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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Anti-EMT properties of CoQ0 attributed to PI3K/AKT/NFKB/MMP-9 signaling pathway through ROS-mediated apoptosis

Fig. 8

In vivo inhibition of proliferation in mice xenografted with MDA-MB-231 by CoQ0. a Time-dependent effect of CoQ0 on growth of MDA-MB-231 xenografted nude mice was evaluated by measurements of body weight and tumor volume every week. Cells were implanted subcutaneously into the flanks of nude mice on day 0, and animals were subsequently treated with 0.075 mg/kg of CoQ0 (three times/week) or vehicle (control). b On the 12th week after tumor implantation, the animals were sacrificed and the tumor tissues removed and weighed. The results are presented as the mean ± SE (n = 5). c Histochemical analysis of proliferation in MDA-MB-231 xenografted tumors. Control and MDA-MB-231 xenografted tumors following CoQ0 (0.75 mg/kg) treatments were sectioned, stained with hematoxylin and eosin and examined using light microscopy (400 × magnification). Arrows indicate mitotic cells (tumor control). d In-situ apoptosis detection using TUNEL staining in tumor sections from control animals and experimental analogues treated with CoQ0 (0.75 mg/kg) (400 × magnifications). The number of apoptotic-positive cells from 3 samples was averaged. e Western blotting results demonstrating the effects of CoQ0 on the total protein content of Cyclin A and Cyclin B in the xenografted tumors from 3 samples. f Xenografted tumor sections were subjected to immunohistochemical analysis for Cyclin A, Cyclin B, CDK1, Bax, p53, and p21. Cells positive for the indicated proteins were counted from 3 fields (200 × magnification) for each tumor sample. Relative changes in protein bands were measured by densitometric analysis, with the control being 100% or 1-fold. The results are the mean (±SE) numbers of cells/microscope field (as percentage) for 5~7 animals per group. Significant at *p < 0.05; **p < 0.01; ***p < 0.001 compared to untreated control cells

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