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

Abstract

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. IntroductionGliomas are a type of tumor formed by neoplastic transformation of neural stem cells, progenitor cells and differentiated glial cells, including astrocytes, oligodendrocytes and ependymal cells (1). Neoplastic cells may spread diffusely to normal brain tissues and damage normal neurological functions, which is the reason why malignant gliomas are detrimental to human health (2). In China, gliomas constitute 44.69% of primary intracranial tumors and 1-3% of generalized malignancies (3). According to the World Health Organization, malignant glioma causes the second highest amount of mortalities in sufferers <34 years old, and the third highest amount of mortalities in sufferers aged 35-54 years old (4). It is estimated that the survival time of the majority of glioma sufferers is ~1 year. Although there are currently various treatments available, including excision, chemotherapy and radiotherapy, the characteristic of strong invasiveness has severely influenced the effectiveness of glioma treatment.MicroRNAs (miRNAs/miRs) are an important molecular mediator of cell genetic changes, and are directly or indirectly associated with the occurrence and development of a number

RETRACTED ARTICLE: The circular RNA ZNF292 alleviates OGD-induced injury in H9c2 cells via targeting BNIP3

“…mTOR prevented the cardiomyocyte necrosis and inflammation but was conducive to functional recovery in ex vivo hearts [44]. CircZNF292 served as a tumor-promoting factor through the mTOR signaling pathway, relying on the expressions of the alkylglycerone phosphate synthase (AGPS) in glioma cells [45]. In addition, previous investigation has reported that the BNIP3 is capable of inhibiting the sensitivity of the mTOR, which plays pivotal roles in autophagic induction.…”

Mass Spectrometry and Computer Simulation Predict the Interactions of AGPS and HNRNPK in Glioma

“…The infiltration of glioma cells into normal brain tissue can destroy normal brain tissue function. In the early stage, it may show irritation symptoms such as localized epilepsy, 10 BioMed Research International and later, it may show symptoms of neurological deficits such as paralysis, which is a sign of deterioration of glioma and the main cause of treatment failure and death [14]. Abnormally expressed lipids can regulate a series of functional genes to turn on and/or off abnormally by participating in the formation of tumor cells and signal transduction process so that tumor cells can acquire various characteristics different from normal cells and induce cell canceration and tumor proliferation, invasion, and apoptosis resistance [15,16].…”

Friend or Foe? The fascinating Tudor-SN protein

“…Tudor-SN is transcriptionally activated by the TGFb and NF-jB pathways [70,73,85] but also participates in the regulation of the gene transcription of TGFb and NF-jB pathway-related members [28,[86][87][88][89]. The PI3K-AKT-mTOR pathway can regulate the translation of the Tudor-SN protein [76], and components of this pathway can also be induced and activated by high Tudor-SN expression [87,90,91]. It is thus hypothesized that activation of the TGFb, NF-jB, and PI3K-AKT-mTOR pathways in tumor cells mediates the overexpression of Tudor-SN by regulating the processes of RNA transcription and protein translation, and the upregulation of Tudor-SN expression, in turn, facilitates the activation of these signaling pathways.…”