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

Zhang,Yongqiang; Jia,Jun; Li,Ying; Chen,Yan‑Ge; Huang,Huan; Qiao,Yang; Zhu,Yu

doi:10.3892/ol.2018.8484

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

Authors:
- Yongqiang Zhang
- Jun Jia
- Ying Li
- Yan‑Ge Chen
- Huan Huang
- Yang Qiao
- Yu Zhu
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Affiliations: Geriatric Ward of Neurology, Department of Geriatrics, Institute of Tianjin Geriatrics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, Department of Surgery of Foot and Ankle, Tianjin Hospital, Tianjin 300211, P.R. China, Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, Basic Medical College, Tianjin Medical University, Tianjin 300070, P.R. China, Department of Clinical Laboratory, Tianjin Key Laboratory of Cerebral Vessels and Neural Degeneration, Tianjin Huanhu Hospital, Tianjin 300350, P.R. China
Published online on: April 13, 2018 https://doi.org/10.3892/ol.2018.8484
Pages: 9553-9558

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Abstract

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)‑κB 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‑κB and miR‑127 retrieval experiments partially reduced the activity of mTOR. Therefore, it was considered that NF‑κB 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.

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