Abstract
Thioamide is one of a group of antithyroid drugs prescribed in the treatment of hyperthyroidism. Thioamide derivative is currently used for the treatment of thyroid disease, tuberculosis, and leprosy. Recent in vitro experiment in our laboratory demonstrated thioamide is highly cytotoxic to human liver carcinoma (HepG2) cells. Although published studies indicate that thioamide derivative has medicinal properties effective against many diseases other than liver cancer, the molecular mechanisms under which this compound induces apoptosis of cancer cells remain largely unknown. In the present study, we proposed to use human liver carcinoma (HepG2) cells as a test model to evaluate the basis apoptotic mechanism of thioamide derivative. To achieve this goal, the expression of annexin V was measured by flow cytometric analysis. Human liver carcinoma (HepG2) cells were treated with different doses of thioamide derivative for 48 hours. Results from the flow cytometric assessment (Annexin V FITC/PI) showed a strong dose‐response relationship between thioamide derivative exposure and annexin V positive cells undergoing early stage apoptosis in HepG2 cells. Taken together, our results indicate that phosphatidylserine externalization was involved in thioamide derivative induced toxicity to HepG2 cells. This grant is supported in part by NIH‐NIGMS Grant R25GM50117 and in part by NIH Grant 2G12RR013459‐11.
Published Version
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