钾离子通道蛋白HERG1可调控部分肿瘤的恶性生物学行为，但在食管癌中报道有限。我们预实验显示：HERG1在食管癌中高表达，能促进食管癌细胞增殖、侵袭及上皮间质转化；HERG1可上调泛素连接酶家族蛋白Cullin2（Cul2）和分泌粒蛋白III（SCG3），Cul2能促进SCG3表达。但尚不清楚HERG1、Cul2和SCG3中间的桥梁分子。已知HERG1能调控AKT/NF-κB信号轴。同时生物信息学预测：NF-κB能与Cul2启动子区结合。Cul2可调控E2F家族成员，而E2F家族成员能调控多种基因。因此我们假设：①HERG1通过Cul2增强SCG3表达，促进食管癌进展；②HERG1通过AKT/NF-κB信号轴调控Cul2表达；③Cul2通过E2F家族成员上调SCG3。本课题拟探讨HERG1在食管癌中的作用，阐明“HERG1-Cul2-SCG3”与食管癌进展的关系，为食管癌防治提供实验依据。

The potassium channel protein HERG1 has been confirmed to be involved in the regulation of malignant biological behaviors of certain tumors; however, there are few reports on its role in esophageal carcinoma. Our prophase research demonstrated that HERG1 was highly expressed in esophageal carcinoma specimens and could promote esophageal carcinoma cell proliferation and invasion, as well as the epithelial-mesenchymal transition; HERG1 induced upregulation of Cullin2 (Cul2), a member of the ubiquitin ligase family, and secretogranin III (SCG3). However, the linking molecules involved in HERG1, Cul2, and SCG3 are not known. HERG1 has been shown to be involved in regulation of the AKT/NF-κB signaling pathway. Bioinformatics prediction revealed that NF-κB binds to the Cul2 promoter region. Meanwhile, HERG1 modulates the E2F family, which is involved in the regulation of numerous genes. Therefore, we proposed that ①HERG1 enhances the expression of SCG3 by targeting Cul2, thus promoting esophageal carcinoma progression; ②HERG1 regulates Cul2 through the AKT/NF-κB signaling pathway; ③Cul2 regulates SCG3 through the E2F family. This study aimed to explore the role of HERG1 in esophageal carcinoma and clarify the potential relationship between "HERG1-Cul2-SCG3" and esophageal carcinoma progression, thus providing experimental evidence that could be beneficial for the prevention and treatment of esophageal carcinoma.