Astragalus polysaccharides inhibits nasopharyngeal carcinoma progression through the mediation of the Akt/mTOR pathway and the induction of oxidative stress.

Abstract

To investigate whether astragalus polysaccharides (APS) can inhibit the progression of nasopharyngeal carcinoma (NPC) and its underlying mechanisms, we conducted both cell and animal experiments. In NPC tissues and cell lines, the level of SNHG12 was significantly elevated, and high levels of SNHG12 were associated with advanced TNM staging, as well as increased cell viability and invasiveness. We further explored the mechanism by which SNHG12 promotes NPC progression and found multiple binding sites between SNHG12 and miR-30a-3p (miR-30a). The expression of miR-30a was significantly decreased in NPC tissues and cell lines, showing a strong negative correlation with SNHG12 levels. Moreover, SNHG12 could counteract the anti-cancer effects of miR-30a, enhancing the viability and migratory ability of CNE-2 cells. Further studies revealed that miR-30a could target and inhibit AKT3 levels, while SNHG12 could antagonize miR-30a and restore AKT3 levels. Thus, SNHG12 can regulate the malignant biological characteristics of NPC by targeting the miR-30a/AKT3 axis. In animal experiments, we found that APS can downregulate SNHG12 and upregulate miR-30a in tumor tissues, effectively suppressing NPC progression. Additionally, APS demonstrated significant antioxidant effects. Therefore, APS can inhibit oxidative stress and suppress NPC progression by targeting the SNHG12/miR-30a/AKT3 signaling pathway.