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Geographical variability of alpha-1-antitrypsin alleles in China: A study on six Chinese populations
Ying Qi-long Zhang Mei-lin Liang Chih-chuan Liu Xiao-po Huang You-wen Wang Rong-xin Zhang Ni-jia Chen Li-chang Chen Luo-fu Yu Ning-chang Muo Xi-ping 《Human genetics》1985,69(2):184-187
Summary Alpha-1-antitrypsin phenotypes of six Chinese Han populations (20°–45°N. latitude) were determined. The frequency of allele M2 increases from North to South China. The north-south change of M2 appears to be mainly at the expense of alleles M1 and M3. Geographical variability of other variants was also observed. In the northern populations, the most common variants are M4 and Etokyo; in the southern populations, Pweishi, a variant which can not be distinguished electrophoretically from Pyasugi. These results form a distribution pattern of alpha-1-antitrypsin alleles in China. 相似文献
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Hsi-Kai Tsou Hsien-Te Chen Ya-Huey Hung Chia-Hao Chang Te-Mao Li Yi-Chin Fong Chih-Hsin Tang 《PloS one》2013,8(1)
Chondrosarcoma is a type of highly malignant tumor with a potent capacity for local invasion and causing distant metastasis. Chondrosarcoma shows a predilection for metastasis to the lungs. Hepatocyte growth factor (HGF) has been demonstrated to stimulate cancer proliferation, migration, and metastasis. However, the effect of HGF on migration activity of human chondrosarcoma cells is not well known. Here, we found that human chondrosarcoma tissues demonstrated significant expression of HGF, which was higher than that in normal cartilage. We also found that HGF increased the migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells. c-Met inhibitor and siRNA reduced HGF-increased cell migration and MMP-2 expression. HGF treatment resulted in activation of the phosphatidylinositol 3′-kinase (PI3K)/Akt/PKCδ/NF-κB pathway, and HGF-induced expression of MMP-2 and cell migration was inhibited by specific inhibitors or siRNA-knockdown of PI3K, Akt, PKCδ, and NF-κB cascades. Taken together, our results indicated that HGF enhances migration of chondrosarcoma cells by increasing MMP-2 expression through the c-Met receptor/PI3K/Akt/PKCδ/NF-κB signal transduction pathway. 相似文献
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Tien-Huang Lin Hsin-Ho Liu Tsung-Hsun Tsai Chi-Cheng Chen Teng-Fu Hsieh Shang-Sen Lee Yuan-Ju Lee Wen-Chi Chen Chih-Hsin Tang 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
Chemokine ligand 2 (CCL2), also known as monocyte chemoattractant protein-1 (MCP-1), belongs to the CC chemokine family which is associated with the disease status and outcomes of cancers. Prostate cancer is the most commonly diagnosed malignancy in men and shows a predilection for metastasis to the bone. However, the effect of CCL2 on human prostate cancer cells is largely unknown. The aim of this study was to examine the role of CCL2 in integrin expression and migratory activity in prostate cancers.Methods
Prostate cancer migration was examined using Transwell, wound healing, and invasion assay. The PKCδ and c-Src phosphorylations were examined by using western blotting. The qPCR was used to examine the mRNA expression of integrins. A transient transfection protocol was used to examine AP-1 activity.Results
Stimulation of prostate cancer cell lines (PC3, DU145, and LNCaP) induced migration and expression of integrin αvβ3. Treatment of cells with αvβ3 antibody or siRNA abolished CCL2-increased cell migration. CCL2-increased migration and integrin expression were diminished by CCR2 but not by CCR4 inhibitors, suggesting that the CCR2 receptor is involved in CCL2-promoted prostate cancer migration. CCL2 activated a signal transduction pathway that includes PKCδ, c-Src, and AP-1. Reagents that inhibit specific components of this pathway each diminished the ability of CCL2 to effect cell migration and integrin expression.Conclusions
Interaction between CCL2 and CCR2 enhances migration of prostate cancer cells through an increase in αvβ3 integrin production.General significance
CCL2 is a critical factor of prostate cancer metastasis. 相似文献5.
Chun-Hao Tsai Yi-Chun Chiang Hsien-Te Chen Po-Hao Huang Horng-Chaung Hsu Chih-Hsin Tang 《Biochimica et Biophysica Acta (BBA)/General Subjects》2013
Background
Diabetes is an independent risk factor of osteoarthritis (OA). Angiogenesis is essential for the progression of OA. Here, we investigated the intracellular signaling pathways involved in high glucose (HG)-induced vascular endothelial growth factor (VEGF) expression in human synovial fibroblast cells.Methods
HG-mediated VEGF expression was assessed with qPCR and ELISA. The mechanisms of action of HG in different signaling pathways were studied using Western blotting. Knockdown of proteins was achieved by transfection with siRNA. Chromatin immunoprecipitation assays were used to study in vivo binding of c-Jun to the VEGF promoter.Results
Stimulation of OA synovial fibroblasts (OASF) with HG induced concentration- and time-dependent increases in VEGF expression. Treatment of OASF with HG increased reactive oxygen species (ROS) generation. Pretreatment with NADPH oxidase inhibitor (APO or DPI), ROS scavenger (NAC), PI3K inhibitor (Ly294002 or wortmannin), Akt inhibitor, or AP-1 inhibitor (curcumin or tanshinone IIA) blocked the HG-induced VEGF production. HG also increased PI3K and Akt activation. Treatment of OASF with HG increased the accumulation of phosphorylated c-Jun in the nucleus, AP-1-luciferase activity, and c-Jun binding to the AP-1 element on the VEGF promoter.Conclusions
Our results suggest that the HG increases VEGF expression in human synovial fibroblasts via the ROS, PI3K, Akt, c-Jun and AP-1 signaling pathway.General significance
We link high glucose on VEGF expression in osteoarthritis. 相似文献6.
