Gao Kang, Song Lina, Niu Deying
Department of Neurosurgery, Zibo Central Hospital, No. 54, Gongqingtuan West Road, Zhangdian District, Zibo, 255000, China.
Neurochem Res. 2025 Sep 4;50(5):281. doi: 10.1007/s11064-025-04539-z.
Long non-coding RNAs (lncRNAs) have emerged as promising cancer biomarkers due to their stability and detectability. This study aimed to investigate the clinical significance and molecular mechanisms of lncRNA MCA3AP-AS1 in glioma. This study collected the clinical data from 177 glioma patients, and the expression of MCM3AP-AS1 was measured in glioma tissues and cell lines. Kaplan-Meier and COX regression analyses were employed to assess its prognostic value in glioma. In the mechanism study, bioinformatics prediction, correlation analysis, and dual-luciferase assays were conducted to validate the regulatory network involving MCM3AP-AS1, miR-23c, and PIK3R3. Functional experiments (CCK-8, Transwell assays, and Western blot) further determined the impact of MCM3AP-AS1 on glioma cell functions and confirmed the potential regulatory mechanism. Upregulation of MCM3AP-AS1 in glioma was related to the WHO grade, KFS scores, and glioma poor prognosis. Correlation analysis, binding site prediction, and the dual-luciferase reporter assay confirmed the interaction relationship among MCM3AP-AS1, miR-23c, and PIK3R3. In mechanism, MCM3AP-AS1 knockdown suppressed the glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). This attenuated effect of downregulated MCM3AP-AS1 expression in glioma cell proliferation, migration, and invasion could be further reversed by miR-23c inhibition. Upregulated MCM3AP-AS1 expression in glioma was associated with the poor prognosis of glioma. MCM3AP-AS1 may promote glioma progression by enhancing cell proliferation, migration, and invasion through the miR-23c/PIK3R3 axis.
长链非编码RNA(lncRNAs)因其稳定性和可检测性已成为有前景的癌症生物标志物。本研究旨在探讨lncRNA MCA3AP-AS1在胶质瘤中的临床意义及分子机制。本研究收集了177例胶质瘤患者的临床资料,并检测了胶质瘤组织和细胞系中MCM3AP-AS1的表达。采用Kaplan-Meier法和COX回归分析评估其在胶质瘤中的预后价值。在机制研究中,进行了生物信息学预测、相关性分析和双荧光素酶测定,以验证涉及MCM3AP-AS1、miR-23c和PIK3R3的调控网络。功能实验(CCK-8、Transwell实验和蛋白质免疫印迹法)进一步确定了MCM3AP-AS1对胶质瘤细胞功能的影响,并证实了潜在的调控机制。胶质瘤中MCM3AP-AS1的上调与世界卫生组织(WHO)分级、KFS评分及胶质瘤预后不良相关。相关性分析、结合位点预测和双荧光素酶报告基因测定证实了MCM3AP-AS1、miR-23c和PIK3R3之间的相互作用关系。机制上,敲低MCM3AP-AS1可抑制胶质瘤细胞的增殖、迁移、侵袭及上皮-间质转化(EMT)。miR-23c抑制可进一步逆转下调MCM3AP-AS1表达对胶质瘤细胞增殖、迁移和侵袭的减弱作用。胶质瘤中MCM3AP-AS1表达上调与胶质瘤预后不良相关。MCM3AP-AS1可能通过miR-23c/PIK3R3轴增强细胞增殖、迁移和侵袭,从而促进胶质瘤进展。