Asia-Pacific Journal of Oncology, Год журнала: 2024, Номер unknown
Опубликована: Окт. 11, 2024
Senescence is irreversible cell cycle arrest that results from therapy-induced stress such as DNA damage. It was initially thought to be a tumor-suppressive mechanism, but now getting attention contribute tumor progression and therapy resistance through the senescence-associated secretory phenotype (SASP). Remodeling microenvironment (TME), SASP can establish conditions conducive progression. In addition, senescence being acknowledged increasingly crucial factor in inducing dormancy, state of reversible quiescence allows cancer cells evade therapeutic clearance survive protective niches. Eventually, both dormancy significantly maintenance stem (CSCs), enhancing their plasticity tumor-initiating potential. Moreover, promote aggressive disease cells, driving epithelial-to-mesenchymal transition (EMT) metastasis. On other hand, dormant act reservoir, serving seeds for metastatic spread which reactivate develop at secondary sites. Understanding mechanisms holds promise overcoming resistance, stemness Therapeutic strategies targeting include senolytics, senomorphics, dormancy-disrupting agents, immunotherapies. Future preclinical clinical research should prioritize integration senescence- dormancy-targeting agents with conventional treatments achieve durable control.
Язык: Английский