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. Author manuscript; available in PMC: 2023 Mar 1.
Published in final edited form as: Pharmacol Ther. 2021 Sep 1;231:107985. doi: 10.1016/j.pharmthera.2021.107985

Figure 2. Senescence and quiescence in cancer stem cells –

Figure 2.

Senescence is a halt mainly in cell cycle G1, induced by persistent DNA damage, reactive oxygen species (ROS), and oncogenic stress. Senescence-associated secretory phenotype, a feature of senescence, induces secretion of cytokines such as IL-6 and IL-8 to promote tumorigenesis via paracrine effects. Senescent cells also undergo reprogramming and activation of stem cell transcriptional factors including WNT/LEF1, OCT4 and NANOG to induce plasticity and stemness activation. The paracrine effect and the genetic reprograming may lead to reversal of cell senescence. Quiescence is a cell state of resting a G0 phase to overcome vulnerabilities and maintain stemness, which is induced by therapeutic stress, ROS, or microenvironmental cues. Quiescence is a reversible state where cells switch into a diving state upon favorable conditions through KDM6, NOTCH/CSL, SOX, AKT1.