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Sökning: WFRF:(Kuo Min Liang)

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2.
  • Chen, Chi-Kuan, et al. (författare)
  • Leukocyte cell-derived chemotaxin 2 antagonizes MET receptor activation to suppress hepatocellular carcinoma vascular invasion by protein tyrosine phosphatase 1B recruitment
  • 2014
  • Ingår i: Hepatology. - Hoboken : Wiley-Blackwell. - 0270-9139 .- 1527-3350. ; 59:3, s. 974-985
  • Tidskriftsartikel (refereegranskat)abstract
    • UNLABELLED: Leukocyte cell-derived chemotoxin 2 (LECT2) has been shown to act as a tumor suppressor in hepatocellular carcinoma (HCC). However, the underlying mechanism has not yet been completely defined. Here, we employ a LECT2-affinity column plus liquid chromatography coupled with tandem mass spectrometry to identify LECT2-binding proteins and found that MET receptor strongly interacted with LECT2 protein. Despite the presence of hepatocyte growth factor, the LECT2 binding causes an antagonistic effect to MET receptor activation through recruitment of protein tyrosine phosphatase 1B. The antagonistic effect of LECT2 on MET activation also mainly contributes to the blockage of vascular invasion and metastasis of HCC. Furthermore, serial deletions and mutations of LECT2 showed that the HxGxD motif is primarily responsible for MET receptor binding and its antagonistic effects.CONCLUSION: These findings reveal a novel, specific inhibitory function of LECT2 in HCC by the direct binding and inactivation of MET, opening a potential avenue for treating MET-related liver cancer.
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3.
  • Chien, Ming-Hsien, et al. (författare)
  • Vascular endothelial growth factor-C (VEGF-C) promotes angiogenesis by induction of COX-2 in leukemic cells via the VEGF-R3/JNK/AP-1 pathway.
  • 2009
  • Ingår i: Carcinogenesis. - : Oxford University Press (OUP). - 0143-3334 .- 1460-2180. ; 30:12, s. 2005-13
  • Tidskriftsartikel (refereegranskat)abstract
    • Vascular endothelial growth factor (VEGF)-C is recognized as a tumor lymphangiogenic factor based on the effects of activated VEGF-R3 on lymphatic endothelial cells. Many tumor cells express VEGF-R3 but the function of this receptor in tumor cells is largely unknown. It has been reported that the VEGF-C/VEGF-R3 axis is activated in subsets of leukemia patients. Herein, we have shown that VEGF-C induces angiogenic activity in the tube formation assay invitro and Matrigel plug assay in vivo by upregulating an angiogenic factor, cyclooxygenase-2 (COX-2), through VEGF-R3 in the human acute myeloid leukemia (AML) cell line, THP-1. COX-2 induction by VEGF-C was also observed in other VEGF-R3(+) human AML cell lines (U937 and HL60). Moreover, immunohistochemical analysis of bone marrow specimens of 37 patients diagnosed with AML revealed that VEGF-C expression in specimens was associated with the expression of COX-2 (P < 0.001). The manner by which signaling pathways transduced by VEGF-C is responsible for COX-2 upregulation was further investigated. Blocking the p42/44 mitogen-activated protein kinase (MAPK) pathway with the MAPK kinase inhibitor, PD 98059, failed to inhibit VEGF-C-mediated COX-2 expression. However, VEGF-C-induced COX-2 upregulation was effectively abolished by overexpression of dominant-negative c-Jun N-terminal kinase (JNK) or treatment with the JNK inhibitor, SP 600125. VEGF-C induced JNK-dependent nuclear translocation of c-Jun. Furthermore, chromatin immunoprecipitation and reporter assays revealed that VEGF-C enhanced c-Jun binding to the cyclic adenosine 3',5'-monophosphate-response element of the COX-2 promoter and induced COX-2 expression. In sum, the data herein highlight the pathogenic role of VEGF-C in leukemia via regulation of angiogenesis through upregulation of COX-2.
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4.
