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Identification of Prostate Cancer LncRNAs by RNA-Seq
Hu, Cheng-Cheng,Gan, Ping,Zhang, Rui-Ying,Xue, Jin-Xia,Ran, Long-Ke Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.21
Purpose: To identify prostate cancer lncRNAs using a pipeline proposed in this study, which is applicable for the identification of lncRNAs that are differentially expressed in prostate cancer tissues but have a negligible potential to encode proteins. Materials and Methods: We used two publicly available RNA-Seq datasets from normal prostate tissue and prostate cancer. Putative lncRNAs were predicted using the biological technology, then specific lncRNAs of prostate cancer were found by differential expression analysis and co-expression network was constructed by the weighted gene co-expression network analysis. Results: A total of 1,080 lncRNA transcripts were obtained in the RNA-Seq datasets. Three genes (PCA3, C20orf166-AS1 and RP11-267A15.1) showed a significant differential expression in the prostate cancer tissues, and were thus identified as prostate cancer specific lncRNAs. Brown and black modules had significant negative and positive correlations with prostate cancer, respectively. Conclusions: The pipeline proposed in this study is useful for the prediction of prostate cancer specific lncRNAs. Three genes (PCA3, C20orf166-AS1, and RP11-267A15.1) were identified to have a significant differential expression in prostate cancer tissues. However, there have been no published studies to demonstrate the specificity of RP11-267A15.1 in prostate cancer tissues. Thus, the results of this study can provide a new theoretic insight into the identification of prostate cancer specific genes.
Hu, Pengwei,Zheng, Dewen,Xian, Yuxi,Hu, Xianhai,Zhang, Qian,Wang, Shanyu,Li, Mingjun,Cheng, Congliang,Liu, Jin,Wang, Ping Materials Research Society of Korea 2021 한국재료학회지 Vol.31 No.6
Bi<sub>2</sub>MoO<sub>6</sub> (BMO) via the structure-directing role of CO(NH<sub>2</sub>)<sub>2</sub> is successfully prepared via a facile solvothermal route. The structure, morphology, and photocatalytic performance of the nanoflake BMO are characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM), fluorescence spectrum analysis (PL), UV-vis spectroscopy (UV-vis) and electrochemical test. SEM images show that the size of nanoflake BMO is about 50 ~ 200 nm. PL and electrochemical analysis show that the nanoflake BMO has a lower recombination rate of photogenerated carriers than particle BMO. The photocatalytic degradation of tetracycline hydrochloride (TC) by nanoflake BMO under visible light is investigated. The results show that the nanoflake BMO-3 has the highest degradation efficiency under visible light, and the degradation efficiency reached 75 % within 120 min, attributed to the unique hierarchical structure, efficient carrier separation and sufficient free radicals to generate active center synergies. The photocatalytic reaction mechanism of TC degradation on the nanoflake BMO is proposed.
Cathepsin K Activity Controls Injury-Related Vascular Repair in Mice
Hu, Lina,Cheng, Xian Wu,Song, Haizhen,Inoue, Aiko,Jiang, Haiying,Li, Xiang,Shi, Guo-Ping,Kozawa, Eiji,Okumura, Kenji,Kuzuya, Masafumi American Heart Association, Inc. 2014 Hypertension Vol.63 No.3
<P>Cathepsin K (CatK) is one of the most potent mammalian collagenases. We showed previously the increased expression of CatK in human and animal atherosclerotic lesions. Here, we hypothesized that ablation of CatK mitigates injury-induced neointimal hyperplasia. Male wild-type (CatK<SUP>+/+</SUP>) and CatK-deficient (CatK<SUP>−/−</SUP>) mice underwent ligation or a combination of ligation and polyethylene cuff-replacement injuries to the right common carotid artery just proximal to its bifurcation, and they were then processed for morphological and biochemical studies at specific time points. On operative day 28, CatK<SUP>−/−</SUP> significantly reduced neointimal formation and neovessel formation in both single- and combination-injured arteries compared with the Cat K<SUP>+/+</SUP> mice. At early time points, CatK<SUP>−/−</SUP> reduced the lesion macrophage contents and medial smooth muscle cell proliferation, the mRNA levels of monocyte chemoattractant