Neurotrophin 3 hinders the growth and metastasis of hepatocellular carcinoma cells
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 w...
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Veröffentlicht in: | Oncology and translational medicine 2020-08, Vol.6 (4), p.143-152 |
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Sprache: | eng |
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Zusammenfassung: | 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. |
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ISSN: | 2095-9621 |
DOI: | 10.1007/s10330-020-0426-6 |