β-lapachone Suppresses Carcinogenesis of Cervical Cancer via Interaction with AKT1

Pan Du ¹ Yue Li ^2* Anna Han ^1* Mengying Wang ^1* Jiajing Liu ^1* Yingshi Piao ¹ Liyan Chen ^1*

• ¹ Yanbian University, Yanji, China
• ² Changchun Center for Disease Control and Prevention, Changchun, Jilin Province, China

Cervical cancer is one of the most prevalent malignant tumors affecting women worldwide, and affected patients often face a poor prognosis due to its high drug resistance and recurrence rates. β-lapachone, a quinone compound originally extracted from natural plants, is an antitumor agent that specifically targets NQO1. In this study, we investigated the effects of β-lapachone on cervical cancer cells both in vitro and in vivo. Database analysis revealed that NQO1 is highly expressed in cervical cancer tissues. β-lapachone significantly inhibited the proliferation and metastasis of cervical cancer cells by regulating glucose metabolism, reducing tumor angiogenesis, and suppressing epithelial-mesenchymal transition (EMT) in cells with high NQO1 expression. Furthermore, we identified the inactivation of the PI3K/AKT/mTOR pathway as the key mechanism underlying these effects. AKT1 was identified as a potential target of β-lapachone in modulating glucose metabolism and EMT in cervical cancer cells. These findings suggest that β-lapachone inhibits the malignant progression of cervical cancer by targeting AKT1 to regulate glucose metabolism in NQO1-overexpressing cells, providing a theoretical basis for developing novel therapeutic strategies for cervical cancer.