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Migration Ability (migration + ability)
Selected AbstractsHonokiol inhibits HepG2 migration via down-regulation of IQGAP1 expression discovered by a quantitative pharmaceutical proteomic analysisPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 7 2010Shufang Liang Abstract Honokiol (HNK), a natural small molecular product, inhibited proliferation of HepG2 cells and exhibited anti-tumor activity in nude mice. In this article, we applied a novel sensitive stable isotope labeling with amino acids in cell culture-based quantitative proteomic method and a model of nude mice to investigate the correlation between HNK and the hotspot migration molecule Ras GTPase-activating-like protein (IQGAP1). The quantitative proteomic analysis showed that IQGAP1 was 0.53-fold down-regulated under 10,,g/mL HNK exposure for 24,h on HepG2 cells. Migration ability of HepG2 cells under HNK treatment was correlated with its expression level of IQGAP1. In addition, the biochemical validation on HepG2 cells and the tumor xenograft model further demonstrated that HNK decreased the expression level of IQGAP1 and its upstream proteins Cdc42/Rac1. These data supported that HNK can modulate cell adhesion and cell migration by acting on Cdc42/Rac1 signaling via IQGAP1 interactions with its upstream Cdc42/Rac1 proteins, which is a new molecular mechanism of HNK to exert its anti-tumor activity. [source] Nucleolar organizer region staining patterns in paraffin-embedded tissue cells from human skin cancersJOURNAL OF CUTANEOUS PATHOLOGY, Issue 5 2005Rosana F. Romão-Corrêa Background:, Increased number of nucleoli (nucleolar organizer regions, NORs) with abnormal shapes and sizes, including small dots, has been used as prognostic tools to evaluate tumor proliferation levels and troublesome borderline lesions. In this study, NOR patterns of skin cancers were performed in the search of a valuable prognostic method to complement other histological procedures. Methods:, Paraffin-embedded tumor tissue was obtained from basal and squamous cell carcinomas, cutaneous malignant melanoma, premalignant lesions, and Skmel-28 human melanoma cells. Slices were dewaxed and AgNOR stained. The patterns were scored and submitted for statistical analyses. Results:, All types of cancer cells showed variable numbers of abnormally shaped nucleoli and dot-like structures. Only tumor cells presented four or more nucleoli, with or without dots, while 85% of the normal cells had one single NOR without dots. Most data were statistically significant when compared to normal cells. As a whole, squamous cell carcinoma and malignant melanoma tumor cells had less NOR alterations than basal cell carcinoma (BCC) tumor types. Conclusions:, Changes in the number and shape of nucleoli present in malignant cells could be attributed to increased levels on rDNA transcription on cancer cells, besides abnormal remodeling of chromatin, which could disrupt proper nucleoli association. Increased genetic alterations on malignant basal cells could contribute to impair invasive and migration abilities of BCC tumors. [source] Bergmann's rule and the mammal fauna of northern North AmericaECOGRAPHY, Issue 6 2004Tim M. Blackburn The observation that "on the whole,,larger species live farther north and the smaller ones farther south" was first published by Carl Bergmann in 1847. However, why animal body mass might show such spatial variation, and indeed whether it is a general feature of animal assemblages, is currently unclear. We discuss reasons for this uncertainty, and use our conclusions to direct an analysis of Bergmann's rule in the mammals in northern North America, in the communities of species occupying areas that were covered by ice at the last glacial maximum. First, we test for the existence of Bergmann's rule in this assemblage, and investigate whether small- and large-bodied species show different spatial patterns of body size variation. We then attempt to explain the spatial variation in terms of environmental variation, and evaluate the adequacy of our analyses to account for the spatial pattern using the residuals arising from our environmental models. Finally, we use the results of these models to test predictions of different hypotheses proposed to account for Bergmann's rule. Bergmann's rule is strongly supported. Both small- and large-bodied species exhibit