Natural products are vastly utilized as a source of chemotherapeutic agents for human cancers. Kochia scopraia is traditionally used for the cure of urological and dermatological diseases. Recently, methanol extract of Kochia scoparia (MEKS) has been shown to have anti-cancer activity to various human cancers. However, there is no report demonstrating the anti-cancer activity of MEKS in human mucoepidermoid carcinoma (MEC) cells. In this study, the authors studied the effects of MEKS on the cell proliferation and underlying mechanism in YD15 human MEC cells. MEKS decreased YD15 cell proliferation proven by trypan blue exclusion assay and induced apoptosis, evidenced by cell cycle analysis and western blotting. Autophagy induction by MEKS was verified by western blotting. In addition, MEKS regulated the expression of phosphorylated Akt, phosphorylated p38 and Nrf2 protein. This results can imply that MEKS might be a potential candidate for the treatment of human MEC cells.

Background: Cisplatin is a well-known platinum-containing anti-cancer drug against bladder, ovarian, lung and testicular cancer. However, the potential effects and molecular targets of cisplatin in human mucoepidermoid carcinoma (MEC) are not fully understood. Here, we investigated the apoptotic effect and underlying mechanism of cisplatin in human MEC cells. Methods: The potential effects of cisplatin were evaluated by trypan blue exclusion assay, Western blotting, 4’-6-diamidino-2-phenylindole (DAPI) staining, live/dead assay and immunocytochemistry. Results: Cisplatin suppressed cell growth and enhanced expression of cleaved PAPR in MC3 and YD15 cells. Cisplatin caused morphological change of nuclei and increased the number of ethidium homodimer-1-stained cells. In addition, cisplatin commonly increased Bax activation in both cells, while other Bcl-2 family proteins were not affected. Conclusions: These results suggest that cisplatin might induce apoptosis by activating Bax protein, which would provide baseline data for development of effective treatment strategy against MEC.

Caffeic acid phenethyl ester (CAPE), a component of propolis, was reported to possess anti-inflammatory, anti-bacterial, anti-viral, and anti-tumor activities. Our aim was to investigate the effect of CAPE on apoptosis in cultured human mucoepidermoid carcinoma (MEC) cell line, MC-3. Apoptotic effects of CAPE were measured by cell viability assays, Western blotting, 4’-6-diamidino-2-phenylindole (DAPI) staining and Live/Dead assay. The result of cell viability assay showed that CAPE displayed a strong growth-inhibitory effect in a concentration-dependent manner against MC-3 cells. Consumption of CAPE resulted in pronounced increase in the cleavage of caspase-3 and PARP, induced nuclear condensation and fragmentation and clearly increased the number of dead cells in MC-3 cells. CAPE also caused the increase in truncated Bid (t-Bid) and the cleavage of caspase-8 and this phenomenon was regulated by death receptor 5 (DR5). In addition, Phosphorylation of AKT and ERK were downregulated by CAPE. Taken together, these results suggest that CAPE is a potent apoptosis-inducing agent in MC-3 cells.

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

Al thou gh calcifi cation is a common finding in inflammatory salivary gland disorders , saliva ry gland tumour ra rely s hows calcifications. A case of clear cell mucoepidermoid carcinoma(MEC) of the hard pa late with extensive intra tumoural calcifïcations vis ible on computed tomog r때hy(CT) scans and histologic sections is described. The calci fï caLion in the sali va ry gland tumour 0 1' the palate recogni zed by a CT scan s hould be considered in the differential diagnosis of a MEC The mechanism of the i ntratumoural calcifi cation in our case is speculated to be a result of a secretory fu nction 0 1' the tumour cells