Lin Xiangdan, Wu Qiong, Lei Wei, Wu Dongyang, Sheng Jianchun, Liang Guobiao, Hou Guojun, Fan Di
Department of Neurosurgery, General Hospital of Northern Theater Command, 83 Wenhua Road, ShenHe District, Shengyang, Liaoning, 110016, China.
Department of Neurosurgery, The first affiliated hospital of Jinzhou medical university, Jinzhou, 121000, China.
Cell Div. 2024 Nov 1;19(1):30. doi: 10.1186/s13008-024-00134-w.
Glioblastomas (GBM) are most common types of primary brain tumors and miRNAs play an important role in pathogenesis of glioblastomas. Here, we reported a new miRNA, miR-3154, which regulates glioblastoma proliferation and metastasis. miR-3154 was elevated in glioblastoma tissue and cell lines, and its elevation was associated with grade of glioblastomas. Knockdown of miR-3154 in cell lines weakened ability of proliferation and colony formation, and caused cell cycle arrested and higher percentage of apoptosis. Knockdown of miR-3154 also impaired ability of migration and invasion in glioblastoma cells. In mechanism, miR-3154 bound directly to Tumor Protein P53 Inducible Nuclear Protein 1 (TP53INP1), down-regulating TP53INP1 expression at both mRNA and protein level. Silence of TP53INP1 reversed the effect of miR-3154 knockdown on proliferation and metastasis of glioblastoma cells. These findings show that miR-3154 promotes glioblastoma proliferation and metastasis via targeting TP53INP1.
胶质母细胞瘤（GBM）是最常见的原发性脑肿瘤类型，而微小RNA（miRNA）在胶质母细胞瘤的发病机制中起重要作用。在此，我们报道了一种新的miRNA，即miR-3154，它可调节胶质母细胞瘤的增殖和转移。miR-3154在胶质母细胞瘤组织和细胞系中表达升高，其升高与胶质母细胞瘤的分级相关。在细胞系中敲低miR-3154会削弱增殖和集落形成能力，并导致细胞周期停滞和更高的凋亡百分比。敲低miR-3154还会损害胶质母细胞瘤细胞的迁移和侵袭能力。机制上，miR-3154直接与肿瘤蛋白P53诱导核蛋白1（TP53INP1）结合，在mRNA和蛋白质水平下调TP53INP1的表达。沉默TP53INP1可逆转miR-3154敲低对胶质母细胞瘤细胞增殖和转移的影响。这些发现表明，miR-3154通过靶向TP53INP1促进胶质母细胞瘤的增殖和转移。
