PRPF19 promotes the proliferation, migration, and inhibits autophagy in prostate cancer by suppressing SLC40A1.

IF 1.4 4区 医学 Q4 PHYSIOLOGY
Guofei Zhang, Wansong Zhang, Mingjiang Dan, Feng Zou, Chunming Qiu, Canbiao Sun
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引用次数: 0

Abstract

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.

PRPF19通过抑制SLC40A1促进前列腺癌症的增殖、迁移和抑制自噬。
癌症(PCa)是一种常见的癌症,也是男性癌症相关死亡的主要原因。研究前信使核糖核酸处理因子19(PRPF19)在前列腺癌增殖、迁移中的作用,并评估PRPF19作为治疗靶点的潜在能力。从癌症基因组图谱和GEPIA数据库中分析PRPF19的表达。进行定量实时聚合酶链反应(qRT-PCR)以评估PRPF9和溶质载体家族40成员1(SLC40A1)的转录。免疫组化(IHC)检测前列腺癌组织中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。采用Transwell方法研究癌症细胞的迁移和侵袭。Western印迹法检测PRPF9、E-钙粘蛋白、波形蛋白和α-平滑肌肌动蛋白(α-SMA)、SLC40A1、LC3、Beclin-1和ATG7的表达水平。进行免疫荧光测定以测量PCa细胞中LC3的表达。生物信息学分析显示PRPF19在前列腺癌中高度表达,qRT-PCR、蛋白质印迹和IHC检测证实了这一点。PRPF19过表达可促进PCa细胞的增殖,而PRPF19敲低可抑制PCa细胞增殖。此外,PRPF19可积极调节前列腺癌细胞的迁移和侵袭,促进E-钙粘蛋白、波形蛋白和α-SMA的表达。此外,LC3、Beclin-1和ATG7的表达受到PRPF19的负调控,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SLC40Al的mRNA并降低其蛋白水平,并且SLC40A2拮抗PRPF19对PCa细胞增殖、迁移和自噬的影响。PRPF19通过减弱SLC40A1的表达促进前列腺癌的增殖和迁移,并抑制自噬,表明PRPF19是前列腺癌治疗的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.30
自引率
5.60%
发文量
36
审稿时长
6-12 weeks
期刊介绍: Chinese Journal of Physiology is a multidisciplinary open access journal. Chinese Journal of Physiology (CJP) publishes high quality original research papers in physiology and pathophysiology by authors all over the world. CJP welcomes submitted research papers in all aspects of physiology science in the molecular, cellular, tissue and systemic levels. Multidisciplinary sciences with a focus to understand the role of physiology in health and disease are also encouraged. Chinese Journal of Physiology accepts fourfold article types: Original Article, Review Article (Mini-Review included), Short Communication, and Editorial. There is no cost for readers to access the full-text contents of publications.
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