Abstract
Anastasis is a newly identified cellular recovery process that enables cells to regain viability after progressing into execution-phase apoptosis. In cancer, this process may allow tumor cells to survive transient cytotoxic stress and subsequently acquire more aggressive phenotypes, including enhanced migration, invasion, and resistance to therapy. Although anastasis has attracted increasing attention, its biological significance and contribution to cancer progression remain incompletely understood. In this review, we summarize the defining features and biological processes of anastasis and critically evaluate current evidence linking post-apoptotic recovery to cancer-associated phenotypes, including apoptosis regulation, metastasis, angiogenesis, oxidative-stress adaptation, and epithelial-mesenchymal transition. We further discuss molecular pathways implicated in anastatic recovery and examine potential therapeutic strategies aimed at limiting post-apoptotic survival in cancer cells. Finally, we highlight major challenges in the field, including the need for more specific biomarkers, physiologically relevant in vivo models, and direct clinical validation, and outline key unresolved questions that should guide future investigation.