# Cellular senescence: a double-edged sword in cancer therapy

## TL;DR

Cellular senescence can both prevent and promote cancer, making it a complex factor in cancer therapy.

## Contribution

The paper reviews the dual role of cellular senescence in cancer and proposes strategies to manage senescent cells.

## Key findings

- Cellular senescence can suppress tumor growth by halting cell division.
- Senescent cells may promote cancer by triggering tumor-like changes in nearby cells.
- Eliminating senescent cells after treatment could improve cancer therapy outcomes.

## Abstract

Over the past few decades, cellular senescence has been identified in cancer patients undergoing chemotherapy and radiotherapy. Senescent cells are generally characterized by permanent cell cycle arrest as a response to endogenous and exogenous stresses. In addition to exiting the cell cycle process, cellular senescence also triggers profound phenotypic changes such as senescence-associated secretory phenotype (SASP), autophagy modulation, or metabolic reprograming. Consequently, cellular senescence is often considered as a tumor-suppressive mechanism that permanently arrests cells at risk of malignant transformation. However, accumulating evidence shows that therapy-induced senescence can promote epithelial-mesenchymal transition and tumorigenesis in neighboring cells, as well as re-entry into the cell cycle and activation of cancer stem cells, thereby promoting cancer cell survival. Therefore, it is particularly important to rapidly eliminate therapy-induced senescent cells in patients with cancer. Here we review the hallmarks of cellular senescence and the relationship between cellular senescence and cancer. We also discuss several pathways to induce senescence in tumor therapy, as well as strategies to eliminate senescent cells after cancer treatment. We believe that exploiting the intersection between cellular senescence and tumor cells is an important means to defeat tumors.