Dual Disruption: Targeting Mitotic Processes and Epigenetic Regulation to Overcome Anticancer Drug Resistance
Komal Bhardwaj1, Aman Jain1, Karan Goel1
1Chitkara College of Pharmacy, Chitkara University, Rajpura, 140401, Punjab, India.
Current Pharmaceutical Design
|May 19, 2026
Summary
Targeting both cell division errors and epigenetic changes offers a novel cancer therapy. This dual approach overcomes drug resistance and eliminates persistent cancer cells, improving treatment outcomes.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Drug resistance is a major challenge in cancer therapy, leading to disease recurrence.
- Mitotic regulators (e.g., AURKA, PLKs) and epigenetic modifiers (e.g., HDACs, BET proteins) are crucial for cell division and chromatin structure.
- Dysregulation of these networks contributes to cancer growth, stemness, and immune evasion.
Purpose of the Study:
- To review the therapeutic potential of simultaneously targeting mitotic and epigenetic regulatory networks in cancer.
- To highlight how dual disruption creates unique vulnerabilities for overcoming drug resistance.
Main Methods:
- Review of current literature on mitotic regulators and epigenetic modifiers in cancer.
- Analysis of combination therapies targeting both pathways.
- Examination of mechanisms underlying cancer cell adaptation and resistance.
Main Results:
- Simultaneous targeting of mitotic fidelity and epigenetic plasticity enhances cancer cell cytotoxicity.
- Combination therapies delay the onset of drug resistance and eliminate drug-tolerant cells.
- This dual approach is effective against aggressive cancers like triple-negative breast cancer and glioblastoma.
Conclusions:
- Dual disruption of mitotic and epigenetic pathways represents an innovative therapeutic strategy.
- Combining mitotic stress induction with prevention of adaptive epigenetic rewiring limits drug tolerance.
- This approach offers a promising avenue for treating resistant and aggressive cancers.
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