Triptolide enhanced decitabine’s effect in preclinical cancer models — News-Medical

Researchers at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins found that the natural compound triptolide may increase cancer cells’ sensitivity to the drug decitabine. As News-Medical reports, in laboratory cell cultures and animal models, the combination of these substances enhanced the reactivation of tumor suppressor genes and the destruction of cancer cells.

How resistance to therapy develops

Triptolide is derived from the plant Tripterygium wilfordii, known as the thunder god vine. Scientists found that the compound blocks the DCTPP1 enzyme. This enzyme can destroy the active form of DNA methyltransferase inhibitors before the drugs are incorporated into the DNA of a tumor cell.

This group of medicines includes decitabine and azacitidine. They can eliminate abnormal DNA methylation, a mechanism through which cancer cells suppress genes that restrain uncontrolled growth. Such drugs are used against certain hematologic cancers, including myelodysplastic syndromes and leukemia, but their effectiveness in solid tumors has been limited due to cellular defense mechanisms.

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The results require further verification

The study also linked high DCTPP1 levels to resistance to DNA methyltransferase inhibitors. The authors believe that suppressing this enzyme could become an approach to overcoming drug resistance and expanding the possibilities of epigenetic therapy.

At the same time, the researchers stressed that the findings are preclinical. The work does not prove that the plant itself is a treatment for cancer. For trials involving humans, DCTPP1 inhibitors with appropriate efficacy, safety, and pharmacological properties must be developed. The results were published on August 26 in the journal Nature Communications.