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Han Ying-Hao,Chen Dong-Qin,Jin Mei-Hua,Jin Ying-Hua,Li Jing,Shen Gui-Nan,Li Wei-Long,Gong Yi-Xi,Mao Ying-Ying,Xie Dan-Ping,Lee Dong-Seok,Yu Li-Yun,Kim Sun-Uk,김지수,권태호,Cui Yu-Dong,Sun Hu-Nan 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.3
Severe inflammatory reactions caused by macrophage activation can trigger a systemic immune response. In the present study, we observed the anti-inflammatory properties of hispidin on LPS induced RAW264.7 macrophage cells. Our results showed that hispidin treatment significantly reduced the production of cellular NO, IL-6 and reactive oxygen species (ROS) while has not inhibitory effect on TNF-α productions. Excitingly, hispidin treatment retains the phagocytosis ability of macrophages which enabling them to perform the function of removing foreign invaders. Signaling studies showed, hispidin treatment dramatic suppressed the LPS induced mitogen activated protein kinases (MAPK) and JAK/STAT activations. In conclusion, our findings suggest that hispidin may be a new therapeutic target for clinical treatment of macrophages-mediated inflammatory responses.
Han Ying-Hao,Mao Ying-Ying,Yu Nan-Nan,Jin Mei-Hua,Jin Ying-Hua,Wang Ai-Guo,Zhang Yong-Qing,Shen Gui-Nan,Cui Yu-Dong,Yu Li-Yun,Lee Dong-Seok,Jo Yu-Jin,Sun Hu-Nan,Kwon Jeongwoo,권태호 한국응용생명화학회 2020 Applied Biological Chemistry (Appl Biol Chem) Vol.63 No.3
In this study, we used RNA sequencing (RNA-seq) to analyze and compare bulk cell samples from wild-type (WT) dermal mesenchymal stem cells (DMSCs) (n = 3) and Prx II knockout DMSCs (n = 3). The purpose of the study was to elucidate the role of Prx II on allogeneic immune rejection of transplanted DMSCs. The results revealed differential expression of 472 genes (176 up-regulated and 296 down-regulated; p ≤ 0.05) between the PrxII+/+ (WT) and PrxII−/− sample groups. When highly regulated genes were categorized according to the Gene Ontology (GO) molecular function classification and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the PrxII−/− samples showed a robust downward trend in allograft rejection. The study identified 43 all immunologically rejected differentially expressed genes, of which 41 showed lower expression in the PrxII−/− vs. PrxII+/+ (WT) samples. These findings suggest that Prx II gene knockout may down-regulate the allograft rejection that occurs during DMSCs transplantation and improve the survival rate of DMSCs in the host. This study provides a new perspective on the clinical treatment of stem cell transplantation.
Association Between XRCC1 Gene Polymorphisms and Risk of Glioma Development: A Meta-analysis
Sun, Jian-Ying,Zhang, Chun-Yang,Zhang, Zhen-Jun,Dong, Yan-Fang,Zhang, An-Long,Wang, Zhi-Wei,Mei, Xiao-Long Asian Pacific Journal of Cancer Prevention 2012 Asian Pacific journal of cancer prevention Vol.13 No.9
Objective: Previous studies of the association between X-ray cross-complementing group 1 (XRCC1) gene polymorphisms and the gliomas risk have yielded conflicting results, and thus a meta-analysis was performed to provide a more accurate estimation. Methods: A computerized literature search of 5 electronic databases was conducted to identify the relevant studies. Fixed or random effect models were selected based on the heterogeneity test. Publication bias was estimated using Begg's funnel plots and Egger's regression test. Results: A total of 11 studies (3,810 cases and 6,079 controls), 7 studies (2,928 cases and 5,048 controls), and 4 studies (1,461 cases and 2,593 controls) were finally included in the analyses of the association between XRCC1 Arg399Gln, Arg194Trp, and Arg280His polymorphisms and glioma risk, respectively. The pooled results showed that GlnGln carriage was associated with moderately increased risk of gliomas in Asians (GlnGln vs. ArgArg, OR=1.490, 95%CI 1.031-2.153; GlnGln/ArgGln vs. ArgArg, OR=1.321, 95%CI 1.037-1.684), whereas a marginal association was revealed in Caucasians. For the Arg194Trp polymorphism, although a significant association was shown in the homozygous genotype comparisons (TrpTrp vs. ArgArg, OR = 2.209, 95%CI 1.398-2.945), no significant link was found on subgroup analysis stratified by ethnicity. With regard to the Arg280His polymorphism, no significant association was found in each comparison. No particular study was found to significantly influence the pooled results, and no potential publication bias was detected. Conclusions: This meta-analysis suggested that the XRCC1 Arg399Gln polymorphism is moderately associated with increased risk of gliomas in Asians, while Arg194Trp and Arg280His polymorphisms demonstrated no significant influence. Due to the limited studies and the potential confounders, further studies are needed to confirm these results.
