Tenascin-C promotes epithelial-to-mesenchymal transition and the mTOR signaling pathway in nasopharyngeal carcinoma.

Abstract

Tenascin-C (TNC) is a large extracellular matrix glycoprotein that promotes cell adhesion and tissue remodeling, and is involved in the transduction of cellular signaling pathways. The present study aimed to investigate the role of TNC and determine its effect in nasopharyngeal carcinoma (NPC). TNC gene transcription and expression were analyzed using the NPC dataset and immunohistochemistry analysis of NPC tissues. Weighted gene co-expression network and gene enrichment analyses were performed to determine the potential molecular mechanisms underlying the effects of TNC in NPC. TNC expression was suppressed in NPC cells, and the effects were determined both in vitro and in vivo. The results demonstrated that TNC gene transcription and expression were high in NPC tissues compared with normal tissues. Notably, TNC knockdown inhibited NPC cell proliferation, migration and invasion. In addition, TNC knockdown inhibited tumor growth in mice. In vitro, TNC knockdown inhibited epithelial-to-mesenchymal transition (EMT) and decreased activity of the PI3K/AKT/mTOR signaling pathway in NPC cells. Taken together, these results suggest that TNC promotes cell proliferation, EMT and activity of the PI3K/AKT/mTOR signaling pathway in NPC cells, and thus functions as an oncogene.