Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review)

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Abstract
Emodin is a naturally occurring anthraquinone being investigated for its anticancer potential due to its ability to modulate the cell cycle and inhibit tumor progression. The cell cycle is composed of a series of events that dictate cell growth and cell division. The G0/G1 checkpoint is the resting stage before the first gap phase (G1), whereas the G2/M checkpoint is the working stage from the second gap phase (G2) before mitosis begins. Emodin exerts its effects by the following means: Cyclins, which propel the cells through the cell cycle stages; cyclin-dependent kinases (CDKs), which are energy sources that, along with cyclins, push the cell cycle further; and finally, CDK inhibitors, such as p21 and p27, which can inhibit CDK activity. G0/G1 arrest is mediated by the suppression of cyclin D/CDK4 and cyclin E/CDK2 activity, whereas G2/M arrest results from the inhibition of cyclin B/CDK1 and the disruption of mitotic progression. G2/M arrest is further reinforced by the activation of the checkpoint kinases, Chk1 and Chk2. These kinases operate downstream of DNA damage sensors and effectors to maintain cell cycle blockade. The present review discusses the mechanisms of emodin-induced cell cycle arrest. In preclinical settings, emodin has been shown to be capable of suppressing tumor cell proliferation in multiple cancer models, both by itself and in combination with standard chemotherapy or radiotherapy. However, suboptimal bioavailability and metabolic instability are obstacles that have hindered its clinical application, with results being inconsistent among cancer types. Future studies are required to develop more efficacious drug delivery systems, identify predictive biomarkers and conduct strong clinical trials. Addressing these issues may position emodin as a viable cancer therapeutic option, either alone or in combination with current therapies.

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