the rule. Our environmental models account for most of the spatial variation in mean, minimum and maximum body mass in this assemblage. Our results falsify predictions of hypotheses relating to migration ability and random colonisation and diversification, but support predictions of hypotheses relating to both heat conservation and starvation resistance. [source] Trypanosoma cruzi infection modulates intrathymic contents of extracellular matrix ligands and receptors and alters thymocyte migrationEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 9 2003Vinícius Cotta-de-Almeida Abstract Several T cell abnormalities have been described in the course of acute Trypanosoma cruzi infection in mice, including severe effects on the thymus. In the present study, looking at the expression of extracellular matrix ligands in the thymus, we observed that deposits of fibronectin and laminin increased progressively during the course of infection, reaching a maximum at the peak of parasitemia and thymic atrophy. Concomitantly, membrane expression of fibronectin and laminin receptors (VLA-4, VLA-5 and VLA-6) was also enhanced on thymocyte subsets of infected mice. These results correlated with changes in intrathymic thymocyte migration ability during the acute phase of infection, when a higher fibronectin-dependent transmigratory activity of CD4+CD8+ thymocytes was observed. Strikingly, we detected higher frequency of immature and high VLA-expressing CD4+CD8+ T cells in the peripheral lymphoid organs of infected mice at thepeak of parasitemia. These cells seemed to be thymus dependent, since significantly lower amounts of them were found in thymectomized mice, and some of them carry "prohibited" V, segments of the TCR. Our data suggest an imbalance in the intrathymic cell trafficking following acute T. cruzi infection, likely due to dysregulated extracellular matrix-dependent interactions. [source] Phenotypic alterations induced by the Hong Kong-prevalent Epstein-Barr virus-encoded LMP1 variant (2117-LMP1) in nasopharyngeal epithelial cellsINTERNATIONAL JOURNAL OF CANCER, Issue 6 2004Angela Kwok Fung Lo Abstract Epstein-Barr virus (EBV) is closely associated with nasopharyngeal carcinoma (NPC), a common cancer in Hong Kong. The EBV-encoded LMP1 protein is believed to play an important role in cell transformation. We have previously identified a prevalent LMP1 variant (2117-LMP1) that is expressed in 86% of primary NPC in Hong Kong. In this study, the biologic phenotypes induced by 2117-LMP1 were compared with those of the prototypic B95.8-LMP1 in an immortalized nasopharyngeal epithelial cell line, NP69. The 2117-LMP1 could induce cell proliferation and resistance to apoptosis induced by growth factor deprivation. Expression of 2117-LMP1 also suppressed expression of p16, p21 and Bax but induced expression of CDK2 and A20. Compared with B95.8-LMP1, 2117-LMP1 could induce a higher migration ability in NP69 cells but was less efficient in inducing morphologic changes, anchorage-independent growth and cell invasion. Relatively weaker ability of 2117-LMP1 than B95.8-LMP1 in upregulation of vimentin, VEGF and MMP9 as well as in downregulation of E-cadherin was observed. 2117-LMP1 could activate higher level of NF-,B activity in HEK 293 cells than B95.8-LMP1. The present study supports a role of 2117-LMP1 in NPC development by enhancing cell proliferation, cell death inhibition and migration in premalignant nasopharyngeal epithelial cells. Furthermore, our study reveals significant functional differences between 2117-LMP1 and the prototypic B95.8-LMP1. Our results provide insights into the pathologic significance of this prevalent LMP1 variant, 2117-LMP1, in the development of NPC in the Hong Kong population. © 2004 Wiley-Liss, Inc. [source] Hepatitis B virus X protein upregulates expression of calpain small subunit 1 via nuclear facter-,B/p65 in hepatoma cellsJOURNAL OF MEDICAL VIROLOGY, Issue 6 2010Feng Zhang Abstract Hepatitis B virus (HBV) infection is closely correlated with the development of hepatocellular carcinoma (HCC), in which hepatitis B virus X protein (HBx) plays crucial roles. HBx is believed to be a multifunctional oncoprotein. It has been reported that the calpain small subunit 1 (Capn4) is upregulated in the HCC tissues and involved in the metastasis of HCC. Therefore, we suppose that HBx may promote hepatoma cell migration through Capn4. In