Taxillus yadoriki (Siebold) Dancer is a parasitic plant that grows on camellia trees and is common on Jeju Island. The branches of T. yadoriki have long been used to treat various diseases, including hypertension, diabetes mellitus, viral infections, and arthritis. Although recent studies reported that T. yadoriki has anticancer effects in various human cancer cell lines, including lung cancer, the exact molecular mechanisms supporting its anticancer effects are not well understood. This study aims to assess the anticancer effect of the methanol extract of T. yadoriki branches (METY) on mucoepidermoid carcinoma (MEC) cell lines (MC3 cells and YD15 cells) and explore its mechanism of action. Inhibitory activity of MEC cell proliferation was assessed using the CCK-8 assay. The mechanism of the anticancer effect on METY-treated MC3 cells and YD15 cells was evaluated with Hoechst 33342 stain and Western blot. After treating MC3 cells and YD15 cells with METY for 48 hours, the cytotoxicity of MC3 and YD15 cells increased, and nuclear fragmentation increased in both METY-treated MEC cells. Caspase-3 and cleaved PARP activation demonstrated apoptosis of METY-treated MEC cells. Cell proliferation inhibition with METY was alleviated in METY-treated MEC cells pretreated with zVAD-FMK, supporting the cell proliferation inhibition effect by apoptosis. METY-induced apoptosis in MEC cells occurs through MAP kinase pathways such as p38 and pAkt. MEC cell. METY-induced apoptosis of MEC cells occurs via the p38 and pAkt MAPK pathways. Therefore, METY may be a promising anticancer candidate for the MEC therapeutic strategy.

Background. Vitamin K (VK) is a fat-soluble vitamin and is known to have anticancer activity in various cancer cell lines. However, there is no report on the anticancer effect of VK2 in mucoepidermoid carcinoma cells. Methods. The effects of VK2 on anti-proliferative and apoptotic activity were recognized by the trypan blue exclusion assay, 4'-6-diamidino-2-phenylindole (DAPI) staining and Western blot analysis. Results. The results showed that VK2 decreased cell viability and induced apoptotic programmed cell death in MC3 cells evidenced by the cleavages of caspase3 and PARP. VK2 treatment clearly increased Bak and truncated Bid (t-Bid) compared with the control treatment whereas it did not alter other Bcl-2 family members. Conclusions. Overall, our results suggest that VK2 can be a good apoptotic inducer accompanied by the increase in Bak and Bid protein. VK2 may be a potent target of anticancer drug candidate for the treatment of oral cancer.

Emodin is a bioactive compound isolated from the root and rhizomes of Rheum plamatum L. (polygenaceae), which is known as a traditional Chinese and Japanese medicine. In the present study, the effect of emodin on YD-15 mucoepidermoid carcinoma cells and its molecular mechanism were investigated. This study shows that emodin significantly inhibits the growth of YD-15 cells. Activation of caspase-3 and PARP is triggered by emodin and it increases sub-G1 population and the number of YD-15 cells with nuclear condensation and fragmentation. In addition, we found that emodin significantly decreases myeloid cell leukemia 1(MCL-1). These results suggest that MCl-1 is an important molecule for emodin-induced apoptosis. Taken together, emodin inhibits cell viability and induces apoptosis via down-regulation of MCL-1 and it can be a new potent anticancer drug candidate for the treatment of mucoepidermoid carcinoma