Dishevelled Segment Polarity Protein 3 (DVL3) Induced by Bacterial LPS Promotes the Proliferation and Migration of Prostate Cancer Cells through the TLR4 Pathway.

BACKGROUND

Chronic inflammation is associated with various malignant tumors. Bacterial lipopolysaccharides (LPSs) play a significant part in the event and development of prostate cancer. Dishevelled segment polarity protein 3 () is a shared component of the Wnt/β-catenin and Notch signaling pathways, which are involved in tumor progression, chemoresistance, and maintenance of stem cell-like properties. According to reports, prostatic cancer cell invasion and proliferation are mediated by toll-like receptor 4 (). However, the role and regulation of in prostate cancer and its relationship with remain unclear.

METHODS

Survival curves were plotted to evaluate the relationship between expression and prognosis in patients with prostate cancer. was silenced in PC3 and DU145 cells using small interfering RNAs (siRNAs). Subsequently, cell counting kit-8 (CCK-8) assay, colony formation assay, transwell migration assay, and quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) were performed to investigate the role of in cell proliferation and migration . The protein markers of potential pathways were analyzed via western blotting.

RESULTS

expression was linked to prognosis in patients with prostate cancer; In particular, patients with high expression had a poor prognosis. LPS stimulation increased ( < 0.01) the expression of in PC3 cells. regulated tumor cell proliferation and migration by mediating the increase ( < 0.01) in expression. Knockout of validated that played a crucial role in LPS-induced expression. Silencing of decreased ( < 0.01) the LPS-induced proliferation and migration of PC3 cells.

CONCLUSIONS

Bacterial LPS-induced promoted the multiplication and migration of prostate cancer cells through the pathway. This study offers a valuable reference for the development and clinical application of targeted drugs for prostate cancer.