SIX1 enhances aerobic glycolysis and progression in cervical cancer through ENO1

Xuelian Liu & Hongbing Cai et al. · 2025-04-15

2Citations
Cervical cancer is a significant threat to women's health, and its incidence in China has been increasing in recent years. Treating advanced and recurrent cervical cancer has become increasingly challenging, highlighting the urgent need to identify new therapeutic targets for this disease. SIX1 is associated with cell proliferation, metastasis, and chemoresistance in various human malignancies. SIX1 overexpression in cervical cancer tissues has been linked to increased clinical stage and lymph node metastasis; however, the regulatory function of SIX1 in cervical cancer remains largely unexplored. In this study, we found that SIX1 promotes cervical cancer cell proliferation, invasion, and migration by enhancing glucose metabolism. Additionally, SIX1 was shown to influence the glycolytic process in cervical cancer by upregulating GLUT1, PFK1, PGK1, ENO1, and PKM2 expression. Furthermore, we identified a binding site for SIX1 in the ENO1 promoter region, demonstrating that SIX1 has a regulatory effect. These results suggest that SIX1 regulates proliferation and glucose metabolism in cervical cancer cells by promoting the transcription of key glycolytic enzymes, such as ENO1. Understanding this regulatory mechanism is crucial for identifying potential therapeutic targets for cervical cancer.
Journal
Human Cell
TL;DR

It is found that SIX1 promotes cervical cancer cell proliferation, invasion, and migration by enhancing glucose metabolism and is shown to influence the glycolytic process in cervical cancer by upregulating GLUT1, PFK1, PGK1, ENO1, and PKM2 expression.

AI-generated by Semantic Scholar

Authors
Xuelian Liu, Hang Ren, Anjin Wang, Ziyan Liang, Su Min, Shijie Yao, Shimeng Wan, Yang Gao, Hua Wang, Hongbing Cai