The double dealing of cyclin D1

TL;DR

This paper reviews the complex roles of cyclin D1 in cell cycle regulation and oncogenesis, highlighting its non-canonical functions, interactions, and implications for targeted cancer therapy.

Contribution

It synthesizes recent findings on cyclin D1's non-traditional roles and its network interactions, providing insights for potential therapeutic strategies.

Findings

Cyclin D1 acts as a mitogenic sensor and cell cycle regulator.

Deregulation of cyclin D1 contributes to tumor development.

Complex networks involving cyclin D1 influence its oncogenic functions.

Abstract

The cell cycle is tightly regulated by cyclins and their catalytic moieties, the cyclin-dependent kinases (CDKs). Cyclin D1, in association with CDK4/6, acts as a mitogenic sensor and integrates extracellular mitogenic signals and cell cycle progression. When deregulated (overexpressed, accumulated, inappropriately located), cyclin D1 becomes an oncogene and is recognized as a driver of solid tumors and hemopathies. Recent studies on the oncogenic roles of cyclin D1 reported non-canonical functions dependent on the partners of cyclin D1 and its location within tumor cells or tissues. Support for these new functions was provided by various mouse models of oncogenesis. Finally, proteomic and transcriptomic data identified complex cyclin D1 networks. This review focuses on these aspects of cyclin D1 pathophysiology, which may be crucial for targeted therapy.