Abstract Title:

Curcumin induces pro-apoptotic endoplasmic reticulum stress in human leukemia HL-60 cells.

Abstract Source:

Biochem Biophys Res Commun. 2007 Feb 23;353(4):1040-5. Epub 2006 Dec 27. PMID: 17198682

Abstract Author(s):

Hyun-Ock Pae, Sun-Oh Jeong, Gil-Saeng Jeong, Ki Mo Kim, Hak Sung Kim, Soon-Ai Kim, Youn-Chul Kim, Sung-Don Kang, Byeong-Nam Kim, Hun-Taeg Chung

Article Affiliation:

Department of Microbiology and Immunology, Wonkwang University School of Medicine, Iksan 570-749, Republic of Korea.

Abstract:

Curcumin has been shown to induce apoptosis in many cancer cells. However, the molecular mechanism(s) responsible for curcumin-induced apoptosis is not well understood and most probably involves several pathways. In HL-60 cells, curcumin induced apoptosis and endoplasmic reticulum (ER) stress as evidenced by the survival molecules such as phosphorylated protein kinase-like ER-resident kinase, phosphorylated eukaryotic initiation factor-2alpha, glucose-regulated protein-78, and the apoptotic molecules such as caspase-4 and CAAT/enhancer binding protein homologous protein (CHOP). Inhibition of caspase-4 activity by z-LEVD-FMK, blockage of CHOP expression by small interfering RNA, and treatment with salubrinal, an ER inhibitor, significantly reduced curcumin-induced apoptosis. Removing two double bonds in curcumin, which was speculated to form Michael adducts with thiols in secretory proteins, resulted in a loss of the ability of curcumin to induce apoptosis as well as ER stress. Thus, the present study shows that curcumin-induced apoptosis is associated with its ability to cause ER stress.

Study Type : In Vitro Study

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