FNBP4 is a Potential Biomarker Associated with Cuproptosis and Promotes Tumor Progression in Hepatocellular Carcinoma

作者全名："Zheng, Kai-Wen; Zhang, Chao-Hua; Wu, Wu; Zhu, Zhu; Gong, Jian-Ping; Li, Chun-Ming"

作者地址："[Zheng, Kai-Wen; Wu, Wu; Zhu, Zhu; Gong, Jian-Ping; Li, Chun-Ming] Chongqing Med Univ, Affiliated Hosp 2, Dept Hepatobiliary Surg, Chongqing, Peoples R China; [Zheng, Kai-Wen] Peoples Hosp Rongchang Dist, Dept Hepatobiliary Surg, Chongqing, Peoples R China; [Zhang, Chao-Hua] Chongqing Med Univ, Affiliated Hosp 2, Dept Gastrointestinal Surg, Chongqing, Peoples R China"

通信作者："Li, CM (通讯作者)，Chongqing Med Univ, Affiliated Hosp 2, Dept Hepatobiliary Surg, Chongqing, Peoples R China."

来源：INTERNATIONAL JOURNAL OF GENERAL MEDICINE

ESI学科分类：　

WOS号：WOS:000931605400001

JCR分区：Q2

影响因子：2.1

年份：2023

卷号：16

期号：　

开始页：467

结束页：480

文献类型：Article

关键词：FNBP4; hepatocellular carcinoma; HCC; cuproptosis; biomarker

摘要："Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors that lacks an efficient therapeutic approach because of its elusive molecular mechanisms. This study aimed to investigate the biological function and potential mechanism of formin-binding protein 4 (FNBP4) in HCC. Methods: FNBP4 expression in tissues and cells were detected by quantitative real-time PCR (qRT-PCR), Western blot, and immunohistochemistry (IHC). The Kaplan-Meier method was used to explore the correlation between the FNBP4 expression and clinical survival. MTT, EdU incorporation, colony formation, and Transwell assays were performed to evaluate the function of FNBP4 in cell proliferation and migration in vitro. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was used to explore the potential mechanism of FNBP4. The prognostic risk signature and nomogram were constructed to demonstrate the prognostic value of FNBP4. Results: We found that FNBP4 was upregulated in patients with HCC and associated with poor overall survival (OS). Furthermore, knockdown of FNBP4 inhibited the proliferation and migration in HCC cells. Then, we performed a KEGG pathway analysis of the coexpressed genes associated with FNBP4 and found that FNBP4 may be associated with tumor-related signaling pathways and cuproptosis. We verified that FNBP4 could cause cell cycle progression and inactivation of the hippo signaling pathway. A prognostic risk signature containing three FNBP4-related differentially expressed cuproptosis regulators (DECRs) was established and can be used as an independent risk factor to evaluate the prognosis of patients with HCC. In addition, a nomogram including a risk score and clinicopathological factors was used to predict patient survival probabilities. Conclusion: FNBP4, as a potential biomarker associated with cuproptosis, promotes HCC cell proliferation and metastasis. We provide a new potential strategy for HCC treatment by targeting FNBP4."

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