肝细胞癌(HCC)是一种常见且致命的肝癌,其特征是病因复杂且治疗选择有限。FAM210B,与各种癌症有关,值得注意的是它在HCC的进展和治疗反应中的潜在作用。然而,它的表达模式,功能影响以及与患者预后的相关性以及对治疗的抵抗力尚不清楚。我们采用了全面的方法来探讨FAM210B在肝癌中的作用,分析其在癌症中的表达,亚细胞定位和对细胞增殖的影响,入侵,迁移,生物富集和免疫微环境。此外,我们研究了它在单细胞中的表达,药物敏感性及其与基因组不稳定性的关系,免疫疗法疗效和关键免疫检查点。虽然FAM210B的表达在不同的癌症中有所不同,肝癌组织与正常组织无明显差异。FAM210B水平升高与生存结果改善相关。亚细胞分析将FAM210B定位在质膜和细胞质中。FAM210B在HCC中普遍下调,它的抑制显著增强了细胞增殖,入侵和迁移。生物富集分析将FAM210B与代谢和免疫应答途径联系起来。此外,其表达改变了肝癌的免疫微环境,影响药物反应性和免疫治疗结果。FAM202B的高表达水平与舒尼替尼的耐药性增加和对免疫疗法的反应性增强相关。正如与肿瘤突变负担的关联所证明的那样,PDCD1、CTLA4和TIDE评分。FAM210B对肝癌有复杂的影响,影响肿瘤细胞行为,代谢途径,免疫微环境和对治疗的反应。
Hepatocellular carcinoma (HCC) is a common and lethal liver cancer characterized by complex aetiology and limited treatment options.
FAM210B, implicated in various cancers, is noteworthy for its potential role in the progression and treatment response of HCC. Yet, its expression patterns, functional impacts and correlations with patient outcomes and resistance to therapy are not well understood. We employed a comprehensive methodology to explore the role of
FAM210B in HCC, analysing its expression across cancers, subcellular localization and impacts on cell proliferation, invasion, migration, biological enrichment and the immune microenvironment. Additionally, we investigated its expression in single cells, drug sensitivity and relationships with genomic instability, immunotherapy efficacy and key immune checkpoints. While FAM210B expression varied across cancers, there was no notable difference between HCC and normal tissues. Elevated levels of
FAM210B were associated with improved survival outcomes. Subcellular analysis located
FAM210B in the plasma membrane and cytosol. FAM210B was generally downregulated in HCC, and its suppression significantly enhanced cell proliferation, invasion and migration. Biological enrichment analysis linked
FAM210B to metabolic and immune response pathways. Moreover, its expression modified the immune microenvironment of HCC, affecting drug responsiveness and immunotherapy outcomes. High expression levels of FAM202B correlated with increased resistance to sunitinib and enhanced responsiveness to immunotherapy, as evidenced by associations with tumour mutation burden, PDCD1, CTLA4 and TIDE scores. FAM210B exerts a complex influence on HCC, affecting tumour cell behaviour, metabolic pathways, the immune microenvironment and responses to therapy.