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Updated: Jan 22, 2026

Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
Published on: October 10, 2025
Bavachinin exhibits antitumor activity against non‑small cell lung cancer by targeting PPARγ
Lu-Na Ge1, Lei Yan2, Cheng Li2
1Shandong Medicinal Biotechnology Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong 250062, P.R. China.
Abstract:
Bavachinin (BNN), one of the main active ingredients of Psoraleacorylifolia, can activate peroxisome proliferator‑activated receptor γ (PPARγ). PPARγ has become a promising therapeutic target in cancer. The aim of the present study was to explore the antitumor effects of BNN in non‑small cell lung cancer (NSCLC). Cell Counting Kit‑8 and lactate dehydrogenase release assays were performed to measure cell toxicity. Western blotting and immunofluorescence were used to analyze the expression of apoptosis‑related factors and PPARγ. The ability of PPARγ to bind to BNN was evaluated by drug affinity responsive target stability (DARTS) and cellular thermal shift assay (CETSA). A reactive oxygen species (ROS) assay kit was used to detect the ROS level. The results revealed that the survival rates and cell viability of A549 cells were reduced by BNN in a dose‑dependent manner. The present results also demonstrated that BNN dose‑dependently changed the expression of Bcl‑2, Bax, caspases‑3/9 and PPARγ. In addition, through the cytotoxic and anti‑proliferative effects, the apoptosis‑related proteins' inhibitive properties of BNN were completely inhibited by the PPARγ antagonists T0070907 and GW9662. The DARTS and CETSA results confirmed the protein binding activity of PPARγ. Furthermore, it was demonstrated that the BNN‑induced ROS generation was dependent on PPARγ activation. Taken together, the present study demonstrated that BNN induced the death of A549 cells by activating PPARγ, an effect mediated by the increased ROS level. These results highlighted the potential role of BNN as a chemotherapeutic agent against NSCLC.
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