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

backgroundLung 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.

methodsThe 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.

resultsTexasin 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.

conclusionsTexasin emerges as a promising non-cytotoxic anti-lung adenocarcinoma cancer compound, significantly inhibiting malignant phenotypes, highlighting its potential for lung adenocarcinoma cancer therapy.