PDF(Pubmed)
Abstract：
UNASSIGNED: Abnormal anillin (ANLN) expression has been observed in multiple tumours and is closely associated with patient prognosis and clinical features. In this study, we systematically elucidated the clinical significance and biological roles of ANLN in patients with clear cell renal cell carcinoma (ccRCC).
UNASSIGNED: We obtained transcriptome and clinical data of patients with ccRCC from public databases. Multi-omics data and clinical samples were combined to analyse the correlation between ANLN expression and the clinical characteristics of patients with renal cancer. Additionally, the immune cell landscape of ANLN expression was evaluated using different immune algorithms in the tumour microenvironment. The tumour-promoting potential of ANLN was confirmed using in vitro assays, including CCK8 and Transwell assays.
UNASSIGNED: Bioinformatics analysis showed that ANLN is over-expressed in patients with ccRCC, as validated by clinical samples. Publicly available clinical data suggest that high ANLN expression may indicate poor outcomes in patients with ccRCC. Moreover, biological function analysis revealed a marked enrichment of the cell cycle and PI3K-Akt pathways. The distribution of immune cells, particularly M2 macrophages, differed in patients with ccRCC. Furthermore, ANLN silencing inhibited the proliferation, migration, and invasion of renal cancer cells in vitro. After ANLN expression was knocked down in 786-O cells, the protein levels of important PI3K signalling pathway components, including PI3K, Akt, and mTOR, drastically decreased.
UNASSIGNED: These findings suggest that ANLN is dysregulated in renal cancer tissues and promotes tumour progression by activating the PI3K/Akt/mTOR signalling pathway.
UNASSIGNED: We obtained transcriptome and clinical data of patients with ccRCC from public databases. Multi-omics data and clinical samples were combined to analyse the correlation between ANLN expression and the clinical characteristics of patients with renal cancer. Additionally, the immune cell landscape of ANLN expression was evaluated using different immune algorithms in the tumour microenvironment. The tumour-promoting potential of ANLN was confirmed using in vitro assays, including CCK8 and Transwell assays.
UNASSIGNED: Bioinformatics analysis showed that ANLN is over-expressed in patients with ccRCC, as validated by clinical samples. Publicly available clinical data suggest that high ANLN expression may indicate poor outcomes in patients with ccRCC. Moreover, biological function analysis revealed a marked enrichment of the cell cycle and PI3K-Akt pathways. The distribution of immune cells, particularly M2 macrophages, differed in patients with ccRCC. Furthermore, ANLN silencing inhibited the proliferation, migration, and invasion of renal cancer cells in vitro. After ANLN expression was knocked down in 786-O cells, the protein levels of important PI3K signalling pathway components, including PI3K, Akt, and mTOR, drastically decreased.
UNASSIGNED: These findings suggest that ANLN is dysregulated in renal cancer tissues and promotes tumour progression by activating the PI3K/Akt/mTOR signalling pathway.
摘要：
■已在多个肿瘤中观察到ANLN异常表达，并且与患者预后和临床特征密切相关。在这项研究中,我们系统地阐明了ANLN在肾透明细胞癌（ccRCC）患者中的临床意义和生物学作用。
■我们从公共数据库获得了ccRCC患者的转录组和临床数据。将多组学数据和临床样本相结合，分析ANLN表达与肾癌患者临床特征的相关性。此外,在肿瘤微环境中使用不同的免疫算法评估了ANLN表达的免疫细胞景观。使用体外试验证实了ANLN的促进肿瘤的潜力，包括CCK8和Transwell测定。
■生物信息学分析显示，ANLN在ccRCC患者中过度表达，经临床样本验证。公开的临床数据表明，高ANLN表达可能表明ccRCC患者的预后不良。此外，生物学功能分析显示细胞周期和PI3K-Akt通路显著富集.免疫细胞的分布,特别是M2巨噬细胞，ccRCC患者不同。此外，ANLN沉默抑制增殖,迁移,肾癌细胞的侵袭能力。在786-O细胞中敲低ANLN表达后，重要的PI3K信号通路组分的蛋白质水平，包括PI3K,Akt,还有MTOR,急剧下降。
■这些研究结果表明，ANLN在肾癌组织中失调，并通过激活PI3K/Akt/mTOR信号通路促进肿瘤进展。
■我们从公共数据库获得了ccRCC患者的转录组和临床数据。将多组学数据和临床样本相结合，分析ANLN表达与肾癌患者临床特征的相关性。此外,在肿瘤微环境中使用不同的免疫算法评估了ANLN表达的免疫细胞景观。使用体外试验证实了ANLN的促进肿瘤的潜力，包括CCK8和Transwell测定。
■生物信息学分析显示，ANLN在ccRCC患者中过度表达，经临床样本验证。公开的临床数据表明，高ANLN表达可能表明ccRCC患者的预后不良。此外，生物学功能分析显示细胞周期和PI3K-Akt通路显著富集.免疫细胞的分布,特别是M2巨噬细胞，ccRCC患者不同。此外，ANLN沉默抑制增殖,迁移,肾癌细胞的侵袭能力。在786-O细胞中敲低ANLN表达后，重要的PI3K信号通路组分的蛋白质水平，包括PI3K,Akt,还有MTOR,急剧下降。
■这些研究结果表明，ANLN在肾癌组织中失调，并通过激活PI3K/Akt/mTOR信号通路促进肿瘤进展。
