Abstract
Cellular dormancy is a major contributor to cancer progression and recurrence. This review explores recent findings on the molecular mechanisms implicated in cancer dormancy and investigates potential strategies to improve therapeutic interventions. Research on cancer dormancy reveals a complex and multifaceted phenomenon. Providing a latent reservoir of tumor cells with reduced proliferation and enhanced drug-tolerance, dormant cancer cells emerge from a clonally diverse population after therapy or at metastatic sites. These cells exhibit distinct transcriptional and epigenetic profiles, involving the downregulation of Myc and mechanistic target of rapamycin (mTOR) pathways, and the induction of autophagy. Senescence traits, under the control of factors such as p53, also contribute significantly. The tumor microenvironment can either promote or prevent dormancy establishment, notably through the involvement of T and NK cells within the dormant tumor niche. Strategies to combat dormancy-related relapse include direct elimination of dormant tumor cells, sustaining dormancy to prolong survival, or awakening dormant cells to re-sensitize them to antiproliferative drugs. Improving our understanding of cancer dormancy at primary and secondary sites provides valuable insights into patient care and relapse prevention.
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