Comprehensive analysis of the role of netrin G1 (NTNG1) in hepatocellular carcinoma cells.

癌症研究 肝细胞癌 生物 基因敲除 流式细胞术 癌变 肝癌 免疫组织化学 癌细胞 污渍 川地163 癌症 病理 细胞凋亡 免疫学 体外 医学 基因 巨噬细胞 生物化学 遗传学
作者
Xing Gao,Yan Lin,Xi Huang,Cheng Lü,Weifeng Luo,Dan Zeng,Yongqiang Li,Ting-Shi Su,Lin Yc,Jiazhou Ye
出处
期刊:European Journal of Pharmacology [Elsevier]
卷期号:963: 176262-176262
标识
DOI:10.1016/j.ejphar.2023.176262
摘要

Netrin G1 (NTNG1) is a member of the Netrin family and plays a crucial role in various human cancers. However, the molecular functions of NTNG1 in HCC and the underlying mechanisms remain unclear. HCC expression data was obtained from the GEO database and analyzed using various bioinformatics tools. The expression of NTNG1 in HCC tissues and liver cancer cells was evaluated through RT-qPCR and western blotting. Cells with stable NTNG1 overexpression and knockdown were established, and CCK-8, colony formation, and flow cytometry assays were conducted in vitro. The xenograft model was utilized to verify the tumorigenesis capacity of NTNG1 in vivo. IHC was employed to analyze the expression of NTNG1 and CD163 proteins. HCC-specific genes were screened, followed by functional enrichment and immune cell infiltration analysis. Finally, the Co-IP was used to detect the interaction between NTNG1 and N-cadherin. NTNG1 was highly expressed in HCC tissues and liver cancer cells, and associated with significantly poorer OS rates. In addition, NTNG1 overexpression in liver cancer cells significantly increased their proliferation, colony growth, invasion, migration, and EMT, while inhibiting apoptosis. Bioinformatics analyses indicated that NTNG1 was closely related to EMT and tumor infiltration. IHC staining revealed a positive correlation between NTNG1 expression and CD163 in HCC tissues. Additionally, an EMT inhibitor attenuated the expression levels of EMT-related markers and counteracted the effects of NTNG1 overexpression in liver cancer cells. This study is the first to identify NTNG1 as a potential therapeutic target in HCC, promoting tumor development and progression by regulating EMT.
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