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Fig. 7 | Journal of Experimental & Clinical Cancer Research

Fig. 7

From: Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3

Fig. 7

CA retards tumor growth in a murine xenograft model by activating ER stress. Typical tumor tissue images after treatment was shown in (a). The tumor volume (b), weight (c) and body weight (d) were recorded after CA treatment for 14 days. e Histological analysis [stained with H&E 200×] of normal tissue (heart, liver, spleen, lung and kidney) in mice induced by CA for 14 days. f In situ detection of apoptotic cells in tumor sections after the treatment of CA for 14 days by optical microscope using the TUNEL assay (apoptotic cell: green fluorescence). g The protein expression of tumor tissue was measured by western blotting. h Protein levels were quantified by grayscale scan and the GAPDH was used as the loading control. i Effect of CA on p-JNK, CHOP, p-AKT and Cleaved caspase-3 expressions in male mice tumor sections were detected by immunocytochemistry (positive cell: claybank). The results are presented as mean ± SD. *p < 0.05 and **p < 0.01 as compared with control group

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