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Expression and Underlying Roles of IGFBP-3 in Paclitaxel-Treated Gastric Cancer Sgc-7901 Cells
Huang, Gang,Dang, Zhong-Feng,Dang, Ya-Mei,Cai, Wei,Li, Yuan,Chen, Yi-Rong,Xie, Xiao-Dong Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.14
Purpose: To study the expression of insulin-like growth factor binding proteins (IGFBPs) in paclitaxel-treated gastric cancer SGC-7901 cells, and to further investigate underlying mechanisms. Materials and Methods: Real time PCR and Western blot assays were applied to detect the mRNA and protein expression of IGFBP-2, -3 and -5 after paclitaxel (10 nM) treatment of SGC-7901 cells. In addition IGFBP-3 expression was silenced by RNA interference to determine effects. Cell viability was determined by MTT assay. Cell cycling and apoptosis were assessed by flow cytometry. Results: Compared to the control group, only IGFBP-3 expression was elevated significantly after paclitaxel (10 nM) treatment (p<0.05). Paclitaxel treatment caused cell cycle arrest and apoptosis via downregulating Bcl-2 expression. However, the effect could be abrogated by IGFBP-3 silencing. Conclusions: IGFBP-3 exhibits anti-apoptotic effects on paclitaxel-treated SGC-7901 cells via elevating Bcl-2 expression.
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Chun-Lian Liu,Xiao-Ping Hu,Wei-Dong Guo,Li Yang,Jie Dang,Hai-Yan Jiao 한국유방암학회 2013 Journal of breast cancer Vol.16 No.4
Purpose: Genetic variation in fibroblast growth factor receptor 2(FGFR2) is a newly described risk factor for breast cancer. Thisstudy aimed to evaluate the association of four single nucleotidepolymorphisms (SNPs) in FGFR2 with breast cancer in Han Chinesewomen. Methods: Two hundred three women with breastcancer and 200 breast cancer-free age-matched controls wereselected. Four SNPs (rs2981579, rs1219648, rs2420946, andrs2981582) and their haplotypes were analyzed to test for theirassociation with breast cancer susceptibility. The presence ofthe four FGFR2 SNPs was determined by polymerase chain reaction-restriction fragment length polymorphism analysis. Results:A statistically significant difference was observed in thefrequency of rs2981582 in the FGFR2 gene (p<0.05) betweencase and control groups. In subjects stratified by menopausalstatus, rs2981582 TT, rs2420946 AA, and rs1219648 CC weresignificantly associated with the risk of breast cancer in postmenopausalsubjects, but no significant associations betweenthese four SNPs and the risk of breast cancer were identified inpremenopausal subjects. Further, there was no significant associationbetween hormone receptor status (estrogen receptor andprogesterone receptor) and breast cancer risk. Six common (>3%) haplotypes were identified. Three of these haplotypes,CGTC (odds ratio [OR], 0.613; 95% confidence interval [CI],0.457-0.82; p=0.001), TGTC (OR, 6.561; 95% CI, 2.064-20.854;p<0.001), and CATC (OR, 12.645; 95% CI, 1.742-91.799; p=0.001) were significantly associated with breast cancer risk. Conclusion:Our findings indicated that the SNP rs2981582 and haplotypesCGTC, TGTC, and CATC in FGFR2 may be associatedwith an increased risk of breast cancer in Han Chinese women.
