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Bufalin down-regulates Axl expression to inhibit cell proliferation and induce apoptosis in non-small-cell lung
Nam-Yi Kim1, Young-Ah Suh2, Soyoung Kim1
1Department of Pharmacology, School of Medicine, Dongguk University, Gyeongju 38066, South Korea.
Abstract:
Axl, a member of the TAM (Tyro3, AXL, Mer) receptor tyrosine kinase family, plays critical roles in cell growth, proliferation, apoptosis, and migration. In the present study, we demonstrated that the anti-cancer activity of bufalin, a major bioactive component of the Chinese traditional medicine Chan Su, is mediated by the down-regulation of Axl in non-small-cell lung cancer (NSCLC) cells. We observed the inhibitory effect of bufalin on the proliferation of A549 and H460 NSCLC cells and the clonogenicity of these cells was reduced by bufalin treatment in a dose-dependent manner. Next, we found that the protein level of Axl was decreased in proportion to the concentration of bufalin in both A549 and H460 cells. Moreover, the promoter activity of the Axl gene was decreased by bufalin in a dose- and time-dependent manner, indicating that bufalin down-regulates Axl gene expression at the transcriptional level. We further examined if the anti-proliferative property of bufalin is influenced by Axl at the protein level. Axl overexpression attenuated the effect of bufalin in inhibiting cell proliferation and colony formation and inducing apoptosis in H460 cells, while knockdown of Axl gene expression induced the opposite effect. Taken together, our data indicate that the anti-proliferative and pro-apoptotic effects of bufalin were associated with the protein level of Axl, suggesting that Axl is a potent therapeutic target of bufalin in suppressing proliferation and inducing apoptosis in NSCLC cells.
Insights
Bufalin, derived from Chan Su, inhibits non-small-cell lung cancer (NSCLC) by down-regulating Axl receptor tyrosine kinase. This suggests Axl is a therapeutic target for NSCLC treatment.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Axl receptor tyrosine kinase (TAM family) is crucial for cell growth, proliferation, apoptosis, and migration.
- Non-small-cell lung cancer (NSCLC) is a major cause of cancer-related deaths worldwide.
- Bufalin, a bioactive component of Chan Su, exhibits anti-cancer properties.
Purpose of the Study:
- To investigate the anti-cancer mechanism of bufalin in NSCLC cells.
- To determine the role of Axl receptor tyrosine kinase in bufalin's anti-cancer activity.
- To explore Axl as a potential therapeutic target for NSCLC.
Main Methods:
- Cell proliferation and clonogenicity assays using A549 and H460 NSCLC cell lines.
- Western blot analysis to assess Axl protein levels.
- Reporter assays to evaluate Axl gene promoter activity.
- Axl overexpression and knockdown experiments.
Main Results:
- Bufalin inhibited proliferation and clonogenicity of NSCLC cells in a dose-dependent manner.
- Bufalin decreased Axl protein levels and Axl gene promoter activity.
- Axl overexpression attenuated bufalin's anti-proliferative and pro-apoptotic effects, while Axl knockdown enhanced them.
- Bufalin down-regulates Axl expression at the transcriptional level.
Conclusions:
- Bufalin exerts anti-cancer effects in NSCLC by down-regulating Axl.
- Axl plays a critical role in mediating bufalin's anti-proliferative and pro-apoptotic activities.
- Targeting Axl represents a potential therapeutic strategy for NSCLC treatment with bufalin.