  • Hua, Kuo-Tai, et al. (författare)
  • N-α-acetyltransferase 10 protein suppresses cancer cell metastasis by binding PIX proteins and inhibiting Cdc42/Rac1 activity
  • 2011
  • Ingår i: Cancer Cell. - : Cell Press. - 1535-6108 .- 1878-3686. ; 19:2, s. 218-231
  • Tidskriftsartikel (refereegranskat)abstract
    • N-α-acetyltransferase 10 protein, Naa10p, is an N-acetyltransferase known to be involved in cell cycle control. We found that Naa10p was expressed lower in varieties of malignancies with lymph node metastasis compared with non-lymph node metastasis. Higher Naa10p expression correlates the survival of lung cancer patients. Naa10p significantly suppressed migration, tumor growth, and metastasis independent of its enzymatic activity. Instead, Naa10p binds to the GIT-binding domain of PIX, thereby preventing the formation of the GIT-PIX-Paxillin complex, resulting in reduced intrinsic Cdc42/Rac1 activity and decreased cell migration. Forced expression of PIX in Naa10-transfected tumor cells restored the migration and metastasis ability. We suggest that Naa10p functions as a tumor metastasis suppressor by disrupting the migratory complex, PIX-GIT- Paxillin, in cancer cells.
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5.
  • Chen, Min-Wei, et al. (författare)
  • H3K9 histone methyltransferase G9a promotes lung cancer invasion and metastasis by silencing the cell adhesion molecule Ep-CAM
  • 2010
  • Ingår i: Cancer Research. - : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 70:20, s. 7830-7840
  • Tidskriftsartikel (refereegranskat)abstract
    • G9a is a mammalian histone methyltransferase that contributes to the epigenetic silencing of tumor suppressor genes. Emerging evidence suggests that G9a is required to maintain the malignant phenotype, but the role of G9a function in mediating tumor metastasis has not been explored. Here, we show that G9a is expressed in aggressive lung cancer cells, and its elevated expression correlates with poor prognosis. RNAi-mediated knockdown of G9a in highly invasive lung cancer cells inhibited cell migration and invasion in vitro and metastasis in vivo. Conversely, ectopic G9a expression in weakly invasive lung cancer cells increased motility and metastasis. Mechanistic investigations suggested that repression of the cell adhesion molecule Ep-CAM mediated the effects of G9a. First, RNAi-mediated knockdown of Ep-CAM partially relieved metastasis suppression imposed by G9a suppression. Second, an inverse correlation between G9a and Ep-CAM expression existed in primary lung cancer. Third, Ep-CAM repression was associated with promoter methylation and an enrichment for dimethylated histone H3K9. G9a knockdown reduced the levels of H3K9 dimethylation and decreased the recruitment of the transcriptional cofactors HP1, DNMT1, and HDAC1 to the Ep-CAM promoter. Our findings establish a functional contribution of G9a overexpression with concomitant dysregulation of epigenetic pathways in lung cancer progression.
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6.
  • Cha, Shih-Ting, et al. (författare)
  • MicroRNA-519c suppresses hypoxia-inducible factor-1alpha expression and tumor angiogenesis.
  • 2010
  • Ingår i: Cancer Research. - : American Association for Cancer Research. - 0008-5472 .- 1538-7445. ; 70:7, s. 2675-2685
  • Tidskriftsartikel (refereegranskat)abstract
    • Hypoxia-inducible factor-1alpha (HIF-1alpha) is widely considered to be one of the key regulators of tumor angiogenesis. The upstream regulation is complex and involves several growth factors, cytokines, and hypoxia. Herein, we have identified miR-519c as a hypoxia-independent regulator of HIF-1alpha, acting through direct binding to the HIF-1alpha 3' untranslated region and leading to reduced tumor angiogenesis. Overexpression of miR-519c resulted in a significant decrease of HIF-1alpha protein levels and reduced the tube formation of human umbilical vein endothelial cells; similarly, antagomir inhibition of miR-519c increased the level of HIF-1alpha protein and enhanced angiogenic activity, suggesting an important role of miR-519c in HIF-1alpha-mediated angiogenesis. Consistent with the overexpression of miR-519c in cancer patients with better prognosis, mice injected with miR-519c-overexpressing cells exhibited dramatically reduced HIF-1alpha levels, followed by suppressed tumor angiogenesis, growth, and metastasis. In addition, we found that hepatocyte growth factor (HGF), a known HIF-1alpha inducer, reduced the miR-519c levels through an Akt-dependent pathway. This regulation was posttranscriptional and may be mediated by suppression of miR-519c maturation. Taken together, our findings provide the first evidence that miR-519c is a pivotal regulator of tumor angiogenesis and that microenvironmental HGF contributes to regulating miR-519c biogenesis in cancer cells.
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7.
