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71.
Khan Salman Khan Mukhtaj Iqbal Nadeem Hussain Tahir Khan Sher Afzal Chou Kuo-Chen 《International journal of peptide research and therapeutics》2020,26(2):795-809
International Journal of Peptide Research and Therapeutics - Piwi interacting RNA (piRNA) molecules belong to a largest class of small non coding RNA molecules which are originally discovered in... 相似文献
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73.
Jenish R Patel Ankur Jain Yi‐ying Chou Alina Baum Taekjip Ha Adolfo García‐Sastre 《EMBO reports》2013,14(9):780-787
The cytosolic pathogen sensor RIG‐I is activated by RNAs with exposed 5′‐triphosphate (5′‐ppp) and terminal double‐stranded structures, such as those that are generated during viral infection. RIG‐I has been shown to translocate on dsRNA in an ATP‐dependent manner. However, the precise role of the ATPase activity in RIG‐I activation remains unclear. Using in vitro‐transcribed Sendai virus defective interfering RNA as a model ligand, we show that RIG‐I oligomerizes on 5′‐ppp dsRNA in an ATP hydrolysis‐dependent and dsRNA length‐dependent manner, which correlates with the strength of type‐I interferon (IFN‐I) activation. These results establish a clear role for the ligand‐induced ATPase activity of RIG‐I in the stimulation of the IFN response. 相似文献
74.
T. E. Mabry C. D. Jones T. S. Chou J. M. Colacino G. B. Grindey J. F. Worzalla 《Nucleosides, nucleotides & nucleic acids》2013,32(5):1125-1133
Abstract The synthesis of β-dFARPP was accomplished by Mitsunobu coupling of 6-cyanopurine with 2-deoxy-2, 2-difluororibose followed by purine ring-expansion under the action of methanolic ammonia. The title compound inhibited the growth of proliferating human leukemic CCRF-CEM cells at 6.1μg/ml but had no effect on plaque formation by a variety of DNA and RNA viruses. 相似文献
75.
Krzysztof Dziewiszek Raymond F. Schinazi Ting-Chao Chou Tsann-Long Su Jolanta M. Dzik Wojciech Rode 《Nucleosides, nucleotides & nucleic acids》2013,32(1-3):77-94
Abstract A number of 1-(2-deoxy-2-fluoro-β-D-arabinofuranosyl)uracil and -cytosine nucleosides substituted at the 5 position with a nitrophenyl or nitrobenzyl group were synthesized from 5-phenyl- and 5-benzyluracil via condensation of the fluorinated sugar, followed by nitration. The corresponding amino analogues were also prepared by reduction of the nitro nucleosides. The uracil nucleosides were converted into the corresponding cytosine nucleosides by way of the triazole intermediates. None of these nucleosides exhibited significant activity against herpes simplex virus type 1 in Vero cells. However, cytosine nucleosides containing the o-nitrophenyl, p-nitrophenyl, p-nitrobenzyl or p-aminobenzyl substituent were found to be toxic (even at 1 μM) to uninfected Vero cells, although they were essentially nontoxic in HL-60 cells. The 5′-monophosphates of the uracil nucleosides were inhibitors of the reaction catalyzed by purified Ehrlich ascites carcinoma thymidylate synthase, the 5-phenyluracil nucleotides causing a strong inhibition, competitive vs dUMP, described by the Ki value of 0.01 μM. 相似文献
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77.
Pei-Shi Hung Chung-Ji Liu Chung-Shan Chou Shou-Yen Kao Cheng-Chieh Yang Kuo-Wei Chang Ting-Hui Chiu Shu-Chun Lin 《PloS one》2013,8(11)
MicroRNAs are short non-coding RNAs that regulate gene expression and are crucial to tumorigenesis. Oral squamous cell carcinoma (OSCC) is a prevalent malignancy worldwide. Up-regulation of miR-146 has been identified in OSCC tissues. However, the roles of miR-146 in carcinogenesis are controversial as it is suppressive in many other malignancies. The present study investigated the pathogenic implications of miR-146a in oral carcinogenesis. Microdissected OSCC exhibits higher levels of miR-146a expression than matched adjacent mucosal cells. The plasma miR-146a levels of patients are significantly higher than those of control subjects; these levels decrease drastically after tumor resection. miR-146a levels in tumors and in patients’ plasma can be used to classify OSCC and non-disease status (sensitivity: >0.72). Exogenous miR-146a expression is significantly increased in vitro oncogenic phenotypes as well as during xenograft tumorigenesis and OSCC metastasis. The plasma miR-146a levels of these mice parallel the xenograft tumor burdens of the mice. A miR-146a blocker abrogates the growth of xenograft tumors. miR-146a oncogenic activity is associated with down-regulation of IRAK1, TRAF6 and NUMB expression. Furthermore, miR-146a directly targets the 3′UTR of NUMB and a region within the NUMB coding sequence when suppressing NUMB expression. Exogenous NUMB expression attenuates OSCC oncogenicity. Double knockdown of IRAK1 and TRAF6, and of TRAF6 and NUMB, enhance the oncogenic phenotypes of OSCC cells. Oncogenic enhancement modulated by miR-146a expression is attenuated by exogenous IRAK1 or NUMB expression. This study shows that miR-146a expression contributes to oral carcinogenesis by targeting the IRAK1, TRAF6 and NUMB genes. 相似文献
78.
