Abstract:
:The existence of multiple-interactive roles between several signaling pathways in tumorigenesis shows the significance of pharmacological factors like heat shock protein 90 (HSP90) inhibitors which control several signaling pathways simultaneously. HSP90 as a molecular chaperone supports the active conformational structure and function of several oncogenic signal proteins, termed "client" proteins, some of them act as a link between cancer and inflammation. Prostaglandin E2 (PGE2) is one of the major mediators of inflammation in colorectal cancer development and progress. However, the relationship between chaperone activity of HSP90 and PGE2 levels remains unclear. We evaluated the inhibitory effects of 17-demethoxy-17-allylamino geldanamycin (1 7-AAG), an HSP90 inhibitor, on PGE2 levels in HT-29 colorectal cancer cells. For the first time, we showed inhibitory effects of 17-AAG, on PGE2 levels in HT-29 colorectal cancer cells. 17-AAG inhibited PMA-induced cyclooxygenase-2 (COX-2) mRNA expression and protein level. We showed 15-hydroxyprostaglandin dehydrogenase (15-PGDH) expression induced by 17-AAG treatment at both mRNA and protein levels. In conclusion, we found that inhibitory effects of 17-AAG on PGE2 levels in HT-29 colorectal cancer cells were mediated through modulating COX-2 and 15-PGDH expression.
journal_name
Inflammationjournal_title
Inflammationauthors
Mohammadi A,Yaghoobi MM,Gholamhoseinian Najar A,Kalantari-Khandani B,Sharifi H,Saravani Mdoi
10.1007/s10753-016-0343-1subject
Has Abstractpub_date
2016-06-01 00:00:00pages
1116-23issue
3eissn
0360-3997issn
1573-2576pii
10.1007/s10753-016-0343-1journal_volume
39pub_type
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