Abstract / Summary
Abstract Oral squamous cell carcinoma (OSCC) is one of the most prevalent malignancies of the head and neck, characterized by high rates of recurrence, metastasis, and, in some cases, resistance to conventional therapies. The overall survival rate remains unsatisfactory despite advances in treatment strategies. This underscores a need for novel targets and therapeutic approaches. The voltage-gated potassium channel Kv10.1 (ether-à-go-go 1; Eag1) is a promising candidate that is minimally expressed in normal somatic tissues but aberrantly upregulated across a wide range of tumor types. Recent studies have shown that Kv10.1 plays an important role in various oncogenic processes, including cellular proliferation and cell survival. The tumor-restricted expression and functional role of Kv10.1 in malignant progression make it a suitable target for therapeutic intervention in cancers. In this study, we investigated for the first time the role of Kv10.1 in OSCCs. We showed by immunofluorescence that OSCCs expressed high levels of Kv10.1. The OSCC cell line HN also expressed Kv10.1. The functional activity of Kv10.1 was validated electrophysiologically. Blocking of Kv10.1 in OSCC cell lines with astemizole and imipramine induced apoptosis. Furthermore, Kv10.1-positive tumors displayed a high level of proliferation marker (Ki67) compared to Kv10.1-negative tumors. Kv10.1 expression was associated with poor clinical outcomes in OSCC patients. We conclude that Kv10.1 is aberrantly expressed in OSCC, enhancing cellular proliferation, suppressing apoptosis, and is associated with poor prognosis in OSCC patients. The tumor-specific expression of KV10.1 makes it a potential target molecule for inhibition in the treatment of OSCCs.