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

  • Authors:
    • Shreya Das
    • Jhansi Kompala
    • Kyle Laney
    • Sneha Pathak
    • Ravi Nayar
    • Sukant Khurana
    • Alfredo Ghezzi
    • Lakshminarayanan Karthik
    • Abhijit G. Banerjee
  • View Affiliations / Copyright

    Affiliations: IonCure Tech Pvt. Ltd., New Delhi 110085, India, University of South Florida, Tampa, FL 33620, USA, Sakra Premium Clinic, Bengaluru 560035, India, Department of Biology, UPR‑Río Piedras, University of Puerto Rico, San Juan, Puerto Rico 00925‑2535, USA, Genomic Bio‑Medicine Research and Incubation, Chhattisgarh (CGBMRI), Durg 491001, India
    Copyright: © Das et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
  • Article Number: 44
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    Published online on: June 19, 2026
       https://doi.org/10.3892/mi.2026.328
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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.
View Figures

Figure 1

Mechanistic overview of
emodin-induced DNA damage response and cell cycle regulation.
Emodin enters the cell and induces DNA damage, activating the
ATM/ATR-Chk1/Chk2 signaling cascade and p53. Activated p53
upregulates CDK inhibitors (p21 and p27), leading to the
suppression of CDK-cyclin complexes. In parallel, emodin directly
modulates CDKs and cyclins. These combined effects result in cell
cycle arrest at G1/S and G2/M checkpoints and promote apoptotic
outcomes.

Figure 2

Emodin exerts potent
anti-proliferative effects across multiple cancer types by
disrupting key regulators of the cell cycle and survival pathways.
It induces cell cycle arrest at G0/G1 and G2/M phases, suppresses
mitotic progression, and promotes apoptosis through modulation of
proteins, such as cyclin D1, Bcl-2, and the Cyclin B/CDK1 complex.
These molecular effects are particularly evident in hepatocellular
and colorectal cancer models, leading to impaired cell cycle
progression and increased cell death. Additionally, emodin reduces
colony formation and induces a senescence-like state in highly
proliferative cancers, including breast, lung, liver and prostate
cancers.
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Copy and paste a formatted citation
Spandidos Publications style
Das S, Kompala J, Laney K, Pathak S, Nayar R, Khurana S, Ghezzi A, Karthik L and Banerjee AG: Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review). Med Int 6: 44, 2026.
APA
Das, S., Kompala, J., Laney, K., Pathak, S., Nayar, R., Khurana, S. ... Banerjee, A.G. (2026). Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review). Medicine International, 6, 44. https://doi.org/10.3892/mi.2026.328
MLA
Das, S., Kompala, J., Laney, K., Pathak, S., Nayar, R., Khurana, S., Ghezzi, A., Karthik, L., Banerjee, A. G."Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review)". Medicine International 6.4 (2026): 44.
Chicago
Das, S., Kompala, J., Laney, K., Pathak, S., Nayar, R., Khurana, S., Ghezzi, A., Karthik, L., Banerjee, A. G."Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review)". Medicine International 6, no. 4 (2026): 44. https://doi.org/10.3892/mi.2026.328
Copy and paste a formatted citation
x
Spandidos Publications style
Das S, Kompala J, Laney K, Pathak S, Nayar R, Khurana S, Ghezzi A, Karthik L and Banerjee AG: Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review). Med Int 6: 44, 2026.
APA
Das, S., Kompala, J., Laney, K., Pathak, S., Nayar, R., Khurana, S. ... Banerjee, A.G. (2026). Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review). Medicine International, 6, 44. https://doi.org/10.3892/mi.2026.328
MLA
Das, S., Kompala, J., Laney, K., Pathak, S., Nayar, R., Khurana, S., Ghezzi, A., Karthik, L., Banerjee, A. G."Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review)". Medicine International 6.4 (2026): 44.
Chicago
Das, S., Kompala, J., Laney, K., Pathak, S., Nayar, R., Khurana, S., Ghezzi, A., Karthik, L., Banerjee, A. G."Emodin‑induced cell cycle arrest: A promising approach for cancer therapy (Review)". Medicine International 6, no. 4 (2026): 44. https://doi.org/10.3892/mi.2026.328
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