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Your search keyword '"Xia, Dianren"' showing total 35 results
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35 results on '"Xia, Dianren"'

11. Prostaglandin [E.sub.2] promotes intestinal tumor growth via DNA methylation

Author

Xia, Dianren, Wang, Dingzhi, Kim, Sun-Hee, Katoh, Hiroshi, and DuBois, Raymond N.

Subjects
Physiological aspects, Development and progression, Research, Methylation -- Physiological aspects -- Research, Prostaglandins E -- Physiological aspects -- Research, DNA -- Physiological aspects -- Research, Tumors -- Development and progression -- Research
Abstract

Although aberrant DNA methylation is considered to be one of the key ways by which tumor-suppressor and DNA-repair genes are silenced during tumor initiation and progression, the mechanisms underlying DNA [...]

Published
2012
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13. Germline and Somatic Smoothened Mutations in Non–Small-Cell Lung Cancer Are Potentially Responsive to Hedgehog Inhibitor Vismodegib

Author

Tsao, Anne S., primary, Wistuba, Ignacio, additional, Xia, Dianren, additional, Byers, Lauren, additional, Diao, Lixia, additional, Wang, Jing, additional, Papadimitrakopoulou, Vassiliki, additional, Tang, Ximing, additional, Lu, Wei, additional, Kadara, Humam, additional, Grigoryev, Dimitry N., additional, Selvan, Myvizhi Esai, additional, Gümüş, Zeynep H., additional, Tan, Zhi, additional, Zhang, Shuxing, additional, Nilsson, Monique, additional, and Heymach, John V., additional

Published
2017
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14. Response of germline and somatic smoothened (SMO) mutations in non-small cell lung cancer (NSCLC) to hedgehog inhibitor vismodegib.

Author

Tsao, Anne S., primary, Wistuba, Ignacio Ivan, additional, Xia, Dianren, additional, Byers, Lauren Averett, additional, Diao, Lixia, additional, Wang, Jing, additional, Papadimitrakopoulou, Vassiliki, additional, Tang, XiMing, additional, Lu, Wei, additional, Kadara, Humam, additional, Gumus, Zeynep H., additional, Tan, Zhi, additional, Zhang, Shuxing, additional, Nilsson, Monique B., additional, and Heymach, John, additional

Published
2017
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15. MIIPhaploinsufficiency induces chromosomal instability and promotes tumour progression in colorectal cancer

Author

Sun, Yan, primary, Ji, Ping, additional, Chen, Tao, additional, Zhou, Xinhui, additional, Yang, Da, additional, Guo, Yuhong, additional, Liu, Yuexin, additional, Hu, Limei, additional, Xia, Dianren, additional, Liu, Yanxue, additional, Multani, Asha S, additional, Shmulevich, Ilya, additional, Kucherlapati, Raju, additional, Kopetz, Scott, additional, Sood, Anil K, additional, Hamilton, Stanley R, additional, Sun, Baocun, additional, and Zhang, Wei, additional

Published
2016
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18. Prostaglandin E2 Induces Human Enhancer of Filamentation 1 to Promote Proliferation of Colorectal Carcinoma Cells

Author

Xia, Dianren, Holla, Vijaykumar R., Wang, Dingzhi, Menter, David G., and DuBois, Raymond N.

Subjects
Cell Cycle, Mice, Nude, Cell Growth Processes, Protein Serine-Threonine Kinases, Phosphoproteins, Article, Dinoprostone, Mice, Aurora Kinases, Cell Line, Tumor, Animals, Humans, lipids (amino acids, peptides, and proteins), RNA, Messenger, Colorectal Neoplasms, Adaptor Proteins, Signal Transducing, Aurora Kinase A
Abstract

