The Importance of Caveolin-1 in Prostate Cancer Metabolism: Tumour Suppressive and Oncogenic Roles
| Autoři | |
|---|---|
| Rok publikování | 2024 |
| Druh | Konferenční abstrakty |
| Fakulta / Pracoviště MU | |
| Citace | |
| Popis | Caveolin-1 (Cav-1) is a key protein involved in cellular signalling and metabolism, playing a complex role in cancer progression. In prostate cancer, Cav-1's function is highly context-dependent and can have both tumour-suppressive and oncogenic functions, as its expression is low in primary tumour cells but increases during cancer progression. Cav-1 has been involved in modulating cellular metabolism, including processes such as oxidative phosphorylation (OXPHOS) and glycolysis, which are critical for metastasis, tumour growth, and survival. In this study, we investigated the impact of Cav-1 on prostate cancer cell behaviour by manipulating its expression in two cell lines: overexpressing Cav-1 in human prostate carcinoma epithelial cell line 22Rv1 and knocking out Cav-1 using CRISPR/Cas9 in a PC-3 cell line initiated from bone metastasis of grade IV prostatic adenocarcinoma. We studied changes in metabolic activity using Seahorse assays, focusing on OXPHOS and glycolysis, alongside evaluating cell proliferation, colony-forming, drug resistance, invasivity and migration. To explore the invasive potential in a more physiologically relevant context, we employed the BioSilk 3D invasion assay, which utilizes recombinant spider silk protein. It provides a biomimetic scaffold that simulates the extracellular matrix, allowing for a more realistic assessment of tumour cell behaviour in a three-dimensional environment. Our complex study highlights the role of Cav-1's in prostate cancer metabolism and progression, suggesting it as a potential therapeutic target. Future research will explore deeper into the metabolic pathways influenced by Cav-1, aiming to unravel the interplay between Cav-1-mediated metabolic regulation and cancer cell behaviour. This could pave the way for developing targeted therapies that disrupt key metabolic processes in prostate cancer. |