Journal Article Summary
The article investigates the potential of combining histone deacetylase inhibitors (HDIs) with compounds that target mitochondrial hexokinases to enhance the effectiveness of cancer treatments, particularly for solid tumors. HDIs have shown success in treating certain blood cancers but have not been effective against solid tumors, which highlights the need for improved treatment strategies. Understanding how to overcome resistance to HDIs could lead to better therapeutic options for patients with solid tumors, which are often more challenging to treat.
In this study, researchers treated various cancer cell lines from breast, kidney, lung, colon, and ovarian cancers with the HDI romidepsin alongside clotrimazole or bifonazole, both of which are known to disrupt hexokinase activity. The results showed that this combination significantly increased cell death compared to using either treatment alone, indicating that targeting hexokinases could enhance the apoptotic effects of HDIs. The study found that the combination treatment led to a notable decrease in mitochondrial hexokinase 2 levels, suggesting that reducing this protein's presence may be key to improving treatment outcomes.
However, the study has limitations, including its reliance on cell line models, which may not fully represent the complexity of human tumors. Additionally, while the findings are promising, the safety and efficacy of these combinations in actual patients need further investigation. Patients should discuss these findings with their healthcare providers, especially if they are considering treatment options involving HDIs or are interested in emerging therapies that target metabolic pathways in cancer cells.
Medication Safety Note
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Article Cited
- McDonald Andrew J., Curt Katherine M., Patel Ruchi P., Kozlowski Hanna, Sackett Dan L., Robey Robert W., Gottesman Michael M., Bates Susan E.. Targeting mitochondrial hexokinases increases efficacy of histone deacetylase inhibitors in solid tumor models. Experimental cell research 2018. DOI: 10.1016/j.yexcr.2018.12.012. PMID: 30579954. PMCID: PMC8130056.
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