Apoptosis induced by caffeic acid phenethyl ester in human oral cancer cell lines: Involvement of Puma and Bax activation. (December 2017)

• Record Type: Journal Article
• Authors: Yu, Hyun-Ju; Shin, Ji-Ae; Yang, In-Hyoung; Won, Dong-Hoon; Ahn, Chi Hyun; Kwon, Hye-Jeong; Lee, Jeong-Sang; Cho, Nam-Pyo; Kim, Eun-Cheol; Yoon, Hye-Jung; Lee, Jae Il; Hong, Seong-Doo; Cho, Sung-Dae
• Is Part Of: Archives of oral biology. Volume 84(2017)
• Page Start: 94
• Page End: 99
• Publication Date: 2017-12
• Subjects: Caffeic acid phenethyl ester (CAPE) -- Oral cancer -- Apoptosis -- Neoplastic cell transformation -- Bax activation -- Puma; Mouth -- Periodicals; Mouth -- Diseases -- Periodicals; Dentistry -- Periodicals; Electronic journals; 617.6005
• DOI: 10.1016/j.archoralbio.2017.09.024
• Languages: English
• ISSNs: 0003-9969

Abstract

Highlights: CAPE suppresses neoplastic cell transformation induced by EGF and TPA. CAPE has apoptotic effect via Puma and Bax activation in oral cancer. Possibility of CAPE as potent apoptosis-inducing agent in oral cancer is proposed. Abstract: Objective: Caffeic acid phenethyl ester (CAPE), a natural honeybee product exhibits a spectrum of biological activities including antimicrobial, anti-inflammatory, antioxidant and antitumor actions. The purpose of this research was to investigate the anticancer potential of CAPE and its molecular mechanism in human oral cancer cell lines (YD15, HSC-4 and HN22 cells). Design: To determine the apoptotic activity of CAPE and identify its molecular targets, trypan blue exclusion assay, soft agar assay, Western blot analysis, DAPI staining, and live/dead assay were performed. Results: CAPE significantly suppressed transformation of neoplastic cells induced by epidermal growth factor (EGF) and 12-O-tetradecanoylphorbol 13-acetate (TPA) without inhibiting growth. CAPE treatment inhibited cell growth, increased the cleavages of caspase-3 and poly (ADP-ribose) polymerase (PARP), and augmented the number of fragmented nuclei in human oral cancer cell lines. CAPE activated Bax protein causing it to undergo a conformational change, translocate to the mitochondrial outer membrane, and oligomere. CAPE also significantly increased Puma expression and interestingly Puma and Bax were co-localized. Conclusion: Overall, these results suggest that CAPE is a potent apoptosis-inducing agent in human oral cancer cell lines. Its action is accompanied by up-regulation of Bax and Puma proteins.