Neurotrophin 3 hinders the growth and metastasis of hepatocellular carcinoma cells*

Author:

Zhao Shengnan1,Chen Aixia1,Cao Jingyu2,Wang Zusen2,Hu Weiyu2,Zhou Fei1,Liang Donghai1,Yu Hongsheng1

Affiliation:

1. Department of Radiation Oncology, the Affiliated Hospital of Qingdao University, Qingdao 266000, China

2. Department of Hepatobilary and Pancreatic Surgery, the Affiliated Hospital of Qingdao University, Qingdao 266000, China

Abstract

Abstract Objective Neurotrophin 3 (NTF3) is involved in numerous biological processes; however, its role in hepatocellular carcinoma (HCC) is not well studied. This study investigated NTF3 function in HCC progression and revealed its underlying molecular mechanisms. Methods The prognostic relevance of NTF3 was determined through a bioinformatical analysis of publicly available TCGA data. Immunohistochemistry of HCC biopsies was performed to explore the expression of NTF3. Cell growth and proliferation were analyzed using a Cell Counting Kit-8 (CCK-8) assay. Cell invasion and migration were analyzed using Boyden Transwell and wound healing assays. Protein expression and mRNA levels were evaluated through immunoblotting and quantitative polymerase chain reaction (qPCR). Cell apoptosis was evaluated with flow cytometry. Results NTF3 expression was significantly lower in HCC tissues than in adjacent non-tumor tissues. Low NTF3 expression was significantly associated with decreased patient survival and specific clinicopathological features. NTF3 overexpression reduced the proliferation, migration, and invasion abilities of HCC cell lines. Conclusion Decreased expression of NTF3 is associated with poor prognosis in HCC patients, likely due to its action in promoting HCC cell proliferation, migration, and invasion. Our findings provide a novel understanding into the pathogenesis of HCC and the role of NTF3 in tumor progression, suggesting that targeting NTF3 has potential therapeutic and diagnostic value for HCC.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Reference36 articles.

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