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.

Purpose Esophageal squamous cell carcinoma is associated with high morbidity and mortality rate for which radiotherapy is the main treatment modality. Niraparib, a Poly (ADP-ribose) polymerase 1 inhibitors (PARPi) was previously reported to confer radiosensitivity in different malignancies including non-small cell lung cancer. In this study, we assessed the in vivo ability of niraparib in conferring radiosensitivity to esophageal squamous cell carcinoma cells. Materials and methods In this study, KYSE-30 and KYSE-150 cell lines were selected as in vivo esophageal squamous cell carcinoma models. The experimental groups were: niraparib tosylate alone, radiotherapy alone, control (no intervention), and combination therapy (radiotherapy + niraparib tosylate). Cell cytotoxicity assay, colony formation assay, flow cytometry, immunofluorescence, Western blotting, immunohistochemistry, lentivirus transfection analysis, and xenograft models were used for confirming radiosensitizing ability of niraparib and to investigate the possible cellular mechanism involved in radiosensitization. Results The colony formation efficiency of the combination group was significantly much lower than that of the single radiation group (P < 0.01). Cell cytotoxicity assay demonstrated a significant reduction in proliferation of irradiated cells after treatment with niraparib tosylate compared to niraparib tosylate alone (P < 0.01). Cell apoptosis significantly increased in the combination group compared to either niraparib tosylate or radiotherapy alone (P < 0.01). Rate of tumor suppression rate was significantly high in the combined treatment group (P < 0.01) but, significantly decreased in nude mice. Western blot and lentivirus infection model suggested overexpression of FANCG genes to confer radiosensitivity. Conclusion These results suggest that the synergistic effect of niraparib tosylate and radiation may be related to the down-regulation of FANCG.