Exploring the impact of insufficient thermal ablation on hepatocellular carcinoma: NDST2 overexpression mechanism and its role in facilitating growth and invasion of residual cancer cells.

IF 3 3区 医学 Q2 ONCOLOGY
International Journal of Hyperthermia Pub Date : 2024-01-01 Epub Date: 2024-05-15 DOI:10.1080/02656736.2024.2353309
Weijun Wan, Danxia Guo, Tong Kang, Jinshu Pang, Yunjing Pan, Jiamin Chen, Wei Liao, Yuji Chen, Peng Lin, Lipeng Li, Hong Yang, Yun He
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Abstract

Objective: Incomplete thermal ablation (ITA) fosters the malignancy of residual cells in Hepatocellular carcinoma (HCC) with unclear mechanisms now. This study aims to investigate the expression changes of NDST2 following ITA of HCC and its impact on residual cancer cells.

Methods: An in vitro model of heat stress-induced liver cancer was constructed to measure the expression of NDST2 using Quantitative Real-Time PCR and Western blotting experiments. The sequencing data from nude mice were used for validation. The clinical significance of NDST2 in HCC was evaluated by integrating datasets. Gene ontology and pathway analysis were conducted to explore the potential signaling pathways regulated by NDST2. Additionally, NDST2 was knocked down in heat stress-induced HCC cells, and the effects of NDST2 on these cells were verified using Cell Counting Kit-8 assays, scratch assays, and Transwell assays.

Results: NDST2 expression levels are elevated in HCC, leading to a decrease in overall survival rates of HCC patients. Upregulation of immune checkpoint levels in high NDST2-expressing HCC may contribute to immune evasion by liver cancer cells. Additionally, the low mutation rate of NDST2 in HCC suggests a relatively stable expression of NDST2 in this disease. Importantly, animal and cell models treated with ITA demonstrate upregulated expression of NDST2. Knockdown of NDST2 in heat stress-induced liver cancer cells results in growth inhibition associated with gene downregulation.

Conclusion: The upregulation of NDST2 can accelerate the progression of residual HCC after ITA, suggesting a potential role for NDST2 in the therapeutic efficacy and prognosis of residual HCC.

探讨热消融不足对肝细胞癌的影响:NDST2 过度表达机制及其在促进残余癌细胞生长和侵袭中的作用。
目的:不完全热消融(ITA)会导致肝细胞癌(HCC)残留细胞恶变,但其机制尚不清楚。本研究旨在探讨 HCC 热消融后 NDST2 的表达变化及其对残余癌细胞的影响:方法:构建热应激诱导肝癌的体外模型,利用定量实时 PCR 和 Western 印迹实验检测 NDST2 的表达。裸鼠的测序数据用于验证。通过整合数据集评估了 NDST2 在 HCC 中的临床意义。通过基因本体论和通路分析来探索 NDST2 调控的潜在信号通路。此外,还在热应激诱导的 HCC 细胞中敲除了 NDST2,并使用细胞计数试剂盒-8 检测法、划痕检测法和 Transwell 检测法验证了 NDST2 对这些细胞的影响:结果:NDST2 在 HCC 中的表达水平升高,导致 HCC 患者的总生存率下降。高 NDST2 表达的 HCC 中免疫检查点水平的上调可能有助于肝癌细胞的免疫逃避。此外,NDST2 在 HCC 中的低突变率表明 NDST2 在这种疾病中的表达相对稳定。重要的是,经 ITA 处理的动物和细胞模型显示 NDST2 表达上调。在热应激诱导的肝癌细胞中敲除 NDST2 会导致与基因下调相关的生长抑制:结论:NDST2的上调可加速ITA后残留HCC的进展,这表明NDST2在残留HCC的疗效和预后中发挥着潜在作用。
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
5.90
自引率
12.90%
发文量
153
审稿时长
6-12 weeks
期刊介绍: The International Journal of Hyperthermia
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