Sun Wei, Shen Xiaoying, Wang Xinyi, Zhang Xiaoyan, Ji Yongling, Wang Jin
Zhejiang Cancer Hospital, Hangzhou, China.
Hangzhou Institute of Medicine (HIM), Chinese Academy of Sciences, Hangzhou, Zhejiang, China.
Histol Histopathol. 2024 Dec;39(12):1659-1667. doi: 10.14670/HH-18-752. Epub 2024 Apr 22.
This study investigates the association between NAT10 expression and clinical parameters while assessing prognostic outcomes in esophageal squamous cell carcinoma (ESCC) patients. Furthermore, the study seeks to elucidate the functional role of NAT10 in neoplastic cell proliferation and apoptosis.
NAT10 expression was assessed in ESCC tissue microarrays through immunohistochemistry (IHC) tests. We employed SPSS software to analyze the correlation between NAT10 staining data, clinical indicators, and their implications for patient prognosis. Small interference RNA (siRNA) was utilized to inhibit NAT10 expression in two esophageal cancer cell lines, TE-1 and KYSE150. Subsequently, we meticulously quantified and compared cellular proliferation and apoptotic ratios among experimental groups. NAT10, Ki67, and Caspase3 expression levels in different groups were evaluated using quantitative polymerase chain reaction (qPCR) and Western blot (WB) assays. Statistical analyses were conducted using GraphPad Prism software, with significance at <0.05.
Our findings indicate that NAT10 is overexpressed in ESCC tissues and exhibits a significant correlation with tumor diameter and overall patient survival. Decreasing NAT10 expression led to the inhibition of tumor cell proliferation and the promotion of apoptosis. Furthermore, siRNA-mediated NAT10 inhibition resulted in the downregulation of Ki67 expression and the concomitant upregulation of Caspase3.
The observed overexpression of NAT10 in ESCC tissues is associated with larger tumor diameters and reduced patient survival. NAT10 appears to play a pivotal role in the progression of esophageal cancer by influencing cell proliferation and apoptosis. These findings suggest potential clinical implications, with Ki67 and Caspase3 potentially participating in this intricate molecular biological process.
本研究调查了NAT10表达与临床参数之间的关联,同时评估了食管鳞状细胞癌(ESCC)患者的预后结果。此外,该研究旨在阐明NAT10在肿瘤细胞增殖和凋亡中的功能作用。
通过免疫组织化学(IHC)检测评估ESCC组织芯片中的NAT10表达。我们使用SPSS软件分析NAT10染色数据、临床指标及其对患者预后的影响之间的相关性。利用小干扰RNA(siRNA)抑制两种食管癌细胞系TE-1和KYSE150中的NAT10表达。随后,我们精心量化并比较了实验组之间的细胞增殖和凋亡率。使用定量聚合酶链反应(qPCR)和蛋白质免疫印迹(WB)分析评估不同组中NAT10、Ki67和Caspase3的表达水平。使用GraphPad Prism软件进行统计分析,显著性水平为<0.05。
我们的研究结果表明,NAT10在ESCC组织中过表达,并且与肿瘤直径和患者总生存期显著相关。降低NAT10表达导致肿瘤细胞增殖受到抑制,凋亡增加。此外,siRNA介导的NAT10抑制导致Ki67表达下调,同时Caspase3上调。
在ESCC组织中观察到的NAT10过表达与更大的肿瘤直径和患者生存期缩短有关。NAT10似乎通过影响细胞增殖和凋亡在食管癌进展中起关键作用。这些发现提示了潜在的临床意义,Ki67和Caspase3可能参与了这一复杂的分子生物学过程。