Search

Your search keyword '"Jao, Tzu-Ming"' showing total 35 results
Start Over Author "Jao, Tzu-Ming"
35 results on '"Jao, Tzu-Ming"'

34. NDST4 Is a Novel Candidate Tumor Suppressor Gene at Chromosome 4q26 and Its Genetic Loss Predicts Adverse Prognosis in Colorectal Cancer.

Author

Tzeng, Sheng-Tai, Tsai, Ming-Hong, Chen, Chi-Long, Lee, Jing-Xing, Jao, Tzu-Ming, Yu, Sung-Liang, Yen, Sou-Jhy, and Yang, Ya-Chien

Subjects
TUMOR suppressor genes, CHROMOSOMES, COLON cancer prognosis, BIOMARKERS, GENE mapping, GENE expression, POLYMERASE chain reaction, MICRODISSECTION
Abstract

Background: Genomic deletion at tumor suppressor loci is a common genetic aberration in human cancers. The study aimed to explore candidate tumor suppressor genes at chromosome 4q25-q28.2 and to delineate novel prognostic biomarkers associated with colorectal cancer (CRC). Methods: Deletion mapping of chromosome 4q25-q28.2 was conducted in 114 sporadic CRC by loss of heterozygosity study with 11 microsatellite markers. A novel candidate tumor suppressor gene, namely NDST4, was identified at 4q26. Gene expression of NDST4 was investigated in 52 pairs of primary CRC tissues by quantitative reverse transcription-polymerase chain reaction. Allelic loss of NDST4 gene was further determined in 174 colorectal carcinomas by loss of heterozygosity analysis, and then was assessed for clinical relevance. Results: One minimal deletion region was delineated between D4S2297 and D4S2303 loci at 4q26, where NDST4 was the only gene that had markedly been downregulated in CRC tumors. By laser capture microdissection, NDST4 RNA expression was demonstrated in colonic epithelial cells, but was undetectable in tumor cells. In total, 30 (57.7%) of 52 colorectal carcinomas showed a dramatic reduction in NDST4 gene expression compared with matched normal mucosae. The genetic loss of NDST4 was significantly associated with advanced pathological stage (P = 0.039) and poorer overall survival of patients (P = 0.036). Conclusions: NDST4 gene is a novel candidate tumor suppressor gene in human cancer, and the loss of its function might be involved in CRC progression. In addition, the loss of heterozygosity assay, which was established to determine the allelic loss of NDST4 gene, could be a cost-effective tool for providing a useful biomarker of adverse prognosis in CRC. [ABSTRACT FROM AUTHOR]

Published
2013
Full Text
View/download PDF

35. Abstract 14169: Latent Transforming Growth Factor-Beta-Binding Protein 4 Deficiency Attenuated Renal Fibrosis After Myocardial Infarction

Author

Su, Chi-Ting, Fang, I-Hsien, Liu, Yen-wen, Jao, Tzu-Ming, and Urban, Zsolt

Abstract

Introduction:After myocardial infarction (MI), renal injury is common and a predictor for poor prognosis. The cross-talk between heart and kidney is complex. Transforming growth factor beta (TGF) is a key cytokine that promotes cardiac and renal fibrosis. Latent transforming growth factor-beta-binding proteins (LTBPs) regulate TGF signaling and activation. Therefore, we investigated the pathophysiological role of LTBP4 in renal impairment after myocardial infarction.Hypothesis:LTBP4 contributes to renal fibrosis after myocardial infarction.Methods:Unilateral nephrectomy was performed one week before inducing myocardial infarction by ligation of the left anterior descending artery in wild-type (WT) and Ltbp4S-/- mice. Sham surgery was performed on control animals. Echocardiogarphy and picrosirius red/fast green-stained histology studies were used to demonstrate the cardiac dysfunction after myocardial infarction. Renal tissues were collected for histology, protein and gene studies at 1, 2, 4, 8, 10, 12 weeks after the surgery. Serum studies for renal functions and urine studies for albumin level were documented in serious.Results:After myocardial infarction, echocardiography demonstrated systolic dysfunction with anterior wall hypokinesia and histology studies revealed obvious cardiac fibrosis. In renal tissues, interleukin 6 (IL- 6) and monocyte chemoattractant protein-1(MCP-1) were significantly up-regulated in MI animals two weeks earlier than in controls. Moreover, 10 weeks after MI surgery, picrosirius red staining revealed renal interstitial fibrosis but the severity was weaker in Ltbp4S-/- mice, compared with WT mice. Enhanced expressions of kidney injury molecule-1 (KIM1), LTBP4 and TGF? and platelet derived growth factor receptor beta (PDGFRB) were elevated in MI animals compared to sham, but the degree of up-regulation was more prominent in WT than in Ltbp4S-/- mice.Conclusions:Cardiac fibrosis can enhance renal inflammation and exacerbate renal fibrosis. Inflammation preceded the expression of fibrotic factors. LTBP4 enhances TGF? signaling and may be a therapeutic target to mitigate post-MI renal injury.

Published
2019
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results