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Salidroside Enhances the Sensitivity of Lung Cancer Cells to Paclitaxel by Regulating the Wnt/β-catenin Signaling
Guo-Liang Pi1, Liang-Hao Cheng2, Bin-Feng Li3
1Department of Radiation Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430079, China.
Objective:
Chemoresistance, such as paclitaxel (PTX) resistance, has become a great obstacle in non-small cell lung cancer (NSCLC) treatment. The natural agent salidroside (SAL) has been shown to exert an antitumor effect on NSCLC. Nonetheless, it is unclear whether SAL can decrease the resistance of NSCLC to PTX.
Methods:
PTX-resistant NSCLC cells (H1299/PTX and A549/PTX) were generated. Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Colony formation assay and flow cytometry were utilized to assess cell proliferation and apoptosis, respectively. Immunofluorescence staining and TOP/FOP flash luciferase assay were employed to estimate β-catenin activation. Western blotting was implemented to estimate the protein levels of apoptosis-, proliferation-, and Wnt/β-catenin signaling-associated markers. A xenograft mouse model was established to investigate the impact of SAL on PTX resistance in vivo.
Results:
SAL increased PTX-induced suppression of proliferation and promoted apoptosis in PTX-resistant NSCLC cells. SAL blocked the Wnt/β-catenin signaling in A549/PTX cells and in tumor-bearing mice. Activating Wnt/β-catenin signaling reversed the SAL-mediated increase in the sensitivity of NSCLC cells to PTX. SAL attenuated PTX resistance in NSCLC in the xenograft mouse model.
Conclusion:
SAL enhances the sensitivity of NSCLC cells to PTX by blocking the Wnt/β-catenin signal transduction.
Insights
Salidroside (SAL) can overcome paclitaxel (PTX) resistance in non-small cell lung cancer (NSCLC) by inhibiting Wnt/β-catenin signaling. This natural agent enhances chemotherapy effectiveness, offering a potential new strategy for NSCLC treatment.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Paclitaxel (PTX) resistance is a major challenge in treating non-small cell lung cancer (NSCLC).
- Salidroside (SAL), a natural compound, exhibits anti-NSCLC properties.
- The effect of SAL on PTX resistance in NSCLC remains largely unknown.
Purpose of the Study:
- To investigate whether salidroside (SAL) can reduce paclitaxel (PTX) resistance in non-small cell lung cancer (NSCLC).
- To elucidate the underlying molecular mechanisms of SAL's action on PTX-resistant NSCLC.
Main Methods:
- Generated paclitaxel-resistant NSCLC cell lines (H1299/PTX, A549/PTX).
- Assessed cell viability, proliferation, and apoptosis using CCK-8, colony formation, and flow cytometry.
- Investigated Wnt/β-catenin signaling activation via immunofluorescence, luciferase assays, and Western blotting.
- Evaluated SAL's efficacy in a xenograft mouse model.
Main Results:
- SAL enhanced PTX-induced proliferation suppression and apoptosis in resistant NSCLC cells.
- SAL inhibited Wnt/β-catenin signaling in resistant cells and in vivo.
- Reactivation of Wnt/β-catenin signaling counteracted SAL's effect on PTX sensitivity.
- SAL treatment reduced PTX resistance in a xenograft mouse model.
Conclusions:
- Salidroside (SAL) resensitizes non-small cell lung cancer (NSCLC) cells to paclitaxel (PTX).
- This effect is mediated by the inhibition of the Wnt/β-catenin signaling pathway.
- SAL represents a promising therapeutic agent to overcome chemoresistance in NSCLC.
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