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Zhi-Fu Guo,Xiang-Yu Long,Pan Dong,Yu-Ming Wei,Li-Ping Bai,Xiao-Xuan Dang,Hao-Lei Wan,Li-Jun Zhang,You-Liang Zheng 한국유전학회 2011 Genes & Genomics Vol.33 No.2
The α-gliadins from Crithopsis delileana (Schult) Roshev (2n=2x=14, KK) were investigated by Acid polyacrylamide gel electrophoresis (A-PAGE) analysis. It was indicated that the electrophoresis mobility of gliadins from C.delileana had obvious difference with those from common wheat in α, γand ω region. Using primers designed from published sequences of α-gliadin genes, three α-gliadin genes were isolated from C. delileana, which were designated as gli-ka1,gli-ka2 and gli-ka3, respectively. Two in-frame stop codons were found in the coding sequences of gli-ka3, indicating that gli-ka3 could be a pseudogene. The gli-ka2 was a gliadin with an odd number of cysteines, resulting from a non-synonymous mutation. This change might lead to the interactive behavior of gli-ka2. Three α-gliadin genes of C. delileana had the similar but not identical primary structures to the corresponding gene sequences from other wheat related species. By the alignment of α-gliadin genes from Triticeae,phylogenetic analysis indicated that three α-gliadin genes of C. delileana clustered together with all α-gliadin genes from Ee genome of Lophopyrum elongatum by an interior paralleled branch.
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miR-98 suppresses melanoma metastasis through a negative feedback loop with its target gene IL-6
Fei Li,Xin-ji Li,Li Qiao,Fei Shi,Wen Liu,You Li,Yu-ping Dang,Weijie Gu,Xiao-gang Wang,Wei Liu 생화학분자생물학회 2014 Experimental and molecular medicine Vol.46 No.-
Dysregulated microRNA (miRNA) expression has a critical role in tumor development and metastasis. However, the mechanism by which miRNAs control melanoma metastasis is unknown. Here, we report reduced miR-98 expression in melanoma tissues with increasing tumor stage as well as metastasis; its expression is also negatively associated with melanoma patient survival. Furthermore, we demonstrate that miR-98 inhibits melanoma cell migration in vitro as well as metastatic tumor size in vivo. We also found that IL-6 is a target gene of miR-98, and IL-6 represses miR-98 levels via the Stat3-NF-κB-lin28B pathway. In an in vivo melanoma model, we demonstrate that miR-98 reduces melanoma metastasis and increases survival in part by reducing IL-6 levels; it also decreases Stat3 and p65 phosphorylation as well as lin28B mRNA levels. These results suggest that miR-98 inhibits melanoma metastasis in part through a novel miR-98-IL-6-negative feedback loop.
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Wang Ying,Li Ze-Xin,Wang Jian-Guo,Li Lu-Hao,Shen Wen-Long,Dang Xiao-Wei 한국유전학회 2023 Genes & Genomics Vol.45 No.2
Background Deubiquitinating enzymes (DUBs) have been shown to be possible targets for hepatocellular carcinoma (HCC) treatment. Objective This study was designed to reveal the effect and underlying mechanism of Josephin-2, a relatively newly defined DUB, in HCC progression. Methods SNU-387 and PLC/PRF/5 cells were used for in vitro functional assays. The levels of Josephin-2 and phosphoglycerate dehydrogenase (PHGDH) were determined using RT-qPCR and western blotting. Cell proliferation, migration and invasion were assessed by CCK-8, colony formation and Transwell. Spheroid-forming assay was performed to assess the cancer stem cell (CSC)-phenotype of HCC cells. A xenograft mice model was applied to verify the effect of Josephin-2 on HCC cell growth in vivo. Results Herein, we showed that Josephin-2 expression was negatively correlated with HCC patient survival in data from the online database. Cell experiments indicated that knockdown of Josephin-2 attenuated HCC cell malignant biological behaviors. Besides, Josephin-2 silencing also decreased the spheroid-formation while inhibited the expression of CSC biomarkers (CD133, OCT4, SOX2 and EpCAM) in HCC cells. Mechanistically, Josephin-2 had a deubiquitinating activity towards the regulation of PHGDH protein, the rate-limiting enzyme in the first step of serine biosynthesis pathway. Depletion of Josephin-2 enhanced the ubiquitination degradation of PHGDH and ultimately inhibited the proliferation and CSC-phenotype of HCC in vitro and in vivo. Conclusion Our work uncovered the regulatory effects of Josephin-2 on PHGDH protein stability and profiled its contribution in HCC malignant progression, which might provide a potential therapeutic target for HCC.
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