With some tumors becoming increasingly resistant to cancer treatments, research is turning to natural compounds that may help weaken this resistance and enhance the effectiveness of available therapies
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In this context, researchers at the Johns Hopkins Kimmel Cancer Center have found that the compound "Triptolide," extracted from the plant "Tripterygium wilfordii," sometimes referred to as "Thunder God Vine," disrupts an enzyme known as DCTPP1, which cancer cells use to break down inhibitors of the enzyme "DNA methyltransferase" (DNMT) before they can take effect effectively.
When triptolide or related compounds were combined with the DNMT inhibitor decitabine, the combination showed an enhanced ability of the drug to reactivate tumor suppressor genes and kill cancer cells in laboratory models, according to results published in the journal Nature Communications.
"This provides a potential breakthrough to address one of the obstacles that hinder the effectiveness of these drugs in multiple types of cancer," said the study's lead author, Vasan Yegnasoparamanian, professor of oncology at the center and director of "inHealth Precision Medicine" at Johns Hopkins University.
DNA methylation is a process that controls gene expression, where DNMT enzymes add methyl groups to DNA. Cancer cells can hijack this process through aberrant methylation, silencing genes that normally prevent uncontrolled growth.
Yegnasoparamanian explained that drugs such as decitabine and azacitidine, used as DNMT inhibitors, have proven effective against some blood cancers, such as myelodysplastic syndromes and leukemias. However, their success remains limited against solid tumors, which may possess defense mechanisms that prevent the treatments from working.
Research teams sought to discover compounds capable of disrupting these defenses and restoring cancer cells' sensitivity to drugs, and triptolide was identified as an active component of the Thunder God Vine. In laboratory studies and animal models, triptolide significantly enhanced gene regulation and the cytotoxic effect of decitabine.
Decitabine works by being converted into its active form within cells, but the enzyme DCTPP1 degrades this form before it can be incorporated. Yagnasoparamanian noted that triptolide inhibits this enzyme, allowing DNMT inhibitors to successfully integrate into tumor DNA and thus exert their effects effectively.
The researchers confirmed that high levels of DCTPP1 are associated with resistance to DNMT inhibitors, supporting the view that the enzyme is an important source of resistance to cancer drugs.
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