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PubMed | Yuhuangding Hospital Yantai, Peoples Hospital of Weifang Weifang and Peoples Hospital of Zhangqiu Zhangqiu
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2015

Background-Little is known about the prognostic significance of elevated serum relaxin in acute myocardial infarction (AMI) patients. The present study is designed to investigate the potential association between serum relaxin levels and the risk of AMI.We measured circulating relaxin levels in 80 patients (median age 62.3 years) who presented with first-time AMI 8 hours after the incident. The circulating relaxin-2 levels in 80 healthy volunteers (median age 61.5 years) was also measured. Relaxin-2 was detected using enzyme immunoassay in both groups.Serum relaxin levels were significantly higher in patients with AMI (27.4 6.3 ng/ml) compared to controls (9.2 2.3 ng/ml) (P < 0.01). We found that a relaxin level > 13.8 ng/ml had a sensitivity of 79% and a specificity of 86% for predicting AMI. Relaxin revealed the higher sensitivity and specificity for diagnosing AMI.Elevated relaxin in plasma may be a novel biomarker for early detection of AMI.


PubMed | Peoples Hospital of Weifang Weifang, Peoples Hospital of Zhangqiu Jinan and Peoples Hospital of Laiwu Laiwu
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2015

Clusterin (CLU) is known as a multifunctional protein involved in a variety of physiological processes including lipid transport, epithelial cell differentiation, tumorigenesis, and apoptosis. Our recent study has demonstrated that knockdown of clusterin sensitizes pancreatic cancer cell lines to gmcitabine treatment. However the details of this survival mechanism remain undefined. Of the various downstream targets of CLU, we examined activation of the NF-kB transcription factor and subsequent transcriptional regulation of BCL-2 gene in pancreatic cancer cell MIA-PaCa-2. The MIA-PaCa-2 cells were transfected with an antisense oligonucleotide (ASO) against clusterin, which led to a decreased protein level of the antiapoptotic gene BCL-2. Furthermore, inhibition of CLU decreased the function of NF-kB, which is capable of transcriptional regulation of the BCL-2 gene. Inhibiting this pathway increased the apoptotic effect of gmcitabine chemotherapy. Re-activated NF-kB resulted in attenuation of ASO-induced effects, followed by the bcl-2 upregulation, and bcl-2 re-inhibition resulted in attenuation of Re-activated NF-kB -induced effects. Animals injected with ASO CLU in MIA-PaCa-2 cells combined with gmcitabine treatment had fewer tumors than gmcitabine or ASO CLU alone. These findings suggest that knockdown of CLU sensitized MIA-PaCa-2 cells to gmcitabine chemotherapy through modulating NF-Kb/bcl-2 pathway.


PubMed | Peoples Hospital of Weifang Weifang, Peoples Hospital of Rizhao Rizhao and Qingdao University
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2015

CIP2A is a recently characterized oncoprotein which involves in the progression of several human malignancies. CIP2A is overexpressed in human ovarian cancer and regulates cell proliferation and apoptosis. This study was performed to investigate the role of CIP2A in ovarian cancer (OC) chemoresistance.Using DDP-resistant SKOV3 cells (SKOV3(DDP)), we first determined the effect of CIP2A silencing by siRNA-mediated knockdown of CIP2A on chemosensitivity in vitro; we then determined the effect of pCDNA3.1-mediated overexpression of CIP2A on chemosensitivity in SKOV3 cells in vitro. To elucidate the molecular mechanisms underlying CIP2A-mediated chemoresistance, the activities of AKT signaling molecules associated with CIP2A were analyzed.Knockdown of endogenous CIP2A in SKOV3(DDP) cells resulted in the reduction in cell growth and increase in the chemosensitivity of SKOV3(DDP) cells to DDP in vitro, which may be caused by CIP2A-induced AKT activity inhibition. Notably, CIP2A overexpression could significantly decrease the sensitivities of SKOV3 cells to cisplatin, which might be ascribed to CIP2A-induced activation of the AKT pathway.Taken together, the results suggest that CIP2A contributes to cisplatin resistance in OC. Thus, CIP2A is a potential therapeutic target for OC.

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