Eupatorin modulates BCPAP in thyroid cancer cell proliferation via suppressing the NF-κB/P13K/AKT signaling pathways

Thyroid carcinoma (TC), the most prevalent endocrine cancer worldwide, has become progressively more common, especially in women. Most TCs are epithelial-derived differentiated TCs, specifically papillary thyroid cancer (PTC). Although there are many therapeutic drugs available, curing TC is a difficult task.

A flavone called eupatorin (EUP) obtained from herbs can prevent the growth of many types of cancerous cells. Nonetheless, the mechanisms of EUP's actions against PTC are still unknown.

The goal of our work was to evaluate the mechanisms of EUP (20 and 30 μM/mL) and examine its antiproliferative and apoptotic effects on human PTC cells BCPAP. The MTT test; dual acridine orange/ethidium bromide (AO/EB), rhodamine-123 (Rh-123), and 4',6-diamidino-2-phenylindole (DAPI) staining; adherence assays; and western blot analyses were used to evaluate the antiproliferative and apoptotic properties of EUP on BCPAP cells.

Our research showed that the quantity-dependent administration of EUP inhibited the proliferation of BCPAP cells, which in turn caused apoptosis through the increase in caspase-9 and p53 protein expression and the reduction of proliferating cell nuclear antigen (PCNA) levels. Additionally, when P13K/AKT signaling is inhibited by nuclear factor kappa B (NF-κB), EUP reduces inflammation and BCPAP proliferation.

By blocking the NF-κB and P13K/AKT pathways, EUP can reduce the growth of BCPAP cells and promote cell death.