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Chengde, China

Xie J.,Qingdao University | Ma C.,Qingdao University | Lin J.,Qingdao University | Wang G.,Qingdao University | And 2 more authors.
Advances in Polymer Technology

This study reports the antitumor effects of radioiodinated antisense oligonucleotides (ASON) mediated by anionic long-circulating liposomes (ALCL) on MCF-7 breast cancer cells in vitro and the pharmacokinetics and tissue distribution of ALCL in vivo. Our results found that ALCL improves the delivery of radioiodinated ASON, characterized by significant apoptosis, decreased cell survival, and suppressed bcl-2 protein expression in MCF-7 cells. ALCL exhibited bicompartmental clearance and demonstrated significantly favorable pharmacokinetic properties including long half-life, slow clearance, and a large concentration-time curve. © 2011 Wiley Periodicals, Inc. Source

Deng X.Z.,Affiliated Hospital
Zhonghua nan ke xue = National journal of andrology

To determine whether testosterone-induced intra-testicular testosterone withdrawal and therefore spermatogenic impairment is associated with looser arrangement of spermatogenic cells in rats. Adult male SD rats received intramuscular injection of testosterone undecanoate at 19 mg/(kg x 15 d) for 130 days, and then testicular tissue blocks were obtained for the preparation of methacrylate resin-embedded sections and observation of the changes in testicular histology. Apart from such changes as impaired spermiogenesis and spermiation, apparently looser arrangement of spermatogenic cells was seen in 11.5% of the seminiferous tubule profiles, with radial cracks (empty spaces) running towards the tubule lumen being formed between lines, bundles or groups of spermatogenic cells (mainly spermatids and spermatocytes). Looser arrangement of spermatogenic cells is one of the key histological changes resulting from intra-testicular testosterone withdrawal in rats. Source

Zhao T.,Affiliated Hospital | Dong Y.,Harbin Medical University | Ren H.,Harbin Medical University
Nucleic Acids Research

Accumulating evidence indicates that microRNAs (miRNAs) can function as oncogenes or tumor suppressor genes by controlling few key targets, which in turn contribute to the pathogenesis of cancer. The identification of cancer-related key miRNA-target interactions remains a challenge. We performed a systematic analysis of known cancer-related key interactions manually curated from published papers based on different aspects including sequence, expression and function. Known cancer-related key interactions show more miRNA binding sites (especially for 8mer binding sites), more reliable binding of miRNA to the target region, higher expression associations and broader functional coverage when compared to non-disease-related interactions. Through integrating these sequence, expression and function features, we proposed a bioinformatics approach termed PCmtI to prioritize cancer-related key interactions. Ten-fold cross-validation of our approach revealed that it can achieve an area under the receiver operating characteristic curve of 93.9. Subsequent leave-one-miRNA-out cross-validation also demonstrated the performance of our approach. Using miR-155 as a case, we found that the top ranked interactions can account for most functions of miR-155. In addition, we further demonstrated the power of our approach by 23 recently identified cancer-related key interactions. The approach described here offers a new way for the discovery of novel cancer-related key miRNA-target interactions. © 2012 The Author(s). Source

Wu C.,Peking Union Medical College | Miao X.,Huazhong University of Science and Technology | Huang L.,Peking Union Medical College | Che X.,Chinese Academy of Sciences | And 34 more authors.
Nature Genetics

Pancreatic cancer has the lowest survival rate among human cancers, and there are no effective markers for its screening and early diagnosis. To identify genetic susceptibility markers for this cancer, we carried out a genome-wide association study on 981 individuals with pancreatic cancer (cases) and 1,991 cancer-free controls of Chinese descent using 666,141 autosomal SNPs. Promising associations were replicated in an additional 2,603 pancreatic cancer cases and 2,877 controls recruited from 25 hospitals in 16 provinces or cities in China. We identified five new susceptibility loci at chromosomes 21q21.3, 5p13.1, 21q22.3, 22q13.32 and 10q26.11 (P = 2.24 × 10 -13 to P = 4.18 × 10 -10) in addition to 13q22.1 previously reported in populations of European ancestry. These results advance our understanding of the development of pancreatic cancer and highlight potential targets for the prevention or treatment of this cancer. Source

Tang B.,Guilin Medical University | Li Y.,Affiliated Hospital | Yuan S.,Guilin Medical University | Tomlinson S.,Medical University of South Carolina | He S.,Guilin Medical University
International Journal of Oncology

The δ opioid receptor (DOR), is the first cloned G protein-coupled receptor. Many recent studies on DOR functions have determined that the DOR is involved in the regulation of malignant transformation and tumor progression in multiple cancers. However, it is still unclear if the DOR is involved in the regulation of malignant transformation and tumor progression in hepatocellular carcinoma (HCC). The purpose of our study was to investigate the expression of the DOR in HCC and to determine its effect on progression to further understand the influence of the DOR on the biological characteristics of HCC. Higher expression of DOR was observed in liver tumor tissue/cells compared to normal liver tissue/cells. When DOR gene expression was silenced or inhibited, the proliferation of HCC cells was inhibited, and tumor cells underwent apoptosis, the cell cycle was arrested and tumor cell invasion and migration were significantly decreased. Nude mice inoculated with cells stably expressing low levels of DOR displayed reduced tumor formation rates and reduced tumor growth. In conclusion, DOR is highly expressed in HCC and is involved in HCC progression, suggesting that DOR is a potential target for HCC treatment. Source

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