Harmine Hydrochloride Induced G2/M Phase Cell Cycle Arrest, Autophagy and Apoptosis in Human Leukemia K562 Cells through Modulation of the MAPK Pathway

Abstract Background Previous studies have indicated that harmine hydrochloride (HAR-HC) has anti-tumor characteristics. However, its potential impact on human leukemia cells is unknown. In this study, we explored the potential mechanism of HAR-HC effects on human leukemia cells in vitro. Methods MTT assay was used to detect cell viability; A flow cytometer was used to analyze the cell cycle; Anexinn V-FITC/PI was used to detect cell apoptosis; Western blotting assay was used to analyze the expression of related proteins. Results The result of flow cytometry suggested G2/M phage arrest in K562 cells induced by HAR-HC. The expression levels of Cyclin E2, Cyclin D1, Bcl-2, Bcl-xL, Mcl-1, pro-caspase-3, and PARP decreased and the expression levels of Cyclin A2, Cyclin B1, p21, Myt-1, p-cdc2 (Tyr15), cleaved -caspase-3 and cleaved-PARP increased. Moreover, the expression of p-JNK and p-ERK1/2 increased and autophagy was induced in the HAR-HC treatment group. Additionally, HAR-HC facilitated autophagy by activating the ERK1/2 pathway. Conclusion HAR-HC induced G2/M phase cell cycle arrest, autophagy and apoptosis by activating the JNK, and ERK1/2 pathways in the human leukemia K562 cells.