protein-1, toll-like receptor-2, toll-like receptor-4, chemokine ligand-12, and the gelatinolytic activity related to matrix metalloproteinase-2/-9. An aorta-explant assay revealed that smooth muscle cell movement was impaired in the CatK<SUP>−/−</SUP> mice compared with the CatK<SUP>+/+</SUP> mice. In addition, the smooth muscle cells and macrophages from CatK<SUP>−/−</SUP> mice had less invasive ability through a reconstituted basement membrane barrier. This vasculoprotective effect was mimicked by Cat inhibition with <I>trans</I>-epoxysuccinyl-L-leucylamido-{4-guanidino} butane (E64<I>d</I>). These results demonstrate an essential role of CatK in neointimal lesion formation in response to injury, possibly via the reduction of toll-like receptor-2/-4–mediated inflammation and smooth muscle cell proliferation, suggesting a novel therapeutic strategy for the control of endovascular treatment–related restenosis by regulating CatK activity.</P>
Yan Cheng,Youjun Feng,Ping Luo,Jiang Gu,Shu Yu,Wei-jun Zhang,Yan-qing Liu,Qing-xu Wang,Quan-ming Zou,Xu-hu Mao 한국미생물학회 2009 The journal of microbiology Vol.47 No.4
Shiga toxin 2 (Stx2) is a major virulence factor for enterohemorrhagic Escherichia coli (EHEC), which is encoded by λ lysogenic phage integrated into EHEC chromosome. Stx2A1, A1 subunit of Stx2 toxin has gathered extensive concerns due to its potential of being developed into a vaccine candidate. However, the substantial progress is hampered in part for the lack of a suitable in vitro expression system. Here we report use of the prokaryotic system pET-28a::espA-Stx2A1/BL21 to carry out the fusion expression of Stx2A1 which is linked to E. coli secreted protein A (EspA) at its N-terminus. Under the IPTG induction, EspA- Stx2A1 fusion protein in the form of inclusion body was obtained successfully, whose expression level can reach about 40% of total bacterial protein at 25°C, much higher than that at 37°C. Western blot test suggested the refolded fusion protein is of excellent immuno-reactivity with both monoclonal antibodies, which are specific to EspA and Stx2A1, respectively. Anti-sera from Balb/c mice immunized with the EspA-Stx2A1 fusion protein were found to exhibit strong neutralization activity and protection capability in vitro and in vivo. These data have provided a novel feasible method to produce Stx2A1 in large scale in vitro, which is implicated for the development of multivalent subunit vaccines candidate against EHEC O157:H7 infections.
Mao, Ping,Joshi, Kaushal,Li, Jianfeng,Kim, Sung-Hak,Li, Peipei,Santana-Santos, Lucas,Luthra, Soumya,Chandran, Uma R.,Benos, Panayiotis V.,Smith, Luke,Wang, Maode,Hu, Bo,Cheng, Shi-Yuan,Sobol, Robert W National Academy of Sciences 2013 PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF Vol.110 No.21
<P>Tumor heterogeneity of high-grade glioma (HGG) is recognized by four clinically relevant subtypes based on core gene signatures. However, molecular signaling in glioma stem cells (GSCs) in individual HGG subtypes is poorly characterized. Here we identified and characterized two mutually exclusive GSC subtypes with distinct dysregulated signaling pathways. Analysis of mRNA profiles distinguished proneural (PN) from mesenchymal (Mes) GSCs and revealed a pronounced correlation with the corresponding PN or Mes HGGs. Mes GSCs displayed more aggressive phenotypes in vitro and as intracranial xenografts in mice. Further, Mes GSCs were markedly resistant to radiation compared with PN GSCs. The glycolytic pathway, comprising aldehyde dehydrogenase (ALDH) family genes and in particular ALDH1A3, were enriched in Mes GSCs. Glycolytic activity and ALDH activity were significantly elevated in Mes GSCs but not in PN GSCs. Expression of ALDH1A3 was also increased in clinical HGG compared with low-grade glioma or normal brain tissue. Moreover, inhibition of ALDH1A3 attenuated the growth of Mes but not PN GSCs. Last, radiation treatment of PN GSCs up-regulated Mes-associated markers and down-regulated PN-associated markers, whereas inhibition of ALDH1A3 attenuated an irradiation-induced gain of Mes identity in PN GSCs. Taken together, our data suggest that two subtypes of GSCs, harboring distinct metabolic signaling pathways, represent intertumoral glioma heterogeneity and highlight previously unidentified roles of ALDH1A3-associated signaling that promotes aberrant proliferation of Mes HGGs and GSCs. Inhibition of ALDH1A3-mediated pathways therefore might provide a promising therapeutic approach for a subset of HGGs with the Mes signature.</P>
