,过表达PPP2R2D可挽救SNHG25沉默诱导的对CRC细胞恶性程度的抑制。SNHG25通过调控miR-329-3p/PPP2R2D轴在CRC中发挥致癌作用。
在线版本包含可在10.1007/s10616-025-00753-3获取的补充材料。