miR-3154 promotes glioblastoma proliferation and metastasis via targeting TP53INP1.

IF 2.8 4区 生物学 Q3 CELL BIOLOGY Cell Division Pub Date : 2024-11-01 DOI:10.1186/s13008-024-00134-w
Xiangdan Lin, Qiong Wu, Wei Lei, Dongyang Wu, Jianchun Sheng, Guobiao Liang, Guojun Hou, Di Fan
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Abstract

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.

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miR-3154 通过靶向 TP53INP1 促进胶质母细胞瘤的增殖和转移。
胶质母细胞瘤(GBM)是最常见的原发性脑肿瘤,而miRNA在胶质母细胞瘤的发病机制中发挥着重要作用。miR-3154在胶质母细胞瘤组织和细胞系中升高,其升高与胶质母细胞瘤的分级有关。在细胞系中敲除 miR-3154 会削弱细胞增殖和集落形成的能力,并导致细胞周期停滞和更高比例的细胞凋亡。敲除 miR-3154 还会削弱胶质母细胞瘤细胞的迁移和侵袭能力。在机制上,miR-3154 直接与肿瘤蛋白 P53 诱导核蛋白 1(TP53INP1)结合,在 mRNA 和蛋白水平下调 TP53INP1 的表达。TP53INP1的沉默逆转了miR-3154敲除对胶质母细胞瘤细胞增殖和转移的影响。这些研究结果表明,miR-3154通过靶向TP53INP1促进胶质母细胞瘤的增殖和转移。
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来源期刊
Cell Division
Cell Division CELL BIOLOGY-
CiteScore
3.70
自引率
0.00%
发文量
5
审稿时长
>12 weeks
期刊介绍: Cell Division is an open access, peer-reviewed journal that encompasses all the molecular aspects of cell cycle control and cancer, cell growth, proliferation, survival, differentiation, signalling, gene transcription, protein synthesis, genome integrity, chromosome stability, centrosome duplication, DNA damage and DNA repair. Cell Division provides an online forum for the cell-cycle community that aims to publish articles on all exciting aspects of cell-cycle research and to bridge the gap between models of cell cycle regulation, development, and cancer biology. This forum is driven by specialized and timely research articles, reviews and commentaries focused on this fast moving field, providing an invaluable tool for cell-cycle biologists. Cell Division publishes articles in areas which includes, but not limited to: DNA replication, cell fate decisions, cell cycle & development Cell proliferation, mitosis, spindle assembly checkpoint, ubiquitin mediated degradation DNA damage & repair Apoptosis & cell death
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