Triptolide impairs LUAD cells through the JAK-STAT signaling pathway by activating autophagy

Abstract Background Triptolide, an extract from the Chinese herb Tripterygium wilfordii , has shown anticancer activity in vitro and in vivo. In our present study, we aimed to investigate its antitumor effects by examining proliferation, migration, and invasion and the potential mechanism of autophagic induction in lung cancer cells. Methods An MTT assay was used to measure triptolide-mediated inhibition of Lung adenocarcinoma (LUAD)cell (A549 and NCI-H1299) viability. Colony formation, EdU, migration and invasion assays were used to examine the effects of triptolide on the proliferation, migration and invasion of lung cancer cells. Western blot analysis was used to examine the expression of various related proteins. Immunofluorescence assays were used to examine the protein expression of LC3B. Reverse transcription-quantitative polymerase chain reaction (RT–qPCR) was used to examine the mRNA levels of MYC and LIF. Bioinformatics analysis (KEGG, etc.) was used to reveal the pathways that are regulated by triptolide. Results Triptolide inhibits proliferation, migration and invasion and induces autophagy in A549 and NCI-H1299 LUAD cells. Inhibition of autophagy can reverse its inhibitory effects. Moreover, triptolide impaired lung cancer cell proliferation, migration and invasion through the JAK-STAT signaling pathway. Conclusion Triptolide attenuated proliferation, migration and invasion in LUAD cells through autophagy initiation resulted in the JAK-STAT signaling pathway. Triptolide has the potential to be an alternative therapeutic agent for lung cancer.