Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.

MC-3 »ç¶÷ À¯Á¡¾×ÆíÆò¼¼Æ÷¾ÏÁ¾ ¼¼Æ÷ÁÖ¿¡¼­ Caffeic Acid Phenethyl Ester ¸Å°³ ¼¼Æ÷µ¶¼º¿¡ °üÇÑ ¿¬±¸

Caffeic Acid Phenethyl Ester-Mediated Cytotoxicity in MC-3 Human Mucoepidermoid Carcinoma Cell Line

´ëÇѱ¸°­¾Ç¾È¸éº´¸®ÇÐȸÁö 2014³â 38±Ç 6È£ p.357 ~ 364
À¯ÇöÁÖ, Á¶³²Ç¥, Á¶¼º´ë,
¼Ò¼Ó »ó¼¼Á¤º¸
À¯ÇöÁÖ ( Yu Hyun-Ju ) - ÀüºÏ´ëÇб³ Ä¡ÀÇÇÐÀü¹®´ëÇпø ±¸°­º´¸®Çб³½Ç
Á¶³²Ç¥ ( Cho Nam-Pyo ) - ÀüºÏ´ëÇб³ Ä¡ÀÇÇÐÀü¹®´ëÇпø ±¸°­º´¸®Çб³½Ç
Á¶¼º´ë ( Cho Sung-Dae ) - ÀüºÏ´ëÇб³ Ä¡ÀÇÇÐÀü¹®´ëÇпø ±¸°­º´¸®Çб³½Ç

Abstract


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 effectin a concentration-dependent manner against MC-3 cells. Consumption of CAPE resulted in pronounced increase in the cleavage ofcaspase-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 deathreceptor 5 (DR5). In addition, Phosphorylation of AKT and ERK were downregulated by CAPE. Taken together, these results suggestthat CAPE is a potent apoptosis-inducing agent in MC-3 cells.

Å°¿öµå

Caffeic acid phenethyl ester (CAPE); Human mucoepidermoid carcinoma (MEC); Apoptosis; Death Receptor 5

¿ø¹® ¹× ¸µÅ©¾Æ¿ô Á¤º¸

 

µîÀçÀú³Î Á¤º¸

KCI