AI Article Synopsis
- Bladder cancer is more common in men and has high recurrence rates, particularly for non-muscle-invasive forms.
- Transient receptor potential canonical channels (TRPCs), especially TRPC3, influence cancer cell behavior through calcium signaling, and the study investigates the effects of the TRPC3 inhibitor Pyr3 on bladder cancer cells.
- Pyr3 treatment led to reduced cell viability, migration, and specific protein levels associated with cancer progression, indicating its potential as a therapeutic agent for bladder cancer by targeting PKC signaling.
Article Abstract
Bladder cancer, more prevalent in men, has high recurrence rates in non-muscle-invasive forms and is highly lethal upon metastasis in muscle-invasive cases. Transient receptor potential canonical channels (TRPCs), specifically TRPC3, play a role in calcium signaling, influencing cancer cell behavior. This study examines the effects of Pyr3, a TRPC3 inhibitor, and TRPC3 knockdown on both muscle-invasive (T24) and non-muscle-invasive (RT4) bladder cancer cells. Pyr3 treatment reduced cell viability, migration, adhesion, and calcium influx in these cells. Additionally, Pyr3 treatment and siTRPC3 downregulated protein kinase C alpha (PKCα), phospho-PKCα, and protein phosphatase 2A (PP2A) levels. While PKC activator phorbol 12-myristate 13-acetate (PMA) could not restore Pyr3-induced viability loss, it reversed the migration inhibition. In a xenograft model, Pyr3 suppressed T24 cell viability, Ki67, phospho-PKCα, PP2A and TRPC3 expression. These findings suggest that Pyr3 inhibits bladder cancer cell migration through PKC signaling and holds potential as a therapeutic agent for bladder cancer.
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| http://dx.doi.org/10.1016/j.ejphar.2024.177235 | DOI Listing |
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