Gao Yan, Li Yan, Song Ziyan, Jin Zhenxing, Li Xiao, Yuan Chunluan
Department of Oncology, The First People's Hospital of Lianyungang, Lianyungang 222061, China.
Department of Pharmacy, The First People's Hospital of Lianyungang, Lianyungang 222061, China.
J Oncol. 2022 Jul 8;2022:6509028. doi: 10.1155/2022/6509028. eCollection 2022.
Recent evidence suggests that promotes carcinogenesis and tumor progression in multiple types of cancers. This study investigates the role of in hepatocellular carcinoma (HCC).
The differentially expressed gene was screened through GEO and TCGA databases. The gene was identified and its expression was then verified by TCGA and HCCDB (a database of hepatocellular carcinoma expression atlas) databases. The Human Protein Atlas database was used to assess the gene expression in tissues. The TCGA and KM-plotter databases were used to study the relationship between and HCC. The correlation between and immune cells was evaluated through the TIMER database. GO and KEGG enrichment analysis was used to investigate the possible mechanism. The role of in cell proliferation and invasion of HCC was further explored through in vitro experiments.
The differentially expressed molecule obtained from database screening was . Its expression was higher in cancer tissues than in paracancerous ones, and it was mainly located in the cytoplasm. The TCGA, KM-plotter databases, and our study data showed that low expression in HCC patients had better overall survival (OS), progression-free survival (PFI), and disease-specific survival (DSS). Further analysis indicated a significant correlation between expression and immune cell infiltration. The gene set enrichment analysis (GSEA) analysis showed that affected the biological events of HCC by participating in the WNT, TGF-BETA, JAK, STAT, and CALCIUM signaling pathways. In vitro, cytological experiments demonstrated reduced expression of PCNA, Ki-67, Vimentin, N-cadherin, and MMP-9 mRNA after knocking down , although E-cadherin expression was promoted. Overall, these processes reduced the ability of proliferation and invasion of HCC cells.
Downregulation of can prolong the OS, PFI, and DSS of HCC patients. Furthermore, due to its link with immune cell infiltration, the gene represents a potentially novel predictive biomarker of HCC. The growth of HCC can be significantly inhibited by interfering with ; therefore, these results provide a potential target for developing anticancer strategies for HCC.
近期证据表明,[具体内容缺失]在多种癌症中促进致癌作用和肿瘤进展。本研究调查[具体内容缺失]在肝细胞癌(HCC)中的作用。
通过GEO和TCGA数据库筛选差异表达基因。鉴定[具体内容缺失]基因,然后通过TCGA和HCCDB(肝细胞癌表达图谱数据库)数据库验证其表达。使用人类蛋白质图谱数据库评估该基因在组织中的表达。利用TCGA和KM-plotter数据库研究[具体内容缺失]与HCC的关系。通过TIMER数据库评估[具体内容缺失]与免疫细胞之间的相关性。采用GO和KEGG富集分析来研究可能的机制。通过体外实验进一步探索[具体内容缺失]在HCC细胞增殖和侵袭中的作用。
从数据库筛选获得的差异表达分子为[具体内容缺失]。其在癌组织中的表达高于癌旁组织,且主要位于细胞质中。TCGA、KM-plotter数据库以及我们的研究数据表明,HCC患者中[具体内容缺失]低表达具有更好的总生存期(OS)、无进展生存期(PFI)和疾病特异性生存期(DSS)。进一步分析表明,[具体内容缺失]表达与免疫细胞浸润之间存在显著相关性。基因集富集分析(GSEA)显示,[具体内容缺失]通过参与WNT、TGF-BETA、JAK、STAT和钙信号通路影响HCC的生物学事件。在体外,细胞学实验表明,敲低[具体内容缺失]后,PCNA、Ki-67、波形蛋白、N-钙黏蛋白和MMP-9 mRNA的表达降低,尽管E-钙黏蛋白表达得到促进。总体而言,这些过程降低了HCC细胞的增殖和侵袭能力。
[具体内容缺失]的下调可延长HCC患者的OS、PFI和DSS。此外,由于其与免疫细胞浸润的关联,[具体内容缺失]基因代表了一种潜在的新型HCC预测生物标志物。干扰[具体内容缺失]可显著抑制HCC的生长;因此,这些结果为开发HCC抗癌策略提供了一个潜在靶点。