FOXD2-AS1 inhibits the proliferation and migration in prostate cancer: an in vitro and in vivo study

Abstract

FOXD2 Adjacent Opposite Strand RNA 1 (FOXD2-AS1), a long noncoding RNA (lncRNA), exhibits specifically elevated in numerous cancerous cells. Numerous studies have shown that FOXD2-AS1 encourages cellular proliferation, migration and invasion. Nevertheless, the exact mechanism through which FOXD2-AS1 contributes to prostate cancer (PCa) remains unclear. Consequently, we aimed to explore the implications of FOXD2-AS1 on the growth of PCa. Initially, an elevation of FOXD2-AS1 observed in PCa cells (PC-3, DU145 and Lncap) than the prostate normal cell line RWPE2. Then, PC-3 cells were tranafected with shFOXD2-AS1, sh-Numerical Control (shNC) or FOXD2-AS1 to assess the implications of FOXD2-AS. Cell growth was measured with cell counting kit-8 (CCK8) and 5-ethynyl-2′-deoxyuridine (EDU) assays, and cell invasion and migration were assessed by Transwell assays, which demonstrated that FOXD2-AS1 silence impeded proliferation, migration and invasion of PC-3 cells. Additionally, we discovered that FOXD2-AS1 bonded with miR-206/programmed cell death protein 10 (PDCD10) trough analyzing the interaction sites of lncRNA, miRNA and protein. Then, these interaction abilities were confirmed by dual-luciferase reporter assays and RT-qPCR, suggesting FOXD2-AS1 could upregulate the amount of PDCD10 through suppressing miR-206. Furthermore, the role of FOXD2-AS1 silencing on PCa carcinogenesis were assessed. In vivo experiment, shFOXD2-AS1 led to a notable reduction in both the size and weight of PCa. These findings indicated that FOXD2-AS1 silencing effectively hindered the progression of prostate cancer. In conclusion, the upregulation of FOXD2-AS1 was observed in PCa, and the knockdown of FOXD2-AS1 could alleviated tumor development by targeting miR-206 to upregulate PDCD10 expression.