Rapamycin Suppresses Tgf-Beta 1-Induced Nasopharyngeal Cancer Stem Cell Metastasis By Inhibiting Mitochondrial Metabolism

Recent studies have shown that mitochondrial metabolism is a potential target for cancer therapy. Rapamycin was reported to suppress cancer stem cells in nasopharyngeal carcinoma by inhibiting mammalian target of rapamycin (mTOR) signaling, a pathway implicated in the regulation of cell metabolism. However, the mechanism of the anti-cancer action of rapamycin is unclear. Here, we investigated mitochondrial metabolism and cell metastasis in nasopharyngeal cancer stem cells (CSCs). We report that mitochondria of nasopharyngeal carcinoma-derived CD133-positive CSCs exhibit a higher inner membrane potential and increased ATP production compared to their CD133-negative counterparts. Rapamycin repressed nasopharyngeal CSC metastasis by inhibiting TGF-beta 1-induced epithelial-mesenchymal transition (EMT). Moreover, rapamycin inhibited TGF-beta 1-induced EMT by decreasing mitochondrial metabolism. The collected data identify a new strategy for targeting nasopharyngeal cancer stem cell metastasis through the inhibition of mitochondrial metabolism.