Biochemical and Biophysical Research Communications
1′-Acetoxychavicol acetate induces apoptosis of myeloma cells via induction of TRAIL
Section snippets
Materials and methods
Cells. Various multiple myeloma cell lines including RPMI8226, IM-9, and U266 cells (obtained from the Japanese Cancer Research Resources Bank, Tokyo, Japan) were maintained in RPMI 1640 medium (Gibco-BRL, Gaithersburg, MD) with 10% FBS (Gibco-BRL), 100 U/ml penicillin, and 100 mg/ml streptomycin in a humidified atmosphere with 5% CO2. Bone marrow samples were obtained from patients with multiple myeloma and healthy volunteers, who provided written informed consent, according to the appropriate
ACA selectively induces the apoptosis of multiple myeloma cells dependent on caspase pathway
We previously demonstrated that ACA induces apoptosis of various myeloma cell lines (RPMI8226, U266, and IM-9), as well as cells from freshly isolated samples obtained from patients with multiple myeloma in dose- and time-dependent manners [7]. ACA-induced apoptosis in myeloma cells has been assessed in terms of both morphologic changes including condensed chromatin and fragmented nuclei with apoptotic bodies and the presence of DNA ladder formation [7]. In the present study, treatment of
Discussion
In a previous study, we reported that a traditional Asian condiment, ACA, induced apoptosis via the inhibition of NF-κB activity in human myeloma cell lines, as well as in cells from freshly obtained samples from patients with multiple myeloma [7]. In this study, we demonstrated that ACA-induced apoptosis in multiple myeloma cell line and in primary cells from patients in association with the induction of TRAIL and TRAIL receptor DR5. Moreover, a TRAIL/R-Fc chimera dramatically attenuated
Acknowledgments
We thank Ms. Kaori Saito for her excellent technical assistance. This work was supported in part by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan; the Takeda Science Foundation; and the Mitsubishi Pharma Research Foundation.
References (31)
- et al.
Management of multiple myeloma: a systemic review and critical appraisal of published studies
Lancet Oncol.
(2003) - et al.
TRAIL/Apo2L ligand selectively induces apoptosis and overcomes drug resistance in multiple myeloma: therapeutic applications
Blood
(2001) - et al.
SHP2 mediates the protective effect of interleukin-6 against dexamethasone-induced apoptosis in multiple myeloma cells
J. Biol. Chem.
(2000) - et al.
Intracellular regulation of tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human multiple myeloma
Blood
(2002) - et al.
Role of NF-κB in the rescue of multiple myeloma cells from glucocorticoid-induced apoptosis by bcl-2
Blood
(1999) - et al.
Multiple myeloma cell adhesion-induced interleukin-6 expression in bone marrow stromal cells involves activation of NF-κB
Blood
(1996) - et al.
Advances in biology of multiple myeloma: clinical applications
Blood
(2004) - et al.
Biologic sequelae of nuclear factor-κB blockade in multiple myeloma: therapeutic applications
Blood
(2002) - et al.
A potent inhibitor of tumor promoter-induced Epstein–Barr virus activation, 1′-acetoxychavicol acetate from Languas galangal, a traditional Thai condiment
Biosci. Biotech. Biochem.
(1993) - et al.
Suppression of tumor promoter-induced oxidative stress and inflammatory responses in mouse skin by a superoxide generation inhibitor 1′-acetoxychavicol acetate
Cancer Res.
(1998)
1′-acetoxychavicol acetate, a superoxide anion generation inhibitor, potently inhibits tumor promotion by 12-O-tetradecanoylphorbol-13-acetate in ICR mouse skin
Oncology
1′-acetoxychavicol acetate inhibits azoxymethane-induced colonic aberrant crypt foci in rats
Carcinogenesis
Chemoprevention of azoxymethane-induced rat colon carcinogenesis by a xanthine oxidase inhibitor 1′-acetoxychavicol acetate
Jpn. J. Cancer Res.
Induction of apoptosis in human myeloid leukemic cells by 1′-acetoxychavicol acetate through a mitochondrial- and Fas-mediated dual mechanism
Clin. Cancer Res.
1′-acetoxychvicol acetate is a novel nuclear factor-κB inhibitor with significant activity against multiple myloma in vitro and in vivo
Cancer Res.
Cited by (18)
Acute and 28-day sub-acute intravenous toxicity studies of 1’-S-1′-acetoxychavicol acetate in rats
2018, Toxicology and Applied PharmacologyCitation Excerpt :In addition, our group has also found significant reduction in human carcinoma xenograft in mice via proinflammatory microenvironment alterations (In et al., 2012). It was revealed that multiple mechanisms are responsible to cause apoptotic actions of ACA, such as, caspase-3 activation (Williams et al., 2013), induction of TRAIL (Ito et al., 2005) and inhibition of NF-κB (Ito et al., 2005; In et al., 2011; Arshad et al., 2015). Furthermore, ACA induced apoptotic activity against human hepatocarcinoma cells and reduced azoxymethane induced colon carcinogenesis (Kato et al., 2014).
1′S-1′-Acetoxyeugenol acetate: A new chemotherapeutic natural compound against MCF-7 human breast cancer cells
2010, PhytomedicineCitation Excerpt :Variations in cell cycle distribution after treatment with AEA, indicated by changes in PI intensity of stained DNA suggest that AEA inhibits cell cycle progression effects at the G0/G1 phase while unaffecting HMEC normal cells. The effect of AEA in terms of cell cycle arrest in this study has been consistent with past reports on ACA, where it strongly increased the population of myeloma cells in the G0–G1 phase and the sub-G1 phase (Ito et al. 2005). Our current cell cycle studies in response to AEA treatments thus necessitates the need for additional molecular signalling studies on specific cyclin regulatory proteins, particularly CDK4 and CDK6 which are involved in G1 progression, and also various CDK inhibitors which may be up-regulated following AEA treatment.
Effect of naturally occurring hydroxychavicol acetate on the cytokine production in T helper cells
2009, International ImmunopharmacologyNatural Products for Cancer Therapy: A Review of Their Mechanism of Actions and Toxicity in the Past Decade
2022, Journal of Tropical Medicine