前列腺癌（PCa）是一种常见癌症，也是男性癌症相关死亡的主要原因。探讨前mRNA加工因子19（PRPF19）在PCa增殖、迁移中的作用，并评估PRPF19作为治疗靶点的潜在能力。 PRPF19 表达通过癌症基因组图谱和 GEPIA 数据库进行分析。进行定量实时聚合酶链反应 (qRT-PCR) 来评估 PRPF9 和溶质载体家族 40 成员 1 (SLC40A1) 的转录。采用免疫组织化学 (IHC) 检测 PCa 组织中 PRPF9 的表达。进行细胞活力和5-乙炔基-2'-脱氧尿苷掺入分析以评估细胞增殖。进行Transwell实验来研究癌细胞的迁移和侵袭。 Western blot检测PRPF9、E-cadherin、Vimentin、α-平滑肌肌动蛋白(α-SMA)、SLC40A1、LC3、Beclin-1、ATG7的表达水平。进行免疫荧光测定来测量 PCa 细胞中 LC3 的表达。生物信息分析显示PRPF19在前列腺癌中高表达，并通过前列腺癌组织中的qRT-PCR、蛋白质印迹和IHC检测证实。 PRPF19过表达可促进PCa细胞的增殖，敲低PRPF19可抑制PCa细胞的增殖。此外，PRPF19可正向调节PCa细胞的迁移和侵袭，促进E-cadherin、Vimentin和α-SMA的表达。此外，LC3、Beclin-1和ATG7的表达受到PRPF19的负调节，表明PRPF19抑制PCa细胞中的自噬。在PRPF19和SLC40A1的双重敲除中，PRPF19抑制SLC40A1的mRNA并降低SLC40A1的蛋白水平，并且SLC40A1拮抗PRPF19对PCa细胞的增殖、迁移和自噬的作用。 PRPF19通过减弱SLC40A1表达促进PCa的增殖和迁移，并抑制自噬，表明PRPF19是PCa治疗的潜在治疗靶点。

Prostate cancer (PCa) is a common cancer and the leading cause of cancer-related death in men. To investigate the role of pre-mRNA processing factor 19 (PRPF19) in proliferation, migration of PCa, and evaluate the potential ability of PRPF19 as a therapeutic target. PRPF19 expression was analyzed from The Cancer Genome Atlas and GEPIA databank. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate the transcription of PRPF9 and solute carrier family 40 member 1 (SLC40A1). Immunohistochemistry (IHC) was used to test PRPF9 expression in PCa tissues. The cell viability and 5-ethynyl-2'-deoxyuridine incorporation analysis were performed to assess cell proliferation. Transwell assay was performed to investigate the migration and invasion of cancer cells. Western blot was used to measure the expression level of PRPF9, E-cadherin, Vimentin and α-smooth muscle actin (α-SMA), SLC40A1, LC3, Beclin-1 and ATG7. Immunofluorescence assay was performed to measure LC3 expression in PCa cells. The bioinformatic analysis revealed PRPF19 was highly expressed in PCa which was certified by qRT-PCR, western blot and IHC detection in PCa tissues. The proliferation of PCa cells could be promoted by PRPF19 overexpression and suppressed by PRPF19 knockdown. Moreover, the migration and invasion of PCa cells could be positively regulated by PRPF19 which promoted the expression of E-cadherin, Vimentin, and α-SMA. Furthermore, the expression of LC3, Beclin-1, and ATG7 was negatively regulated by PRPF19, indicating that PRPF19 inhibited autophagy in PCa cells. In the double knockdown of PRPF19 and SLC40A1, PRPF19 repressed the mRNA and reduced protein level of SLC40A1, and SLC40A1 antagonized effects of PRPF19 on proliferation, migration and autophagy of PCa cells. PRPF19 promoted proliferation and migration, and inhibited autophagy in PCa by attenuating SLC40A1 expression, indicating PRPF19 was a potential therapeutic target for PCa treatment.