Astaxanthin Combine With Human Serum Albumin To Abrogate Cell Proliferation, Migration, And Drug-Resistant In Human Ovarian Carcinoma SKOV3 Cells.

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Astaxanthin Combine With Human Serum Albumin To Abrogate Cell Proliferation, Migration, And Drug-Resistant In Human Ovarian Carcinoma SKOV3 Cells.

Anticancer Agents Med Chem. 2019 Feb 25;:

Authors: Su XZ, Chen R, Wang CB, Ouyang XL, Jiang Y, Zhu MY

Abstract
BACKGROUND: Astaxanthin (AST) shows a large range of beneficial effects together with anti-cancer and antioxidation properties. Human serum albumin (HSA) is the most abundant protein in blood plasma which plays the role of depot and transport protein for many exogenous compounds. However, whether HSA could enhance AST-induced cytotoxic effects in human ovarian cancer cells has not been examined to date.
OBJECTIVE: This study aims to explore the anticancer effect and the molecular mechanism of AST combine with HSA induced cytotoxicity in ovarian cancer SKOV3 cells.
METHOD: The ovarian cancer SKOV3 cells were treated by AST combined with HSA to study the effects of cell proliferation, cell morphology, cell cycle arrest, related protein expression, nuclear transfer, cell migration, and drug-resistant.
RESULTS: Our data confirmed that AST+HSA treatment enhanced the anticancer effects of AST, arrested G1 phase cell cycle and induced apoptosis in SKOV3 cells. AST+HSA induced apoptosis via mitochondrial apoptotic pathways was related to the increased ratio of Bcl-2/Bax and activation of caspase-3. Besides, exposure of cells to AST+HSA triggered the inactivation of NF-κB and activation p53 and MAPKs signaling pathways. Furthermore, AST+HSA significantly overcome the drug-resistant and inhibited the migration of SKOV3 cells.
CONCLUSION: AST combined treatment with HSA considerably inhibited NF-κB expression and translocation to nucleus, thereby improving the AST-induced cytotoxic effect on SKOV3 cells. These findings may provide rationale to combine AST with HSA for the treatment of ovarian cancer.

PMID: 30799797 [PubMed - as supplied by publisher]

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