Parthenolide-Induced Apoptosis, Autophagy and Suppression of Proliferation in HepG2 Cells
Sun, Jing,Zhang, Chan,Bao, Yong-Li,Wu, Yin,Chen, Zhong-Liang,Yu, Chun-Lei,Huang, Yan-Xin,Sun, Ying,Zheng, Li-Hua,Wang, Xue,Li, Yu-Xin Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.12
Purpose: To investigate the anticancer effects and underlying mechanisms of parthenolide on HepG2 human hepatocellular carcinoma cells. Materials and Methods: Cell viability was assessed by MTT assay and cell apoptosis through DAPI, TUNEL staining and Western blotting. Monodansylcadaverin(MDC) and AO staining were used to detect cell autophagy. Cell proliferation was assessed by Ki67 immunofluorescence staining. Results: Parthenolide induced growth inhibition in HepG2 cells. DAPI and TUNEL staining showed that parthenolide could increase the number of apoptotic nuclei, while reducing the expression of the anti-apoptotic protein Bcl-2 and elevating the expression of related proteins, like p53, Bax, cleaved caspase9 and cleaved caspase3. Parthenolide could induce autophagy in HepG2 cells and inhibited the expression of proliferation-related gene, Ki-67. Conclusions: Parthenolide can exert anti-cancer effects by inducing cell apoptosis, activating autophagy and inhibiting cell proliferation.
Sun, Ying,Chien, Shang-Chieh,Yip, Hin-Lap,Chen, Kung-Shih,Zhang, Yong,Davies, Joshua A.,Chen, Fang-Chung,Lin, Baoping,Jen, Alex K.-Y. The Royal Society of Chemistry 2012 Journal of materials chemistry Vol.22 No.12
<P>A detailed model study has shown that thin film morphology and bulk-heterojunction solar cell performance can be significantly improved by systematic tuning of the surface energy of the conjugated donor polymer through side-chain functionalization. Thiophene-flanked diketopyrrolopyrrole (DPP) moieties with different contents of cyanohexane side chains were incorporated into three low band-gap conjugated copolymers (<B>PIDTDPP1</B>, <B>PIDTDPP2</B> and <B>PIDTDPP3</B>) consisting of indacenodithiophene (IDT) donors and DPP acceptors. The resulting polymers possessed good solubility in common organic solvents and showed similar energy levels, bandgaps, and hole mobilities. However, the introduction of cyano groups onto the terminal of side-chains significantly changed their surface energy. Topographical images obtained from atomic force microscopy (AFM) proved that a better matched surface energy between polymer and PC<SUB>71</SUB>BM had led to enhanced miscibility, which resulted in better BHJ film morphology. Consistent with the surface energy enhancement, the performance of BHJ photovoltaic devices increased from 0.97% for <B>PIDTDPP1</B>, to 2.16% for <B>PIDTDPP2</B> then to 3.67% for <B>PIDTDPP3</B>. These results clearly reveal that tuning surface energy is an effective way to improve the morphology of the BHJ active layer and efficiency of the photovoltaic device.</P> <P>Graphic Abstract</P><P>We have shown that significantly improved thin film morphology and bulk-heterojunction solar cell performance can be achieved by systematically tuning the surface energy of conjugated polymer donors through side-chain functionalization. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c2jm15517f'> </P>
Sun, Ying,Chien, Shang-Chieh,Yip, Hin-Lap,Zhang, Yong,Chen, Kung-Shih,Zeigler, David F.,Chen, Fang-Chung,Lin, Baoping,Jen, Alex K.-Y. Royal Society of Chemistry 2011 Journal of materials chemistry Vol.21 No.35
