食道癌是全球最恶性的肿瘤之一。干扰素α诱导蛋白6（IFI6）的功能紊乱已与多种人类疾病，包括癌症有关。我们进行了这项研究，以探究IFI6在食道鳞状细胞癌（ESCC）细胞中的功能和潜在分子途径。利用数据库派生数据和石蜡包埋组织样本分析了IFI6的表达。利用CCK-8基于分析、EdU染色、克隆形成、β-半乳糖苷酶染色以及Annexin V/PI双染色法，确定了IFI6对细胞生长、衰老和凋亡的影响。在小鼠异种移植瘤模型中研究了体内肿瘤生长。采用RNA测序(RNA-seq)分析了IFI6所影响的转录本和途径。结果显示，IFI6的表达在ESCC中升高，并与不良临床预后相关（P<0.05）。使用慢病毒在TE-1和TE-10细胞中过表达和沉默IFI6。IFI6的上调促进了体外和体内的细胞生长，而下调则产生相反效果。IFI6过表达抑制了细胞衰老和凋亡，但不影响细胞周期进程，而IFI6下调则增加了细胞衰老和凋亡。RNA-seq显示，3个mRNAs（EPHA5、CLIP1和GTF2F2）与IFI6的过表达和沉默均有一致的关联。IFI6似乎通过复杂的机制调节TE-1细胞。总之，IFI6在体外和体内都对ESCC细胞的增殖起着积极的作用，可能成为治疗ESCC的新的治疗靶点。

Oesophageal cancer is one of the most malignant tumors worldwide. Dysfunction of interferon alpha-inducible protein 6 (IFI6) has been implicated in numerous human diseases, including cancer. We performed the study to investigate the function and potential molecular pathways of IFI6 in oesophageal squamous cell carcinoma (ESCC) cells. IFI6 expression was analysed using databases-derived data and paraffin-embedded tissue samples. CCK-8-based analyses and EdU staining, colony formation, β-galactosidase staining and Annexin V/PI double-staining assays were used to determine the influence of IFI6 on cell growth, senescence and apoptosis. Tumor growth in vivo was investigated in mouse xenograft models. RNA sequencing (RNA-seq) was performed to identify the transcripts and pathways affected by IFI6. The results showed that IFI6 expression was elevated in ESCC and correlated with poor clinical prognosis (P<0.05). IFI6 was overexpressed and silenced in TE-1 and TE-10 cells using lentiviruses. Upregulation of IFI6 promoted cell growth both in vitro and in vivo, whereas downregulation induced opposite effects. IFI6 overexpression inhibited cell senescence and apoptosis but did not influence cell cycle progression, while IFI6 downregulation increased cell senescence and apoptosis. RNA-seq revealed that 3 mRNAs (EPHA5, CLIP1 and GTF2F2) were consistently associated with both IFI6 overexpression and silencing. IFI6 appeared to modulate TE-1 cells via complex mechanisms. In conclusion, IFI6 plays a positive role in the proliferation of ESCC cells both in vitro and in vivo, which could be a novel therapeutic target for treating ESCC.