Elevated expression of cyclooxygenase-2 (COX-2) and one of its downstream enzymatic products, prostaglandin E2 (PGE2) have been directly linked to colorectal carcinogenesis in a number of ways. Among which, PGE2 promotes cell proliferation, cell cycle progression, and thus tumor growth. All of the mechanism(s) by which PGE2 signaling regulates cell growth are not completely understood. Here, we demonstrate that PGE2 treatment induces human enhancer of filamentation 1 (HEF1) expression and its link with cell cycle machinery in colorectal cancer cells. PGE2 rapidly stimulated the expression of HEF1 mRNA and protein in colorectal cancer cells. Both PGE2 treatment and HEF1 overexpression resulted in similar effects on cell proliferation, cell cycle progression, and tumor growth. Moreover, knockdown of HEF1 using shRNA suppressed PGE2-driven cell proliferation and cell cycle progression. Cell cycle alterations involved HEF1 fragmentation as well as co-distribution of HEF1 and Aurora A along spindle asters during cell division. Furthermore, HEF1 co-immunoprecipitated with and activated Aurora A. Intriguingly, HEF1 expression was increased in 50% of human colorectal cancers compared with expression in paired normal tissue. These data suggest that PGE2 induces HEF1 expression, which in turn promotes cell cycle progression through its interaction and activation of Aurora A. Clearly, HEF1 is a downstream mediator of PGE2 action during colorectal carcinogenesis.

Published
2010

32. Molecular Cloning and Expression Analysis of a Putative Terpene Synthase Gene from Citrus.

Author

Ying Jia, Xia, Dianren, and Louzada, E. S.

Subjects
*MOLECULAR cloning, *PLANT genetics, *TERPENES, *CITRUS, *GENOMICS, *BOTANY
Abstract

A cDNA coding for a putative terpene synthase (Grips) was isolated from ‘Rio Red’ grapefruit (Citrus paradisi Macf.) mature fruit by differential display RT-PCR and the corresponding full-length cDNA and genomic clone were subsequently obtained. The isolated cDNA clone was 1644 bp in length encoding a protein of 548 amino acids with a predicted molecular mass of 64 kDa and of pI 5.38. The genomic clone was 3203 bp in length with 6 introns and 7 exons. This Grips appears to be a sesquiterpene synthase based on molecular weight, genomic organization, and similarity with the other terpene synthases. Both RT-PCR and Northern blot expression analysis indicated that Grips is not expressed in immature fruits, roots, or leaves, but only in mature fruits. Southern blot analysis of genomic DNA demonstrated that Grtps is one of the members in the family of terpene synthases. [ABSTRACT FROM AUTHOR]

Published
2005
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33. Prostaglandin E2 promotes intestinal tumor growth via DNA methylation.

Author

Xia, Dianren, Wang, Dingzhi, Kim, Sun-Hee, Katoh, Hiroshi, and DuBois, Raymond N

Subjects
PROSTAGLANDINS E, INTESTINAL tumors, TUMOR growth prevention, DNA methylation, TRANSFORMING growth factors, DNA repair
Abstract

Although aberrant DNA methylation is considered to be one of the key ways by which tumor-suppressor and DNA-repair genes are silenced during tumor initiation and progression, the mechanisms underlying DNA methylation alterations in cancer remain unclear. Here we show that prostaglandin E2 (PGE2) silences certain tumor-suppressor and DNA-repair genes through DNA methylation to promote tumor growth. These findings uncover a previously unrecognized role for PGE2 in the promotion of tumor progression. [ABSTRACT FROM AUTHOR]

Published
2012
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34. Targeted deletion of MKK4 gene potentiates TNF-induced apoptosis through the down-regulation of NF-kappa B activation and NF-kappa B-regulated antiapoptotic gene products.

Author

Sethi G, Ahn KS, Xia D, Kurie JM, and Aggarwal BB

Subjects
Animals, Apoptosis genetics, Apoptosis Regulatory Proteins biosynthesis, Apoptosis Regulatory Proteins genetics, Cell Line, Cyclin D1 biosynthesis, Cyclin D1 genetics, Cyclooxygenase 2 biosynthesis, Cyclooxygenase 2 genetics, Down-Regulation genetics, Fibroblasts cytology, Fibroblasts enzymology, Fibroblasts immunology, MAP Kinase Kinase 4 deficiency, MAP Kinase Kinase 4 physiology, Matrix Metalloproteinase 9 biosynthesis, Matrix Metalloproteinase 9 genetics, Mice, Mice, Inbred C57BL, Mice, Knockout, NF-kappa B metabolism, NF-kappa B physiology, Receptors, Tumor Necrosis Factor, Type I biosynthesis, Receptors, Tumor Necrosis Factor, Type I genetics, Receptors, Tumor Necrosis Factor, Type II biosynthesis, Receptors, Tumor Necrosis Factor, Type II genetics, Apoptosis immunology, Apoptosis Regulatory Proteins antagonists & inhibitors, Down-Regulation immunology, Gene Deletion, Gene Targeting, MAP Kinase Kinase 4 genetics, NF-kappa B antagonists & inhibitors, Tumor Necrosis Factor-alpha physiology
Abstract