<P>Two new semiconducting polymers based on indacenodithiophene and thiadiazolo[3,4-<I>c</I>]pyridine units were synthesized <I>via</I> Stille coupling polymerization. The polymers, PIDTPyT and PIDTDTPyT, exhibited main absorption bands in the range of 550–800 nm while their absorption maxima were located at around 700 nm in films. With two additional thiophene spacers, PIDTDTPyT showed a broader absorption band but a 20 nm blue-shifted maximum peak compared to that of PIDTPyT. Both of the polymers possess low bandgaps (∼1.6 eV) and deep energy levels for both the highest occupied molecular orbital (HOMO) and the lowest unoccupied molecular orbital (LUMO). Organic field-effect transistors (OFETs) device measurements indicate that PIDTPyT and PIDTDTPyT have high hole carrier mobilities of 0.066 and 0.045 cm<SUP>2</SUP> V<SUP>−1</SUP> s<SUP>−1</SUP>, respectively, with the on/off ratio on the order of 10<SUP>6</SUP>. Bulk heterojunction photovoltaic devices consisting of the copolymers and PC<SUB>71</SUB>BM gave power conversion efficiencies (PCE) as high as 3.91% with broadband photo-response in the range of 300–800 nm. The relationships between the photovoltaic performance and film morphology, energy levels, hole mobilities are discussed.</P> <P>Graphic Abstract</P><P>Low bandgap regiorandom polymers based on indacenodithiophene and thiadiazolo[3,4-<I>c</I>]pyridine units showed excellent OFET hole mobilities and promising photovoltaic device performance as high as 3.91%. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c1jm11564b'> </P>
Ying-ying Xu,Hai-ru Yu,Jia-yi Sun,Zhao Zhao,Shuang Li,Xin-feng Zhang,Zhi-xuan Liao,Ming-ke Cui,Juan Li,Chan Li,Qiang Zhang 대한암학회 2019 Cancer Research and Treatment Vol.51 No.2
Purpose Although the interferon (IFN) signaling and the paired-like homeodomain transcription factor 2 (PITX2) have both been implicated in the progression of breast cancer (BCa), it remains obscure whether these two pathways act in a coordinated manner. We therefore aimed to elucidate the expression and function of PITX2 during the pathogenesis of endocrine resistance in BCa. Materials and Methods PITX2 expression was assessed in BCa tissues using quantitative reverse transcription polymerase chain reaction (RT-qPCR) and immunohistochemistry and in experimentally induced letrozole-resistant BCa cells using RT-qPCR and immunoblotting. Effects of PITX2 deregulation on BCa progression was determined by assessing MTT, apoptosis and xenograft model. Finally, using multiple assays, the transcriptional regulation of interferon-inducible transmembrane protein 1 (IFITM1) by PITX2 was studied at both molecular and functional levels. Results PITX2 expression was induced in letrozole-resistant BCa tissues and cells, and PITX2 induction by IFN signaling powerfully protected BCa cells against letrozole insult and potentiated letrozole-resistance. Mechanistically, PITX2 enhanced IFN-induced AKT activation by transactivating the transcription of IFITM1, thus rendering BCa cells unresponsive to letrozoleelicited cell death. Additionally, ablation of IFITM1 expression using siRNA substantially abolished IFN-elicited AKT phosphorylation, even in the presence of PITX2 overexpression, thus sensitizing BCa cells to letrozole treatment. Conclusion These results demonstrate that constitutive upregulation of PITX2/IFITM1 cascade is an intrinsic adaptive mechanism during the pathogenesis of letrozole-resistance, and modulation of PITX2/IFITM1 level using different genetic and pharmacological means would thus have a novel therapeutic potential against letrozole resistance in BCa.