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Abstract：
UNASSIGNED: PLAUR has been found upregulated in various tumors and closely correlated with the malignant phenotype of tumor cells. The aim of this study was to investigate the relationship between PLAUR and clear cell renal cell carcinoma (ccRCC) and its potential mechanism of promoting tumor progression.
UNASSIGNED: The expression levels and clinical significance of PLAUR, along with the associated signaling pathways, were extensively investigated in ccRCC samples obtained from The Cancer Genome Atlas (TCGA). PLAUR expression in 20 pairs of ccRCC tumor tissues and the adjacent tissues was assessed using qRT-PCR and IHC staining. Additionally, a series of in vitro experiments were conducted to investigate the impact of PLAUR suppression on cellular proliferation, migration, invasion, cell cycle progression, and apoptosis in ccRCC. The Western blot analysis was employed to investigate the expression levels of pivotal genes associated with the PI3K/AKT/mTOR signaling pathway.
UNASSIGNED: The expression of PLAUR was significantly upregulated in ccRCC compared to normal renal tissues, and higher PLAUR expression in ccRCC was associated with a poorer prognosis than low expression. The in-vitro functional investigations demonstrated that knockdown of PLAUR significantly attenuated the proliferation, migration, and invasion capabilities of ccRCC cells. Concurrently, PLAUR knockdown effectively induced cellular apoptosis, modulated the cell cycle, inhibited the EMT process, and attenuated the activation of the PI3K/AKT/mTOR signaling pathway. PLAUR may represent a key mechanism underlying ccRCC progression.
UNASSIGNED: The involvement of PLAUR in ccRCC progression may be achieved through the activation of the PI3K/AKT/mTOR signaling pathway, making it a reliable biomarker for the identification and prediction of ccRCC.
UNASSIGNED: The expression levels and clinical significance of PLAUR, along with the associated signaling pathways, were extensively investigated in ccRCC samples obtained from The Cancer Genome Atlas (TCGA). PLAUR expression in 20 pairs of ccRCC tumor tissues and the adjacent tissues was assessed using qRT-PCR and IHC staining. Additionally, a series of in vitro experiments were conducted to investigate the impact of PLAUR suppression on cellular proliferation, migration, invasion, cell cycle progression, and apoptosis in ccRCC. The Western blot analysis was employed to investigate the expression levels of pivotal genes associated with the PI3K/AKT/mTOR signaling pathway.
UNASSIGNED: The expression of PLAUR was significantly upregulated in ccRCC compared to normal renal tissues, and higher PLAUR expression in ccRCC was associated with a poorer prognosis than low expression. The in-vitro functional investigations demonstrated that knockdown of PLAUR significantly attenuated the proliferation, migration, and invasion capabilities of ccRCC cells. Concurrently, PLAUR knockdown effectively induced cellular apoptosis, modulated the cell cycle, inhibited the EMT process, and attenuated the activation of the PI3K/AKT/mTOR signaling pathway. PLAUR may represent a key mechanism underlying ccRCC progression.
UNASSIGNED: The involvement of PLAUR in ccRCC progression may be achieved through the activation of the PI3K/AKT/mTOR signaling pathway, making it a reliable biomarker for the identification and prediction of ccRCC.
摘要：
■已发现PLAUR在各种肿瘤中上调，并与肿瘤细胞的恶性表型密切相关。本研究旨在探讨PLAUR与肾透明细胞癌（ccRCC）的关系及其促进肿瘤进展的潜在机制。
■PLAUR的表达水平和临床意义,以及相关的信号通路，在从癌症基因组图谱（TCGA）获得的ccRCC样品中进行了广泛的研究。使用qRT-PCR和IHC染色评估20对ccRCC肿瘤组织和邻近组织中的PLAUR表达。此外,进行了一系列体外实验，以研究PLAUR抑制对细胞增殖的影响，迁移,入侵,细胞周期进程，ccRCC细胞凋亡。采用蛋白质印迹分析来研究与PI3K/AKT/mTOR信号通路相关的关键基因的表达水平。
■与正常肾组织相比，ccRCC中PLAUR的表达明显上调，ccRCC中较高的PLAUR表达比低表达与较差的预后相关。体外功能研究表明，敲低PLAUR显著减弱增殖，迁移,和ccRCC细胞的侵袭能力。同时,PLAUR敲低有效诱导细胞凋亡，调节细胞周期，抑制了EMT过程，并减弱PI3K/AKT/mTOR信号通路的激活。PLAUR可能代表ccRCC进展的关键机制。
■PLAUR参与ccRCC进展可能是通过激活PI3K/AKT/mTOR信号通路实现的,使其成为ccRCC识别和预测的可靠生物标志物。
■PLAUR的表达水平和临床意义,以及相关的信号通路，在从癌症基因组图谱（TCGA）获得的ccRCC样品中进行了广泛的研究。使用qRT-PCR和IHC染色评估20对ccRCC肿瘤组织和邻近组织中的PLAUR表达。此外,进行了一系列体外实验，以研究PLAUR抑制对细胞增殖的影响，迁移,入侵,细胞周期进程，ccRCC细胞凋亡。采用蛋白质印迹分析来研究与PI3K/AKT/mTOR信号通路相关的关键基因的表达水平。
■与正常肾组织相比，ccRCC中PLAUR的表达明显上调，ccRCC中较高的PLAUR表达比低表达与较差的预后相关。体外功能研究表明，敲低PLAUR显著减弱增殖，迁移,和ccRCC细胞的侵袭能力。同时,PLAUR敲低有效诱导细胞凋亡，调节细胞周期，抑制了EMT过程，并减弱PI3K/AKT/mTOR信号通路的激活。PLAUR可能代表ccRCC进展的关键机制。
■PLAUR参与ccRCC进展可能是通过激活PI3K/AKT/mTOR信号通路实现的,使其成为ccRCC识别和预测的可靠生物标志物。
