Tudor-staphylococcal nuclease regulates the expression and biological function of alkylglycerone phosphate synthase via nuclear factor-κB and microRNA-127 in human glioma U87MG cells
Tudor-staphylococcal nuclease regulates the expression and biological function of alkylglycerone phosphate synthase via nuclear factor-κB and microRNA-127 in human glioma U87MG cells
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DOI：
10.3892/ol.2018.8484
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发表时间：
2018-06-01
期刊：
影响因子：
2.9
通讯作者：
Zhu, Yu
中科院分区：
文献类型：
--
作者：
Zhang, Yongqiang;Jia, Jun;Zhu, Yu
胶质瘤是危害人类健康的恶性肿瘤之一，因此，寻找新的靶点和治疗方法具有重要意义。Tudor-staphylococcal nuclease（SN）和alkylglycerone phosphate synthase（AGPS）表达下调可降低肿瘤恶性度，过表达可提高多种肿瘤细胞的存活率和迁移能力，但AGPS在胶质瘤增殖和迁移中的作用以及两者在人脑胶质瘤中的相关性尚不清楚。在本研究中，确定AGPS沉默抑制胶质瘤U87 MG细胞的增殖和迁移能力，并抑制环状RNA circ-ubiquitin-associated protein 2、circ-zinc finger protein 292和circ-homeodomain-interacting protein kinase 3的表达，以及长非编码RNA H19印迹母源表达转录本的表达（非蛋白编码）、结肠癌相关转录物1（非蛋白编码）和肝细胞癌上调长非编码RNA。此外，Tudor-SN沉默抑制了AGPS的表达;然而，核因子（NF）-kappa B和microRNA（miR）-127修复实验部分降低了AGPS的表达。此外，确定Tudor-SN沉默抑制雷帕霉素（mTOR）信号传导途径的机制靶标的活性，并且NF-κ B和miR-127恢复实验部分地降低mTOR的活性。因此，认为NF-κ B和miR-127可能是Tudor-SN通过mTOR信号通路调节AGPS的介质。这些结果提高了我们对Tudor-SN和AGPS在人脑胶质瘤中的作用机制的认识。
Glioma is one of the malignant tumor types detrimental to human health; therefore, it is important to find novel targets and therapeutics for this tumor. The downregulated expression of Tudor-staphylococcal nuclease (SN) and alkylglycerone phosphate synthase (AGPS) can decrease cancer malignancy, and the overexpression of them can the increase viability and migration potential of various tumor cell types; however, the role of AGPS in the proliferation and migration of glioma, and the association of Tudor-SN and AGPS in human glioma is not clear. In the present study, it was determined that AGPS silencing suppressed the proliferation and migration potential of glioma U87MG cells, and suppressed the expression of the circular RNAs circ-ubiquitin-associated protein 2, circ-zinc finger protein 292 and circ-homeodomain-interacting protein kinase 3, and the long non-coding RNAs H19 imprinted maternally expressed transcript (non-protein coding), colon cancer-associated transcript 1 (non-protein coding) and hepatocellular carcinoma upregulated long non-coding RNA. Furthermore, Tudor-SN silencing suppressed the expression of AGPS; however, nuclear factor (NF)-kappa B and microRNA (miR)-127 retrieval experiments partially reduced the expression of AGPS. Additionally, it was determined that Tudor-SN silencing suppressed the activity of the mechanistic target of rapamycin (mTOR) signaling pathway, and NF-kappa B and miR-127 retrieval experiments partially reduced the activity of mTOR. Therefore, it was considered that NF-kappa B and miR-127 may be the mediators of Tudor-SN-regulated AGPS via the mTOR signaling pathway. These results improve on our knowledge of the mechanisms underlying Tudor-SN and AGPS in human glioma.