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Toosendanin Induces Lung Squamous Cell Carcinoma Cell Apoptosis and Inhibits Tumor Progression via the BNIP3/AMPK
Fabing Liu1,2, Guangxue Wang3, Liming Zhao4
1Department of Cardiothoracic Surgery, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Abstract:
Lung squamous cell carcinoma (LUSC) is the second most common type of non-small cell lung cancer. Toosendanin can target critical cancer cell survival and proliferation. However, the function of toosendanin in LUSC is limited. Cancer cell proliferative capacity is detected using cell morphology, colony formation, and flow cytometry. The invasiveness of the cells is detected by a Transwell assay, western blotting, and RT-qPCR. Nude mice are injected with H226 (1×106) and received an intraperitoneal injection of toosendanin every 2 days for 21 days. RNA sequence transcriptome analysis is performed on toosendanin-treated cells to identify target genes and signaling pathways. With increasing concentrations of toosendanin, the rate of cell proliferation decreases and apoptotic cells increases. The number of migrated cells significantly reduces and epithelial-mesenchymal transition is reversed. Injection of toosendanin in nude mice leads to a reduction in tumor volume, weight, and the number of metastatic tumors. Furthermore, KEGG shows that genes related to the AMPK pathway are highly enriched. BNIP3 is the most differentially expressed gene, and its expression along with phosphorylated-AMPK significantly increases in toosendanin-treated cells. Toosendanin exerts anticancer effects, induces apoptosis in LUSC cells, and inhibits tumor progression via the BNIP3/AMPK signaling pathway.
Insights
Toosendanin inhibits lung squamous cell carcinoma (LUSC) progression by inducing apoptosis and reducing cell proliferation. This natural compound targets the BNIP3/AMPK pathway, offering a potential therapeutic strategy for LUSC.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Lung squamous cell carcinoma (LUSC) is a prevalent non-small cell lung cancer subtype.
- Toosendanin demonstrates potential in targeting cancer cell survival and proliferation.
- The specific role of toosendanin in LUSC requires further investigation.
Purpose of the Study:
- To investigate the anticancer effects of toosendanin in LUSC.
- To elucidate the molecular mechanisms underlying toosendanin's action in LUSC.
- To evaluate the therapeutic potential of toosendanin in preclinical models of LUSC.
Main Methods:
- Cell proliferation assays (morphology, colony formation, flow cytometry) and invasion assays (Transwell).
- Western blotting and RT-qPCR for molecular analysis.
- In vivo studies using nude mice xenografts and RNA sequence transcriptome analysis.
Main Results:
- Toosendanin decreased LUSC cell proliferation and increased apoptosis in a dose-dependent manner.
- Toosendanin inhibited cell invasion and reversed epithelial-mesenchymal transition.
- In vivo, toosendanin reduced tumor growth, volume, weight, and metastasis.
- KEGG analysis revealed enrichment of the AMPK pathway, with increased BNIP3 and phosphorylated-AMPK expression.
Conclusions:
- Toosendanin exhibits significant anticancer effects against LUSC.
- The compound induces apoptosis and inhibits tumor progression by activating the BNIP3/AMPK signaling pathway.
- Toosendanin represents a promising therapeutic agent for LUSC treatment.
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