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Shanghai, China

Huang J.,85 Hospital of PLA | Jia J.,Jilin University | Tong Q.,85 Hospital of PLA | Liu J.,85 Hospital of PLA | And 4 more authors.
Tumor Biology | Year: 2015

Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a recently identified human oncoprotein that can stabilize some proteins by inhibiting degradation mediated by protein phosphatase 2A (PP2A), and its level in cancer is associated with resistance to chemotherapy. However, whether CIP2A could increase chemoresistance of prostate cancer (PCa) cells to chemotherapeutic agent cabazitaxel remains unclear. To determine whether CIP2A serves as a potential therapeutic target of human PCa, we utilized small interference RNA (siRNA) to knock down CIP2A expression in human PCa cells and analyzed their phenotypic changes. The data demonstrated that CIP2A was significantly elevated in mCRPC cell lines C4-2 and ARCaPM at both the mRNA and protein levels. CIP2A silencing led to decreased proliferation and enhanced chemosensitivity and apoptosis to cabazitaxel in human PCa cells, as well as reduced Akt phosphorylation. Our data suggesting critical roles of CIP2A in PCa cells chemoresistance to cabazitaxel and raising the possibility of CIP2A inhibition as a promising approach for chemosensitization of metastatic castration-resistant prostate cancer (mCRPC). © 2014, International Society of Oncology and BioMarkers (ISOBM). Source

Mao A.,85 Hospital of PLA | Huang H.,85 Hospital of PLA | Ding K.,85 Hospital of PLA | Xin H.,85 Hospital of PLA | And 2 more authors.
Zhonghua wei zhong bing ji jiu yi xue | Year: 2015

OBJECTIVE: To study the modulation in number and function of endothelial progenitor cell (EPC) in multiple organ dysfunction syndrome (MODS) after trauma in swine, and to investigate its pathogenesis.METHODS: Forty pigs were divided into sham group and MODS group (each, n=20). The model of MODS of "two-hit" injury, namely hemorrhagic shock and endotoxemia, was reproduced. The peripheral blood was collected before hemorrhage (T1) and endotoxin injection (T2), and 1 hour (T3), 24 hours (T4), 48 hours (T5) after endotoxin injection. Phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK ) in mononuclear cell was determined by Western Blot, the content of tumor necrosis factor-α (TNF-α) was determined with enzyme linked immunosorbent assay (ELISA), and the number of EPC was determined with flow cytometry.RESULTS: Model of MODS was successfully reproduced in 17 pigs. In model group, the expression of p-p38MAPK (A value) peaked at T3 (4.83±0.52), and gradually declined at T4 and T5 (4.36±0.43, 1.93±0.33), and the expression of p-p38MAPK at T3-T5 was significantly higher than that at T1 (1.00±0.22, all P<0.01). The plasma concentration of TNF-α (ng/L) at T3 in MODS group was obviously elevated compared with that of sham group (532.43±52.17 vs. 129.03±20.45, t=31.163, P<0.001), and it peaked at T3, it then gradually lowered, and it was significantly higher at T4 and T5 than that in sham group (T4: 398.93±35.75 vs. 131.12±29.53, t=26.562, P<0.001; T5: 287.48±27.26 vs. 126.44±26.96, t=17.861, P<0.001). The number of EPC (×10(7)/L) was apparently increased in MODS group at T3 compared with sham group (4.832±0.624 vs. 3.545±0.363, t=9.542, P<0.001), and it peaked at T3, then gradually decreased, and the number of EPC at T4 and T5 was significantly lower than that in sham group (T4: 2.628±0.627 vs. 3.442±0.325, t=5.043, P<0.001; T5: 2.203±0.711 vs. 3.471±0.323, t=2.972, P<0.001).CONCLUSIONS: Phosphorylation of p38MAPK could increase the plasma concentration of TNF-αand decrease the quantity of EPC in MODS,which may be one of the mechanisms of MODS. Source

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