Cancer-associated fibroblasts-derived exosome PIK3AP1 promotes the malignant progression and immune escape of prostate cancer cells.

BACKGROUND

Prostate cancer (PCa) is a common malignant cancer. Cancer-associated fibroblasts (CAFs) play an important role in occurrence and development of tumors. B-cell adapter protein (PIK3AP1) is related to cell growth, inhibits cell apoptosis and mediates tumor therapy. Thereby, this study aims to explore the role and mechanism of CAFs exosomes and PIK3AP1 in PCa.

METHODS

Normal fibroblasts (NFs), CAFs, and exosomes were characterized by morphology observation and western blot. The proliferation, migration, invasion, and cell viability were examined by 5-Ethynyl-2'-deoxyuridine (EdU), transwell, and cell counting kit-8 (CCK8) assays, respectively. Proliferation and apoptosis of CD8+T cells were tested using flow cytometry. Gene expression was analyzed using qRT-PCR and western blot. Animal experiments were utilized to analyze the role of CAF-derived exosome PIK3AP1 in vivo.

RESULTS

CAFs-derived exosomes promoted the PCa cell proliferation, migration, invasion, cell viability, and immune escape. PIK3AP1 was up-regulated in CAFs and PCa cells and related to tumor immune escape. PIK3AP1 facilitated the malignant behavior of PCa and the immune escape in vivo and in vitro. CAFs-derived exosome promoted PCa progression and immune escape via carrying PIK3AP1.

CONCLUSIONS

CAFs-derived exosomes promote the malignant behavior and immune escape of PCa cells by PIK3AP1.