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.