HDAC6 as a therapeutic target for HPV E7-driven cervical cancer
摘要
Cervical cancer is one of the most prevalent malignant tumors of the female reproductive system. While its occurrence and progression is influenced by various factors, recent research has highlighted roles for histone deacetylase 6 (HDAC6) and the human papillomavirus E7 (HPV E7) protein in cervical cancer pathogenesis. HPV E7 promotes cancer cell survival and proliferation by regulating the cell cycle, inhibiting apoptosis, and integrating into the genome. Meanwhile, HDACs mediate cancer development and invasiveness by regulating key physiological processes, including cell proliferation, apoptosis, motility, epithelial–mesenchymal transition, and angiogenesis. HDAC6, specifically, contributes to cellular stress responses by deacetylating various substrate proteins and interacting with other proteins that together enhance tumor cell survival. In this review, we summarize recent advances in understanding the role of HDACs in HPV E7-induced cervical cancer, including HDAC structure and function, and HDAC6 involvement in tumor initiation and progression. We then explore the potential of HDAC6 as a therapeutic target for cervical cancer.