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Differential expression of Axl and correlation with invasion and multidrug resistance in cancer cells
Yongfu Zhao1, Xiance Sun, Lili Jiang
1College of Laboratory Medicine, Dalian Medical University, Dalian, China.
Abstract:
Dysregulation of Axl receptor tyrosine kinases is implicated in the pathogenesis of several sensitive and refractory cancers. In this study we showed that Axl expression was upregulated in drug-resistant cancer cells, as compared to those in parental cells. Downregulation of Axl expression by RNAi led to a decrease of K562/ADR and MCF-7/ADR cells invasion, proliferation in soft agar, and increased cells chemosensitivity in vitro. In nude mice bearing xenografts, downregulation of Axl in MDR cells enhanced the anticancer activity of intraperitoneally applied chemotherapeutic drugs. Our observations suggest that Axl represents a promising gene for overcoming MDR in cancer therapy.
Insights
Axl receptor tyrosine kinase is upregulated in drug-resistant cancers. Inhibiting Axl can decrease cancer cell invasion and increase chemosensitivity, offering a potential strategy to overcome multidrug resistance (MDR) in cancer therapy.
Area of Science:
- Molecular oncology
- Cancer biology
- Drug resistance mechanisms
Background:
- Axl receptor tyrosine kinases play a role in cancer development.
- Axl is often dysregulated in difficult-to-treat cancers.
- Upregulation of Axl is observed in multidrug-resistant (MDR) cancer cells compared to sensitive cells.
Purpose of the Study:
- To investigate the role of Axl in multidrug-resistant (MDR) cancer.
- To evaluate the therapeutic potential of targeting Axl to overcome MDR.
Main Methods:
- Compared Axl expression in drug-resistant versus parental cancer cells.
- Utilized RNA interference (RNAi) to downregulate Axl expression.
- Assessed effects on cancer cell invasion, proliferation, and chemosensitivity in vitro.
- Evaluated Axl downregulation in xenograft models in nude mice.
Main Results:
- Axl expression was significantly higher in drug-resistant cancer cells.
- Downregulation of Axl reduced invasion and proliferation of MDR cells (K562/ADR and MCF-7/ADR).
- Reduced Axl levels increased cancer cell chemosensitivity in vitro.
- In vivo, Axl downregulation enhanced chemotherapy efficacy in MDR xenografts.
Conclusions:
- Axl receptor tyrosine kinase is a key factor in cancer multidrug resistance (MDR).
- Targeting Axl holds promise for overcoming MDR.
- Axl represents a potential therapeutic target for enhancing cancer treatment efficacy.