  • Johansson, Gunnar, et al. (författare)
  • Soluble AXL : a possible circulating biomarker for neurofibromatosis type 1 related tumor burden
  • 2014
  • Ingår i: PLOS ONE. - San Francisco : Public Library of Science. - 1932-6203. ; 9:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Neurofibromatosis type 1 (NF1) is the most common tumor predisposition disorder affecting 1/3500 worldwide. Patients are at risk of developing benign (neurofibromas) and malignant peripheral nerve sheath tumors (MPNST). The AXL receptor tyrosine kinase has been implicated in several kinds of cancers, but so far no studies have investigated the role of AXL in NF1 related tumorigenesis. Recently, the soluble fraction from the extracellular domain of AXL (sAXL) has been found in human plasma, and its level was correlated to poor prognosis in patients with renal cancer. Compared to normal human Schwann cells, a significantly high expression level of AXL was found in three of the four MPNST cell lines and two of the three primary MPNST tissues. Similarly, the level of sAXL in conditioned media corresponded to the protein and mRNA levels of AXL in the MPNST cell lines. Furthermore, in two different human MPNST xenograft models, the human sAXL could be detected in the mouse plasma. Its level was proportionate to the size of the xenograft tumors, while no human sAXL was detect prior to the formation of the tumors. Treatment with a newly developed photodynamic therapy, prevented further tumor growth and resulted in drastically reduced the levels of sAXL compared to that of the control group. Finally, the level of sAXL was significantly increased in patients with plexiform tumors compared to patients with only dermal neurofibromas, further supporting the role of sAXL as a marker for NF1 related tumor burden.
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8.
  • Su, Jen-Liang, et al. (författare)
  • Function and regulation of let-7 family microRNAs
  • 2012
  • Ingår i: MicroRNA (Shāriqah, United Arab Emirates). - : Bentham. - 2211-5366 .- 2211-5374. ; 1:1, s. 34-39
  • Tidskriftsartikel (refereegranskat)abstract
    • MicroRNAs (miRNAs) are a group of small noncoding RNAs capable of regulating specific gene expression. Let-7 miRNA was first discovered in Caenorhabditis elegans and it is highly conserved in human tissues. The human let- 7 family of miRNA contains 12 members of miRNA. Today, these members have become the most studied miRNAs and they have attracted attention of researchers in various fields, such as development, stem cell biology, aging, and metabolism. Furthermore, there is a large body of evidence linking the loss of let-7 expression and the development of poorly differentiated, aggressive cancers. In addition to the canonical biogenesis pathway, let-7 has been found to be regulated by protein factors, such as RNA binding proteins previously identified as regulators of protein-coding mRNAs. Moreover, the direct interaction between miRNAs has recently been identified as a novel pathway to control let-7 expression. In this review, we discuss the multifaceted roles of let-7 and provide an overview of its regulation at multiple levels.
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9.
  • Löwemark, Ludvig, et al. (författare)
  • Glacio-eustatic influence on deep water circulation in the South China Sea over the past 500 kyrs – implications for global biogeochemical cycling
  • 2008
  • Ingår i: Western Pacific Geophysics Meeting, American Geophysical Union, Cairns, Australia, July/August 2008.
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • We provide new evidence for the development of a stable estuarinecirculation characterized by stagnating water bodies, nutrient recycling and increased primary productivity in the South China Seaduring glacial intervals caused by the closure of the shallow andnarrow straits connecting the South China Sea in the south and west. Our main evidence comes from records of Mn concentrations and Mn/Al ratios in two sedimentary cores from the northern and southeastern South China Sea covering the last 500 ky. Concentrations and Mn/Al ratios of the redox sensitive element Mn show clear glacial-interglacial cycles with maxima during interglacial periods and minima during glacial periods. These cycles indicate ventilation cycles of the bottom water connected to the glacial-interglacial changes in sea level. In contrast, total organic carbon (TOC) concentrations display an opposite pattern with pronounced maxima during glacial times, especially in the southern part of the basin. The variations in TOC can be ascribed to two factors. Firstly to variations in primary productivity controlled by variations in theintensity of the winter monsoon. Secondly to the degree of preservation of TOC controlled by variations in ventilation, ultimately controlled by sea level. Variations in TOC consequentlyrepresent a superimposition of sea level influenced preservationcontrol and primarily winter monsoon driven variations in primaryproductivity intensity. The decrease in Mn correspond to times when sea level dropped below 40-50 m. Larger amplitude of the variations in TOC and Mn in the southern part of the basin compared to the northern sites suggest that oxygen depletion and nutrient recycling was stronger in the parts of the basin situated the furthest from the only remaining opening to the open Pacific, the Luzon strait.
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