MAPK kinase 4 (MKK4) is a dual-specificity kinase that activates both JNK and p38 MAPK. However, the mechanism by which MKK4 regulates TNF-induced apoptosis is not fully understood. Therefore, we used fibroblasts derived from MKK4 gene-deleted (MKK4-KO) mice to determine the role of this kinase in TNF signaling. We found that when compared with the wild-type cells, deletion of MKK4 gene enhanced TNF-induced apoptosis, and this correlated with down-regulation of TNF-induced cell-proliferative (COX-2 and cyclin D1) and antiapoptotic (survivin, IAP1, XIAP, Bcl-2, Bcl-x(L), and cFLIP) gene products, all regulated by NF-kappaB. Indeed we found that TNF-induced NF-kappaB activation was abrogated in MKK4 gene-deleted cells, as determined by DNA binding. Further investigation revealed that TNF-induced I kappaB alpha kinase activation, I kappaB alpha phosphorylation, I kappaB alpha degradation, and p65 nuclear translocation were all suppressed in MKK4-KO cells. NF-kappaB reporter assay revealed that NF-kappaB activation induced by TNF, TNFR1, TRADD, TRAF2, NIK, and I kappaB alpha kinase was modulated in gene-deleted cells. Overall, our results indicate that MKK4 plays a central role in TNF-induced apoptosis through the regulation of NF-kappaB-regulated gene products.

Published
2007
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35. Akt phosphorylates and suppresses the transactivation of retinoic acid receptor alpha.

Author

Srinivas H, Xia D, Moore NL, Uray IP, Kim H, Ma L, Weigel NL, Brown PH, and Kurie JM

Subjects
Animals, Cell Line, Chlorocebus aethiops, DNA metabolism, DNA-Binding Proteins genetics, DNA-Binding Proteins metabolism, Down-Regulation genetics, Humans, Ligands, Mutation genetics, Phosphorylation drug effects, Phosphoserine metabolism, Protein Binding, Proto-Oncogene Proteins c-akt genetics, Retinoic Acid Receptor alpha, Retinoids pharmacology, Substrate Specificity, Proto-Oncogene Proteins c-akt metabolism, Receptors, Retinoic Acid antagonists & inhibitors, Receptors, Retinoic Acid metabolism, Transcriptional Activation genetics
Abstract

The transactivation of nuclear receptors is regulated by both ligand binding and phosphorylation. We previously showed that RARalpha (retinoic acid receptor alpha) phosphorylation by c-Jun N-terminal kinase contributes to retinoid resistance in a subset of NSCLC cells (non-small cell lung cancer cells), but the aetiology of this resistance in the remainder has not been fully elucidated [Srinivas, Juroske, Kalyankrishna, Cody, Price, Xu, Narayanan, Weigel and Kurie (2005) Mol. Cell. Biol. 25, 1054-1069]. In the present study, we report that Akt, which is constitutively activated in NSCLC cells, phosphorylates RARalpha and inhibits its transactivation. Biochemical and functional analyses showed that Akt interacts with RARalpha and phosphorylates the Ser96 residue of its DNA-binding domain. Mutation of Ser96 to alanine abrogated the suppressive effect of Akt. Overexpression of a dominant-negative form of Akt in an NSCLC cell line decreased RAR phosphorylation, increased RAR transactivation and enhanced the growth-inhibitory effects of an RAR ligand. The findings presented here show that Akt inhibits RAR transactivation and contributes to retinoid resistance in a subset of NSCLC cells.

Published
2006
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