抽象的
Oncology Drugs and Anticancer Herbs: Target GT198
Hawra JohnsonAngiogenesis in tumours is a characteristic of cancer. There are clinically effective therapeutic pharmacological inhibitors of angiogenesis. Previously, we discovered that the oncoprotein GT198 (gene symbol PSMC3IP, commonly known as Hop2) causes tumour angiogenesis in human malignancies, including oral cancer. In this study, we demonstrate that numerous oncology medications and several clinically effective anticancer medicines directly target the GT198 protein. A DNA repair protein that binds to DNA is called GT198. We examined the 129 cancer medications in the National Cancer Institute's approved oncology drug set VII using an in vitro DNA-binding assay. Known inhibitors of GT198 include mitoxantrone, doxorubicin, paclitaxel, etoposide, dactinomycin, and imatinib, among others. Higher binding affinities are shared by paclitaxel and etoposide, but higher binding efficacy is shared by doxorubicin due to competitive inhibition. As DNA topoisomerases are known drug targets and GT198 shares protein sequence homology with them, it is possible that GT198 represents a novel therapeutic target that has not yet been identified. We investigated more anticancer plant extracts in our search for more potent GT198 inhibitors. Clinically effective anticancer herbs include allspice from Jamaica; Gleditsia sinensis, or honey locust, from China; and BIRM from Ecuador. These herbs also have high affinity and efficacy. When the activity is observed by the in vitro DNA-binding assay utilising GT198 as a target, partial purification of allspice employing an organic chemical technique indicates excellent feasibility of natural product purification. Our research as a whole identifies GT198 as a brand-new targeting mechanism for oncology medications. The study also provides a great pharmacological target that can be used for purifying natural products and identifying compounds. This study offers a unique chance to quickly identify natural medicines with high efficacy and minimal toxicity.