Cell cycle proteins are critical to pituitary development, but their contribution to lineage-specific tumorigenesis has not been well-elucidated. Emerging evidence from in vitro human tumor analysis and transgenic mouse models indicates that G1/S-related cell cycle proteins, particularly cyclin E, p27, Rb, and E2F1, drive molecular mechanisms that underlie corticotroph-specific differentiation and development of Cushing disease. The aim of this review is to summarize the literature and discuss the complex role of cell cycle regulation in Cushing disease, with a focus on identifying potential targets for therapeutic intervention in patients with these tumors.
Bibliographical noteFunding Information:
The authors thank Shira Berman for technical advice and assistance. This work was supported by NIH grants R21DK103198 (N-AL) and T32DK007770 (TA). The funding sources had no role in study design, data analysis, or decision to publish.
© 2018 Araki and Liu.
- Cell cycle
- Cushing disease
- Cyclin E
- Pituitary tumor