[Mechanism of emodin in influencing proliferation and migration of nasopharyngeal carcinoma cells by regulating autophagy].

This study aims to investigate the effects of emodin on proliferation, migration, epithelial-mesenchymal transition(EMT), and autophagy in HONE-1 and CNE-2 cells of nasopharyngeal carcinoma(NPC). HONE-1 and CNE-2 cells were cultured in vitro and divided into control group, low-(7.5 μg·mL~(-1)), and high-(10 μg·mL~(-1)) dose group of emodin. The cells were treated with emodin of different concentrations for 48 h. CCK-8 and EdU experiments detected the proliferation ability of HONE-1 and CNE-2 cells, and clony formation assay detected the clony formation ability of HONE-1 and CNE-2 cells. Transwell assay detected the migration ability of HONE-1 and CNE-2 cells. A stem cell pellet experiment detected the dryness of HONE-1 and CNE-2 cells. Immunofluorescence staining analyzed the expression level of microtubule-associated protein 1 light chain 3β(LC3B) in HONE-1 and CNE-2 cells, and Western blot detected the expression levels of EMT-related proteins and autophagy-related proteins in HONE-1 and CNE-2 cells. The results showed that the IC_(50) of HONE-1 and CNE-2 cells treated with emodin for 48 h were 10.0 and 9.4 μg·mL~(-1), respectively. Compared with the control group, emodin could increase the cell proliferation inhibition rate of HONE-1 and CNE-2 cells, and the effect increased with time or drug dose. Emodin could inhibit the clony formation, migration, and stem cell pelletizing ability of HONE-1 and CNE-2 cells. Emodin could increase the expression level of LC3B in HONE-1 and CNE-2 cells and improve autophagy activity. Compared with the control group, the experimental group exhibited elevated expression levels of EMT-associated protein E-cadherin, reduced expression level of vimentin, increased expression levels of autophagy-related protein 5(ATG5) and LC3B, and decreased expression level of sequestosome 1(p62). In conclusion, emodin can promote the autophagy of human nasopharyngeal carcinoma cells and inhibit the proliferation, cloning, EMT, and pelletizing ability of tumor stem cells.