Fragrance Composition in Six Tree Peony Cultivars
Zhao, Jing,Hu, Zeng-Hui,Leng, Ping-Sheng,Zhang, Hui-Xiu,Cheng, Fang-Yun Korean Society of Horticultural Science 2012 원예과학기술지 Vol.30 No.6
Tree peony is a traditional famous flower of China, and plays an important role in Chinese traditional culture. But the floral scent of tree peony in vivo is little known. In this study, in order to explore the floral composition of tree peony, floral volatiles of six cultivars, including Paeonia suffruticosa 'Zhaofen' (ZF), P. suffruticosa 'Luoyanghong' (LYH), P. ostii 'Fengdanbai' (FDB), P. ${\times}$ lemonei 'High noon' (HN), P. ${\times}$ lemonei 'Renown' (R), and P. rockii 'Gaoyuanshenghuo' (GYSH) were collected by dynamic headspace and then identified by Automated Thermal Desorption-Gas Chromatography/Mass Spectometry. The results showed that floral fragrances of the six cultivars were qualitatively and quantitatively distinct. A total of 105 volatiles involving ten categories were detected. But not all volatile categories were emitted from these cultivars. The six peony cultivars emitted some shared compounds and peculiar compounds. The total released amounts of volatiles emitted from six cultivars were found significantly different, which was greatest for 'GYSH'. The most abundant volatile compounds detected from 'ZF', 'LYH', 'FDB', 'HN', 'R', and 'GYSH' were respectively ${\alpha}$-pinene, 2,3-dihydroxy propanal, 3-methyl-1-butanol, 2-ethyl-1-hexanol, acetic acid 1-methylethyl ester, and 5-ethyl-2,2,3-trimethyl heptane. This result may contribute to exploring the biosynthesis and emission mechanism of floral scent in tree peony.
Luo, Ai-Ping,Luo, Zhi-Chao,Xu, Wen-Cheng,Cui, Hu The Optical Society 2010 Optics express Vol.18 No.6
<P>A wavelength switchable all-fiber comb filter with flat-top spectral response based on a double-loop Mach-Zehnder (M-Z) interferometer is proposed and demonstrated. The proposed flat-top filter consists of a rotatable polarizer and a double-loop M-Z interferometer composed of two fiber couplers with a polarization controller (PC) in the first loop. In the theoretical analysis, when the second coupler of the M-Z interferometer is a non-3dB one, with proper settings of the polarization state of the input light and the PC, the wavelength switchable comb filter with flat-top passband can be obtained. Theoretical prediction was verified by experimental demonstration. The measured 1 dB bandwidth was 0.51 nm with a channel spacing of 0.98 nm, indicating that the flat-top passband of 1 dB bandwidth extends to about 50% of the comb spacing.</P>
Up-regulation of NICE-3 as a Novel EDC Gene Could Contribute to Human Hepatocellular Carcinoma
Wei, Yuan-Jiang,Hu, Qin-Qin,Gu, Cheng-Yu,Wang, Yu-Ping,Han, Ze-Guang,Cai, Bing Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.9
The epidermal differentiation complex (EDC) contains a large number of gene products which are crucial for the maturation of the human epidermis and can contribute to skin diseases, even carcinogenesis. It is generally accepted that activation of oncogenes and/or inactivation of tumor suppressor genes play pivotal roles in the process of carcinogenesis. Here, NICE-3, a novel EDC gene, was found to be up-regulated in human hepatocellular carcinoma (HCC) by quantitative real-time RT-PCR. Furthermore, overexpression of exogenous NICE-3 by recombinant plasmids could significantly promote cell proliferation, colony formation and soft agar colony formation in Focus and WRL-68 HCC cell lines. Reversely, NICE-3 silencing by RNA interference could markedly inhibit these malignant phenotypes in YY-8103 and MHCC-97H cells. Moreover, cell cycle analysis of MHCC-97H transfected with siRNA by flow cytometry showed that NICE-3 knockdown may inhibit cell growth via arrest in G0/G1 phase and hindering entry of cells into S phase. All data of our findings indicate that NICE-3 may contribute to human hepatocellular carcinoma by promoting cell proliferation.