Umbilical cord tissue-derived mesenchymal stem cells induce apoptosis in PC-3 prostate cancer cells through activation of JNK and downregulation of PI3K/AKT signaling

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• 作者：Ihn Han (5)
  Miyong Yun (5)
  Eun-Ok Kim (5)
  Bonglee Kim (5)
  Min-Hyung Jung (6)
  Sung-Hoon Kim (5)
  
  5. Cancer Preventive Material Development Research Center ; College of Oriental Medicine ; Kyung Hee University ; 1 Hoegi-dong ; Dongdaemun-gu ; Seoul ; 130-701 ; Republic of Korea
  6. School of Medicine ; Kyung Hee University ; Seoul ; 130-701 ; Republic of Korea
  
• 刊名：Stem Cell Research & Therapy
• 出版年：2014
• 出版时间：June 2014
• 年：2014
• 卷：5
• 期：2
• 全文大小：926 KB
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• 刊物主题：Stem Cells; Cell Biology;
• 出版者：BioMed Central
• ISSN：1757-6512

文摘

Introduction Although mesenchymal stem cells (MSCs) have antitumor potential in hepatocellular carcinoma and breast cancer cells, the antitumor mechanism of human umbilical cord mesenchymal stem cells (hUCMSCs) in prostate cancer cells still remains unclear. Thus, in the present study, we elucidated the antitumor activity of hUCMSCs in PC-3 prostate cancer cells in vitro and in vivo. Methods hUCMSCs were isolated from Wharton jelly of umbilical cord and characterized via induction of differentiations, osteogenesis, and adipogenesis. Antitumor effects of UCMSCs on tumor growth were evaluated in a co-culture condition with PC-3 prostate cancer cells. PC-3 cells were subcutaneously (sc) injected into the left flank of nude mice, and UCMSCs were sc injected into the right flank of the same mouse. Results We found that hUCMSCs inhibited the proliferation of PC-3 cells in the co-culture condition. Furthermore, co-culture of hUCMSCs induced the cleavage of caspase 9/3 and PARP, activated c-jun NH2-terminal kinase (JNK), and Bax, and attenuated the phosphorylation of phosphatidylinositol 3-kinase (PI3K)/ AKT, extracellular signal-regulated kinase (ERK), and the expression of survival genes such as Bcl-2, Bcl-xL, Survivin, Mcl-1, and cIAP-1 in PC-3 cells in Western blotting assay. Conversely, we found that treatment of specific JNK inhibitor SP600125 suppressed the cleavages of caspase 9/3 and PARP induced by hUCMSCs in PC-3 cells by Western blotting and immunofluorescence assay. The homing of hUCMSCs to, and TUNEL-positive cells on, the K562 xenograft tumor region were detected in Nu/nu-BALB/c mouse. Conclusions These results suggest that UCMSCs inhibit tumor growth and have the antitumor potential for PC-3 prostate cancer treatment.