cytostasis

Cytostasis refers to the cessation of cell division while preserving cell viability. It is a functional state in which cells exit the cell cycle or slow its progression without undergoing apoptosis or necrosis. Cytostasis can be temporary or more persistent, depending on the context, and it is distinct from both cell death and simple metabolic slowdown.

Cytostasis can result from physiological processes such as contact inhibition or nutrient deprivation, as well as from pharmacological agents known as cytostatics that arrest the cell cycle at various checkpoints. Mechanistically, it often involves activation of CDK inhibitors (such as p21, p27, and p16) and the suppression of cyclin-CDK activity, leading to arrest at G0/G1, S, or G2. Signaling pathways including p53 and the retinoblastoma (Rb) pathway, along with cellular metabolic cues, influence the establishment and maintenance of cytostasis.

Applications of cytostasis occur in research and medicine. In the laboratory, cytostasis is used to synchronize cell populations or to preserve cells without expanding them. Clinically, cytostatic therapies aim to halt tumor cell proliferation, and sublethal or targeted exposures (for example, CDK inhibitors like palbociclib) can induce sustained growth arrest. It is important to distinguish cytostasis from cytotoxicity, which involves cell death, whereas cytostasis preserves viability, at least for a time. In cancer biology, cytostasis may limit tumor growth but does not always eliminate malignant cells, and combination with cytotoxic or immune-based approaches is often considered. Related concepts include cellular senescence, which is typically a more permanent arrest with distinct phenotypic changes.