Background:Suppressor of Cytokine Signalling 6 (SOCS6) is a cytokine signalling suppressor that regulates receptor tyrosine kinase pathways by promoting degradation of signalling proteins, thereby controlling cell growth and survival. One of these tyrosine kinase receptors, Erythropoietin Receptor (EPOR), plays a critical role in CRC progression by enhancing tumour metabolism, angiogenesis, proliferation, and growth. This study investigates the molecular mechanisms governing SOCS6’s role in CRC pathogenesis using in vitro cell models and examines its interaction with EPOR expression following gene knockdown.Methods:Bioinformatics interaction between SOCS6 and EPOR were investigated using molecular visualization. HT-29 and COLO 320DM colorectal cancer cells were transfected with SOCS6 siRNA followed by measurement of SOCS6 and EPOR expression levels by qRT-PCR. The selected knockdown concentration was used in functional assays assessing cell viability, colony formation, migration, apoptosis, and invasion.Results:Bioinformatic results showed interaction between SOCS6 and EPOR through polar bonds. Furthermore, SOCS6 silencing increased cell viability and colony formation in both cell lines and significantly enhanced migration in COLO 320DM cells. Active caspase-3 levels were elevated markedly in HT-29 cells post SOCS6 knockdown, consistent with caspase-3’s reported oncogenic role in CRC. Moreover, EPOR knockdown selectively altered SOCS6 expression in HT-29 cells, indicating a regulatory feedback loop. EPOR silencing elevated cell viability at 24 h in both cell lines but caused a significant decrease in COLO 320DM cells at 72 h.Conclusions:These findings identify the SOCS6–EPOR axis as a potential target for personalized CRC therapy, supporting SOCS6’s tumour-suppressive and diagnostic roles.
背景：细胞因子信号传导抑制因子6（SOCS6）是一种细胞因子信号传导抑制因子，通过促进信号蛋白降解来调控受体酪氨酸激酶通路，从而控制细胞生长与存活。其中，促红细胞生成素受体（EPOR）作为一种酪氨酸激酶受体，通过增强肿瘤代谢、血管生成、增殖和生长，在结直肠癌（CRC）进展中发挥关键作用。本研究利用体外细胞模型探讨SOCS6在CRC发病机制中的分子调控机制，并分析基因敲低后其与EPOR表达的相互作用。 方法：通过分子可视化技术分析SOCS6与EPOR之间的生物信息学相互作用。使用SOCS6 siRNA转染HT-29和COLO 320DM结直肠癌细胞系，通过qRT-PCR检测SOCS6和EPOR的表达水平。选取的敲低浓度用于功能实验，评估细胞活力、克隆形成、迁移、凋亡和侵袭能力。 结果：生物信息学分析显示SOCS6与EPOR通过极性键相互作用。此外，沉默SOCS6可增强两种细胞系的细胞活力与克隆形成能力，并显著促进COLO 320DM细胞的迁移。在HT-29细胞中敲低SOCS6后，活化的caspase-3水平显著升高，这与caspase-3在CRC中已被报道的促癌作用一致。值得注意的是，EPOR敲低能选择性改变HT-29细胞中SOCS6的表达，提示存在调控反馈环路。EPOR沉默在24小时可提升两种细胞系的细胞活力，但在72小时导致COLO 320DM细胞活力显著下降。 结论：本研究证实SOCS6–EPOR信号轴可作为个体化CRC治疗的潜在靶点，进一步支持了SOCS6在肿瘤抑制与诊断中的作用。
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