Consistently, hUCMSCs treatment attenuated the e pression of survival genes, such as Bcl 2, Bcl L, Survivin, Mcl 1, and cIAP 1 in PC 3 cells, imply ing an inhibitory effect of hUCMSCs on antiapoptotic proteins. To confirm the role of JNK in hUCMSCs induced apoptosis in PC 3 cells, JNK inhibitor study was carried out. Conversely, treatment of JNK inhibitor SP600125 reversed the apoptotic ability of hUCMSCs to cleave caspase 9 3 and PARP in PC 3 cells by Western blotting and immunofluorescence assay, indicating that the JNK pathway mediates hUCMSCs induced apoptosis in PC 3 cells. Consistent with our data, Aikin et al. claimed that PI3K inhibition led to increased JNK phosphoryl ation and pancreas islet cell death, which could be re versed by the specific JNK inhibitor SP600125.

Of note, the homing of hUCMSCs to PC 3 cells and TUNEL positive cells as an apoptotic feature was Drug_discovery de tected in the tumor section of PC 3 cells, implying that hUCMSCs on the left flank can move to PC 3 cells on the right flank, as the homing of hUCMSCs to PC 3 cells, possibly for cell death. Likewise, Liang et al. reported that systemically infused hUCMSCs could home to the inflamed colon and effectively ameliorate colitis via modulation of IL 23 IL 17 by live in vivo im aging and immunofluorescent microscopy. Overall, our findings demonstrate the antitumor po tential of hUCMSCs for PC 3 prostate cancer treat ment, but further study is required for animal tumor study via direct or indirect injection of hUCMSCs in the near future.

Conclusions Based on our results, UCMSCs inhibit the tumor growth and have an antitumor potential for PC 3 prostate can cer treatment. Introduction The two main hallmarks of Alzheimers disease are e tracellular deposits composed of B amyloid peptide and intracellular filamentous aggregates composed of self assembled hyperphosphorylated Tau proteins. Histopathological studies show that these hallmarks spread, each in their own stereotyped fashion, within specific regions of the brain during disease evolution. This progression follows neuro anatomical pathways and could be the sign of ne opathy related processes. A large body of evidence indicates that neurons affected in AD follow a dying back pattern of degeneration, where abnormalities in synaptic function and a onal integrity long precede somatic cell death. Since neurons are highly polarized, this raises the question whether local AB and Tau protein abnormalities in the vicinity of different neuronal subparts lead to local degenerative pro cesses or could initiate distant dysfunction within neurons or even within neuronal networks, through synap tic alterations.