Purpose: To investigate the potential function of BTBD7 in prostate cancer (PCa) development and the underlying molecular mechanism.
Methods: Serum levels of BTBD7 in PCa patients were examined by qRT-PCR. Regulatory effects of BTBD7 on viability and invasiveness were detected by CCK-8 and Transwell assay, respectively. Moreover, Western blot analysis was conducted to examine protein levels of epithelial-mesenchymal transition (EMT) markers (E-cadherin and N-cadherin) in PCa cells intervened by BTBD7.
Results: Serum level of BTBD7 was increased in PCa patients, especially those with Gleason score ≥8 or TNM staging Ⅲ+Ⅳ. Knockdown of BTBD7 attenuated the viability and invasiveness of PCa cells, which upregulated E-cadherin and downregulated N-cadherin.
Conclusion: Serum level of BTBD7 increases in PCa patients. It accelerates PCa development by triggering proliferative and invasive potentials, as well as EMT.