LncRNA LINC00184 promotes docetaxel resistance and immune escape via miR-105-5p/PD-L1 axis in prostate cancer

Abstract

BackgroundDocetaxel (DTX) resistance is a common factor in metastatic prostate cancer (PC) chemotherapy that leads to treatment failure. Because lncRNA is involved in a variety of regulatory processes in tumor progression, this study aimed to explore the function and mechanism of LINC00184 in docetaxel resistance of PC. MethodsTwo PC cell lines and their docetaxel resistant cell lines (DU145/DTX and PC3/DTX) were used. The expression of LINC00184 in both cell lines and PC patient samples were evaluated. SiRNA knocking down was used to test the function of LINC00184 in proliferation and colony formation. Interaction between LINC00184 and its target miR-105-5p, as well as miR-105-5p and PD-L1 was checked by luciferase reporter assay and RNA pull-down assay. PC cell line and CD8 + T cell co-culture system was established, miR-105-5p inhibitor was co-transfected with LINC00184 siRNA to investigate the underline mechanism. ResultsLINC00184 was found to be associated with docetaxel resistance and adverse prognosis of prostate cancer. It regulated docetaxel resistance and T-cell-mediated immune response in prostate cancer cells. LINC00184 was induced by adsorption of miR-105-5p and negatively regulated it, subsequently inhibited the expression level of PD-L1. ConclusionsLINC00184 promoted docetaxel resistance and immune escape in prostate cancer cells by adsorption of miR-105-5p, resulted in upregulation of the expression of PD-L1. LINC00184 could possibly be considered as a potential target for treatment in prostate cancer patients with docetaxel-resistance.