the present study, we investigated the effect of HBx on regulating Capn4 expression in human HCC cells. Our data showed that HBx could increase promoter activity of Capn4 and upregulate the expression of Capn4 at the levels of mRNA and protein in human hepatoma HepG2 (or H7402) cells using luciferase reporter gene assay, real-time quantitative RT-PCR assay and Western blot analysis. While, the RNA interference targeting HBx mRNA was able to abolish the upregulation. Interestingly, we found that the inhibition of nuclear factor-,B (NF-,B) mediated by siRNA targeting NF-,B/p65 mRNA or PDTC (an inhibitor of NF-,B) could attenuate the upregulation of Capn4. While, HBx failed to increase the promoter activity of Capn4 in hepatoma cells when the putative NF-,B binding site of the Capn4 promoter was mutant, suggesting that NF-,B is involved in the activation of Capn4 mediated by HBx. In function, wound healing assay showed that HBx could significantly enhance the migration ability of HepG2 cells through upregulating Capn4. Thus, we conclude that HBx upregulate Capn4 through NF-,B/p65 to promote migration of hepatoma cells. J. Med. Virol. 82:920,928, 2010. © 2010 Wiley-Liss, Inc. [source] Inflammation: A new candidate in modulating adult neurogenesisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 6 2008Sulagna Das Abstract Any pathological perturbation to the brain provokes a cascade of molecular and cellular events, which manifests in the form of microglial activation and release of various proinflammatory molecules. This eventually culminates in a profound neuroinflammatory reaction that characterizes the brain's response to stress, injury, or infection. The inflammatory cascade is an attempt by the system to eliminate the challenge imposed on the brain, clear the system of the dead and damaged neurons, and rescue the normal functioning of this vital organ. However, during the process of microglial activation, the proinflammatory mediators released exert certain detrimental effects, and neural stem cells and progenitor cells are likely to be affected. Here we review how the proliferation, maturation, and migration of the neural stem cells are modulated under such an inflammatory condition. The fate of the noncommitted neural stem cells and its differentiation potency are often under strict regulation, and these proinflammatory mediators seem to disrupt this critical balance and finely tune the neurogenesis pattern in the two niches of neurogenesis, the subventricular zone and the subgranular zone of the hippocampus. Moreover, the migration ability of these stem cells, which is important for localization to the proper site, is also affected in a major way by the chemokines released following inflammation. © 2007 Wiley-Liss, Inc. [source] Bone morphogenetic protein 7 induces mesenchymal-to-epithelial transition in melanoma cells, leading to inhibition of metastasisCANCER SCIENCE, Issue 11 2009Yi-Rang Na Bone morphogenetic protein (BMP) 7 counteracts physiological epithelial-to-mesenchymal transition, a process that is indicative of epithelial plasticity in developmental stages. Because epithelial-to-mesenchymal transition and its reversed process mesenchymal-to-epithelial transition (MET) are also involved in cancer progression, we investigated whether BMP7 plays a role in WM-266-4 melanoma cell growth and metastasis. An MTT assay was conducted in WM-266-4 and HEK293T cell lines to show the cell growth inhibition ability of BMP7 and cisplatin. Semiquantitative RT-PCR was used to determine MET in morphologically changed BMP7-treated melanoma cells. MET-induced cells expressed less a basic helix-loop-helix transcription factor (TWIST) in western blot analysis, and we confirm that BMP receptor (Alk2) siRNA transduction could restore TWIST protein expression via blocking of Smad 1, 5 and 8 signaling. Matrigel invasion and cell migration assays were done to investigate the BMP7-induced metastasis inhibition ability. BMP7 treatment only slightly reduced cell growth rate, but induced apparent MET. BMP7 also reduced the invasion and migration ability. Furthermore, BMP7 reduced the resistance of WM-266-4 cells to cisplatin. Collectively, our findings indicate that the metastatis inhibition ability of BMP7 is involved in MET, and that BMP7 could be used as a potential metastasis inhibitor in human melanoma cells. (Cancer Sci 2009) [source] | |||||||||||||