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(Phi)L7 is a lytic phage infecting the gram-negative Xanthomonas campestis pv. campestris, a plant pathogen. To study phage-host interaction, a (phi)L7-resistant mutant was isolated from strain Xc17 by mini-Tn5 transposition and designated CH7LR. CH7LR could not plate (phi)L7 in double-layered assay and formed turbid clearing zones when the cell lawn was dropped with a high titer of (phi)L7. Sequence analysis showed that the mutated gene is xanA coding for phosphoglucomutase/phosphomannomutase, required for the synthesis of lipopolysaccharide and exopolysaccharide (xanthan). The involvement of xanA was confirmed by isolating another mutant with interrupted xanA and complementing with the cloned wild-type gene. Nonmucoid mutants are still sensitive to (phi)L7, indicating that xanthan is not involved in (phi)L7 adsorption. Since the mutants still exhibited low efficiencies of phage adsorption, we predict, by analogy with the cases in other bacteriophages of gram-negative bacteria, that other outer membrane components such as a protein are required for the formation of a complex receptor. 相似文献
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Ching-Hung Lin Chen-Yang Shen Jih-Hsiang Lee Chiun-Sheng Huang Chih-Hsin Yang Wen-Hung Kuo Dwan-Ying Chang Chia-Ni Hsiung Kuan-Ting Kuo Wei-Wu Chen I-Chun Chen Pei-Fang Wu Sung-Hsin Kuo Chien-Jen Chen Yen-Shen Lu Ann-Lii Cheng 《PloS one》2015,10(4)
Background
A rapid surge of female breast cancer has been observed in young women in several East Asian countries. The BIM deletion polymorphism, which confers cell resistance to apoptosis, was recently found exclusively in East Asian people with prevalence rate of 12%. We aimed to evaluate the possible role of this genetic alteration in carcinogenesis of breast cancer in East Asians.Method
Female healthy volunteers (n = 307), patients in one consecutive stage I-III breast cancer cohort (n = 692) and one metastatic breast cancer cohort (n = 189) were evaluated. BIM wild-type and deletion alleles were separately genotyped in genomic DNAs.Results
Both cancer cohorts consistently showed inverse associations between the BIM deletion polymorphism and patient age (≤35 y vs. 36-50 y vs. >50 y: 29% vs. 22% vs. 15%, P = 0.006 in the consecutive cohort, and 40% vs. 23% vs. 13%, P = 0.023 in the metastatic cohort). In healthy volunteers, the frequencies of the BIM deletion polymorphism were similar (13%-14%) in all age groups. Further analyses indicated that the BIM deletion polymorphism was not associated with specific clinicopathologic features, but it was associated with poor overall survival (adjusted hazard ratio 1.71) in the consecutive cohort.Conclusions
BIM deletion polymorphism may be involved in the tumorigenesis of the early-onset breast cancer among East Asians. 相似文献9.
Chiu-Hsia Chiu Chih-Hsin Cheng Wen-Ren Gua Yuan-Kuang Guu Winton Cheng 《Fish & shellfish immunology》2010,29(6):1053-1059
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Fibronectin (Fn) is involved in early stages of bone formation and basic fibroblast growth factor (bFGF) is an important factor regulating osteogenesis. bFGF increased Fn expression, which was attenuated by phosphatidylinositol phospholipase inhibitor (U73122), protein kinase C inhibitor (GF109203X), Src inhibitor (PP2), NF-kappaB inhibitor (PDTC), IkappaBalpha phosphorylation inhibitor (Bay 117082), or IkappaB protease inhibitor (TPCK). bFGF-induced increase of Fn-luciferase activity was antagonized by cells transfected with Fn construct without NF-kappaB regulatory site. Stimulation of osteoblasts with bFGF activated IkappaB kinase alpha/beta (IKK alpha/beta) and increased IkappaBalpha phosphorylation, IkappaBalpha degradation, p65 and p50 translocation from the cytosol to the nucleus, the formation of an NF-kappaB-specific DNA-protein complex and kappaB-luciferase activity. bFGF-mediated an increase of IKKalpha/beta activity and DNA-binding activity was inhibited by U73122, GF109203X, or PP2. The binding of p65 to the NF-kappaB element, as well as the recruitment of p300 and the enhancement of p50 acetylation on the Fn promoter was enhanced by bFGF. Overexpression of constitutively active FGF receptor 2 (FGFR2) increased Fn-luciferase activity, which was inhibited by co-transfection with dominant negative (DN) mutants of PLCgamma2, PKCalpha, c-Src, IKKalpha, or IKKbeta. Our results suggest that bFGF increased Fn expression in rat osteoblasts via the FGFR2/PLCgamma2/PKCalpha/c-Src/NF-kappaB signaling pathway. 相似文献