Voltage-gated potassium channel subfamily A member 1 (KCNA1/Kv1.1) is an important component of type A potassium channels, which has been found to be involved in various tumors. This study aimed to identify the role of KCNA1 in cervical cancer and explore the related mechanism. The levels of KCNA1 in cervical cancer tissues and cell lines were examined by Western blot and qPCR. Cell proliferation and invasion were assessed by CCK-8 and transwell assays, respectively. Protein levels of Hedgehog (Hhg), Wnt and Notch were detected by Western blot. The mitochondrial capacity was examined by immunostaining with MitoTracker Red CMXRos. KCNA1 was highly expressed in cervical cancer tissues and cell lines, and correlated with poor prognosis. In addition, depletion of KCNA1 suppressed growth, proliferation, migration and invasion of HeLa cells. Moreover, KCNA1 could regulate the Hhg, Wnt and Notch signaling pathways and cause mitochondrial dysfunction. The present study has demonstrated that KCNA1 is an oncogene excessively expressed in cervical cancer, and promotes tumor progression by regulating the Hhg, Wnt and Notch signaling pathways and the mitochondrial capacity. Therefore, our results provide a theoretical basis for the discovery of novel clinical treatment against cervical cancer.

电压门控钾通道亚家族A成员1（KCNA1 / Kv1.1）是A型钾通道的重要组成部分，已发现其参与了多种肿瘤。本研究旨在确定KCNA1在宫颈癌中的作用，并探讨其相关机制。通过蛋白质印迹和qPCR检查宫颈癌组织和细胞系中KCNA1的水平。分别通过CCK-8和transwell测定法评估细胞增殖和侵袭。用Western blot检测刺猬蛋白（Hhg），Wnt和Notch的蛋白水平。通过用MitoTracker Red CMXRos免疫染色检查线粒体容量。KCNA1在宫颈癌组织和细胞系中高表达，并与不良预后相关。此外，KCNA1的消耗抑制了HeLa细胞的生长，增殖，迁移和侵袭。此外，KCNA1可能调节Hhg，Wnt和Notch信号通路并引起线粒体功能障碍。本研究表明，KCNA1是在宫颈癌中过度表达的致癌基因，并通过调节Hhg，Wnt和Notch信号通路以及线粒体能力促进肿瘤进展。因此，我们的结果为发现针对宫颈癌的新型临床治疗方法提供了理论基础。