Yu-Ru Lee Dah-Shyong Yu Ya-Chun Liang Kuo-Feng Huang Shih-Jie Chou Tsung-Chih Chen Chia-Chung Lee Chun-Liang Chen Shih-Hwa Chiou Hsu-Shan Huang 《PloS one》2013,8(2)
Poly (ADP-ribose) polymerase-1 (PARP-1) and telomerase, as well as DNA damage response pathways are targets for anticancer drug development, and specific inhibitors are currently under clinical investigation. The purpose of this work is to evaluate anticancer activities of anthraquinone-derived tricyclic and tetracyclic small molecules and their structure-activity relationships with PARP-1 inhibition in non-small cell lung cancer (NSCLC) and NSCLC-overexpressing Oct4 and Nanog clone, which show high-expression of PARP-1 and more resistance to anticancer drug. We applied our library selected compounds to NCI''s 60 human cancer cell-lines (NCI-60) in order to generate systematic profiling data. Based on our analysis, it is hypothesized that these drugs might be, directly and indirectly, target components to induce mitochondrial permeability transition and the release of pro-apoptotic factors as potential anti-NSCLC or PARP inhibitor candidates. Altogether, the most active NSC747854 showed its cytotoxicity and dose-dependent PARP inhibitory manner, thus it emerges as a promising structure for anti-cancer therapy with no significant negative influence on normal cells. Our studies present evidence that telomere maintenance should be taken into consideration in efforts not only to overcome drug resistance, but also to optimize the use of telomere-based therapeutics. These findings will be of great value to facilitate structure-based design of selective PARP inhibitors, in general, and telomerase inhibitors, in particular. Together, the data presented here expand our insight into the PARP inhibitors and support the resource-demanding lead optimization of structurally related small molecules for human cancer therapy. 相似文献
79.
Kuan-Chung Hsiao Neng-Yao Shih Hsun-Lang Fang Tze-Sing Huang Ching-Chuan Kuo Pei-Yi Chu Yi-Mei Hung Shao-Wen Chou Yi-Yuan Yang Gee-Chen Chang Ko-Jiunn Liu 《PloS one》2013,8(7)
In previous research, we found α-enolase to be inversely correlated with progression-free and overall survival in lung cancer patients and detected α-enolase on the surface of lung cancer cells. Based on these findings, we hypothesized that surface α-enolase has a significant role in cancer metastasis and tested this hypothesis in the current study. We found that α-enolase was co-immunoprecipitated with urokinase-type plasminogen activator, urokinase-type plasminogen activator receptor, and plasminogen in lung cancer cells and interacted with these proteins in a cell-free dot blotting assay, which can be interrupted by α-enolase-specific antibody. α-Enolase in lung cancer cells co-localized with these proteins and was present at the site of pericellular degradation of extracellular matrix components. Treatment with antibody against α-enolase in vitro suppressed cell-associated plasminogen and matrix metalloproteinase activation, collagen and gelatin degradation, and cell invasion. Examination of the effect of treatment with shRNA plasmids revealed that down regulation of α-enolase decreases extracellular matrix degradation by and the invasion capacity of lung cancer cells. Adoptive transfer of α-enolase-specific antibody to mice resulted in accumulation of antibody in subcutaneous tumor and inhibited the formation of tumor metastasis in lung and bone. This study demonstrated that surface α-enolase promotes extracellular matrix degradation and invasion of cancer cells and that targeting surface α-enolase is a promising approach to suppress tumor metastasis. 相似文献
80.
Ai-Hsiang Chou Chia-Chyi Liu Jui-Yuan Chang Renee Jiang Yi-Chin Hsieh Amanda Tsao Chien-Long Wu Ju-Lan Huang Chang-Phone Fung Szu-Min Hsieh Ya-Fang Wang Jen-Ren Wang Mei-Hua Hu Jen-Ron Chiang Ih-Jen Su Pele Choi-Sing Chong 《PloS one》2013,8(11)