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Desloratadine, a Novel Antigrowth Reagent for Bladder Cancer
Jianfeng Ma1, Jinchun Qi2, Shoubin Li3
1Department of Urology Surgery, Baoding No. 1 Hospital, Baoding, China.
Abstract:
Desloratadine, a potent antagonist for human histamine H1 receptor, has been revealed to exhibit antihistaminic activity and anti-inflammatory activity. However, it is not yet known whether desloratadine has any effect on the biological behaviors of tumor cells. In this study, we aimed to investigate the effects of desloratadine on cell growth and invasion in bladder cancer EJ and SW780 cells in vitro. We observed that desloratadine inhibited cell viability of EJ and SW780 cells in a dose- and time-dependent manner. Desloratadine treatment was also revealed to suppress colony-formation ability and induce cell cycle arrest at G1 phase in EJ cells. Desloratadine promoted cell apoptosis via modulating the expression of Bcl-2, Bax, cleaved caspase 3, and cleaved caspase 9 in EJ and SW780 cells. Western blot resulted showed that desloratadine also impaired the expression of autophagy-related proteins, such as Beclin 1, P62, and LC3I/II in EJ and SW780 cells; while autophagy inhibitor LY294002 reversed the effects of desloratadine on these proteins. Moreover, desloratadine remarkably attenuated cell migration and invasion. Furthermore, we illustrated that desloratadine downregulated the expression of N-cadherin, Vimentin, Snail1, and Snail2, while upregulated the expression of E-cadherin in EJ and SW780 cells in vitro. The level of interleukin 6 was reduced in desloratadine-treated cells, while upregulation of interleukin 6 significantly abolished the anticancer activity of desloratadine in cell invasion and Bcl-2, Bax, Beclin1, LC3-I/II, N-cadherin, and E-cadherin expression in EJ cells. Taken together, our data suggest a potential anticancer activity of desloratadine on cell growth and invasion for bladder cancer, which may be mediated by diminishing the epithelial-to-mesenchymal transition and interleukin 6.
Insights
Desloratadine, an H1 receptor antagonist, shows potential anticancer effects by inhibiting bladder cancer cell growth, invasion, and promoting apoptosis. It also reduces epithelial-to-mesenchymal transition and interleukin-6 levels.
Area of Science:
- Oncology
- Pharmacology
Background:
- Desloratadine is a known H1 receptor antagonist with antihistaminic and anti-inflammatory properties.
- Its effects on tumor cell biology, specifically bladder cancer, are not well-established.
Purpose of the Study:
- To investigate the in vitro effects of desloratadine on bladder cancer cell growth and invasion.
- To explore the underlying mechanisms of desloratadine's action in bladder cancer cells.
Main Methods:
- Cell viability, colony formation, cell cycle, and apoptosis assays were performed on EJ and SW780 bladder cancer cells.
- Western blot analysis was used to assess protein expression related to apoptosis, autophagy, and epithelial-to-mesenchymal transition (EMT).
- The role of interleukin-6 (IL-6) was investigated by modulating its levels and observing the effects on desloratadine's activity.
Main Results:
- Desloratadine inhibited bladder cancer cell viability, colony formation, and induced G1 cell cycle arrest and apoptosis.
- It modulated apoptosis-related proteins (Bcl-2, Bax, caspase 3/9) and impaired autophagy-related proteins (Beclin 1, P62, LC3I/II).
- Desloratadine reduced cell migration and invasion by downregulating EMT markers (N-cadherin, Vimentin, Snail1/2) and upregulating E-cadherin, with IL-6 playing a significant role.
Conclusions:
- Desloratadine exhibits potential anticancer activity against bladder cancer cell growth and invasion in vitro.
- Its mechanism involves promoting apoptosis, inhibiting EMT, and reducing IL-6 levels.
- Further research is warranted to explore desloratadine as a therapeutic agent for bladder cancer.
