Skip to main content
. Author manuscript; available in PMC: 2016 Feb 16.
Published in final edited form as: Cancer Lett. 2014 Sep 10;355(1):141–147. doi: 10.1016/j.canlet.2014.09.006

Fig. 5.

Fig. 5

(A) Inhibition of AR prevents the expression of inflammatory and preneoplastic markers in HG-induced HT29 human colon cancer cells. HT29 cells were growth-arrested in 0.1% FBS in the presence or absence of AR inhibitor, fidarestat (10 µM) for 24 h, followed by stimulation with HG for another 48 h. For HG stimulation, the medium was replaced with fresh medium containing 25 mM glucose (added 19.5 mM glucose to McCoy’s 5A medium that already contained 5.5 mM glucose) in the absence and presence of fidarestat. Expressions of XIAP, survivin, COX-2, iNOS, β-catenin, NF-κB and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were determined by using Western blot. Western blot analysis was performed using equal amounts of proteins from each group and representative blots are shown (n = 3). The fold-changes were calculated after densitometry and normalized with the loading control. (B) HAEC and HT29 cells were treated with fidarestat ± HG for 24 and cell viability was determined by MTT assay. Data are mean ± SD (n = 6) *P < 0.001 vs control and #p < 0.001 Vs HG. Con, control; Fid, fidarestat; AOM, azoxymethane; AOM+ Fid, azoxymethane + fidarestat.