Document Detail

Antineoplastic effect of calycosin on osteosarcoma through inducing apoptosis showing in vitro and in vivo investigations.
MedLine Citation:
PMID:  24797937     Owner:  NLM     Status:  Publisher    
Recently, increasing studies have documented that tumorigenesis closely relates to apoptotic processes. Thus, inducing apoptosis is an anti-cancer strategy against osteosarcoma. Here we investigated the anti-proliferative effect of calycosin on human osteosarcoma cell (143B) in vitro. The results showed that calycosin dose-dependently inhibited 143B cell proliferation as reflected in tetrazolium salt (MTT) assay (P<0.01). In addition, calycosin effectively down-regulated cellular mRNA expressions of IκBα, NF-κB p65 and cyclin D1 through RT-PCR assay (P<0.01). Next, calycosin-mediated inhibitory effect on 143B tumor-bearing nude mice and the underlying mechanism were evaluated and discussed. As a result, calycosin administration significantly blocked solid tumor growth in 143B-harboured nude mice (P<0.01). Furthermore, intracellular Bcl-2 protein expression was effectively reduced in 143B-harboured tumor tissue through western blotting analysis (P<0.01), while intratumoral Apaf-1, cleaved Caspase-3 protein levels were up-regulated, respectively (P<0.01). Taken together, calycosin possesses the anti-osteosarcoma potential, in which the mechanism involved was associated with activation of apoptotic, thus inducing apoptosis.
Rubiao Qiu; Gang Ma; Chenguang Zheng; Xiaoxia Qiu; Xinning Li; Xueyu Li; Jianlan Mo; Zhengzhao Li; Yun Liu; Linjian Mo; Guan Bi; Yu Ye
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-5-2
Journal Detail:
Title:  Experimental and molecular pathology     Volume:  -     ISSN:  1096-0945     ISO Abbreviation:  Exp. Mol. Pathol.     Publication Date:  2014 May 
Date Detail:
Created Date:  2014-5-6     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370711     Medline TA:  Exp Mol Pathol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Inc.
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