Texasin, A main product from Caragana Jubata (Pall.) Poir, induces proliferation arrest and protective autophagy in lung adenocarcinoma.

BACKGROUND: Lung cancer, a leading cause of mortality worldwide, necessitates effective therapeutic strategies. Caragana jubata, a traditional Chinese medicinal plant, harbors Texasin, a potential anti-tumor agent. This study aimed to evaluate the anti-cancer effects of Texasin on lung cancer cells, while assessing its impact on normal lung cells. METHODS: The study utilized cell lines H1299 and A549, alongside normal lung embryonic cells, to investigate Texasin's effects through Cell Counting Kit-8, Transwell, and wound healing assays. Transcriptome sequencing and analysis were performed to identify potential mechanisms. β-galactosidase activity and Retinoblastoma(RB) protein expression were assessed, and autophagy and apoptosis were explored through chloroquine co-treatment. Mice bearing H1299 cell-derived tumors were treated with Texasin. Tumor changes were assessed through in vivo imaging, and autophagy levels within the tumors were analyzed. RESULTS: Texasin inhibited lung cancer cell proliferation, migration, and invasion without harming normal cells. It promoted cell senescence, arrested the cell cycle in G1 phase, and upregulated β-galactosidase and RB protein expression. Texasin induced protective autophagy, which could be converted to apoptosis by chloroquine co-treatment. Texasin inhibits the proliferation of lung adenocarcinoma cells in vivo, as evidenced by immunohistochemistry showing an increase in autophagy levels within the tumors. CONCLUSIONS: Texasin emerges as a promising non-cytotoxic anti-lung adenocarcinoma cancer compound, significantly inhibiting malignant phenotypes, highlighting its potential for lung adenocarcinoma cancer therapy.