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Sci Rep. 2016 Jun 28;6:28773. doi: 10.1038/srep28773.

Bisdemethoxycurcumin inhibits ovarian cancer via reducing oxidative stress mediated MMPs expressions.

Author information

1
Department of Cardiology, Chengdu Military General Hospital, Chengdu 610083, China.
2
Department of Orthopedics, Chengdu Military General Hospital, Chengdu 610083, China.
3
Department of Obstetrics and Gynecology, Affiliated Guangren Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an 710004, China.

Abstract

As one main active compound of curcuminoids, Bisdemethoxycurcumin (BDMC) possesses several biological activities, such as anti-inflammation and anti-cancer activities. However, the detailed mechanism of BDMC's anti-metastasis activity in ovarian cancer has not been clearly elucidated yet. In the present study, cell proliferation, wound healing motility, cell adhesion and invasion with or without BDMC were determined. In addition, western blot was used to examine proteins expressions. The lucigenin-enhanced luminescence was introduced to assess cellular oxidative stress. The luciferase reporter gene assay was introduced to evaluate the transcriptional activity of NF-κB. Finally, BDMC significantly inhibited the adhesion, migration, invasion and metastasis of SKOV-3 cells. Moreover, BDMC inhibited expressions of several degradation-associated proteins, such as matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), CD147, urokinase plasminogen activator (uPA), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), whereas increased expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), in a dose-dependent manner. In addition, BDMC reduced generation of cellular superoxide in a dose-dependent manner. Furthermore, BDMC inhibited the phosphorylation levels of NF-κB p65 and IκB-α, and consequently reduced NF-κB-driven luciferase expression. Collectively, BDMC serves as a therapeutic medicine to suppress ovarian cancer, perhaps via inhibiting cellular oxidative stress and subsequently inactivating NF-κB pathway.

PMID:
27349797
PMCID:
PMC4923879
DOI:
10.1038/srep28773
[Indexed for MEDLINE]
Free PMC Article

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