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Invasion Ability (invasion + ability)
Selected AbstractsAdhesion and invasion to epithelial cells by fimA genotypes of Porphyromonas gingivalisMOLECULAR ORAL MICROBIOLOGY, Issue 6 2006J. E. Umeda Adhesion to and invasion of epithelial cells by the periodontopathogen Porphyromonas gingivalis is promoted by the major fimbriae, encoded by fimA. The microorganism can be classified in six genotypes, based on fimA sequence, and genotype II strains are more prevalent than others in periodontitis patients. This study aimed to determine the adhesive and invasive abilities on KB cells of different fimA allelic variants of P. gingivalis isolates. Twenty-two isolates and six reference strains representing the six fimA genotypes and non-typeable strains were screened for their adhesion and invasion abilities on KB cells, using standard methods. All strains were able to adhere and, except for one, to invade KB cells. However, these properties were not homogeneous among strains belonging to the same genotype. There was no correlation between adhesion and invasion efficiencies. Isolate KdII 865 (fimA genotype II) was the most invasive and the second most adhesive strain, whereas reference strain ATCC 33277 (fimA I) showed a low adhesion ability but was highly invasive. These data indicated that fimA genotypes of P. gingivalis are not related to the adhesion and invasion abilities on KB cells, suggesting that the increased prevalence and proportion of certain genotypes may be attributed to other characteristics besides FimA variation. [source] Up-regulation of CD147 and matrix metalloproteinase-2, -9 induced by P-glycoprotein substrates in multidrug resistant breast cancer cellsCANCER SCIENCE, Issue 11 2007Qing-Quan Li Treatment of animals bearing multidrug resistant (MDR) tumor cells with P-glycoprotein (P-gp) substrates could worsen host survival. It is assumed that this is due to increased tumor metastasis. To clarify the mechanism(s) underlying this observation, the MDR human breast cancer cell line, MCF-7/AdrR, and its sensitive parental line, MCF-7, was treated with various concentrations of P-gp substrate drugs (vincristine, paclitoxel, adriamycin) and a P-gp non-substrate drug (bleomycin) in serum-free media. Increased production of CD147, and matrix metalloproteinases (MMP)-2, -9 was observed only in MDR cancer cells exposed to P-gp substrates, as determined using real-time polymerase chain reaction, western blotting and zymography. Correspondingly, P-gp substrates significantly enhanced the in vitro invasion abilities of MCF-7/Adr cells. It was also found that the drug-induced promotion of CD147, and MMP-2, -9 was consistent with increased expression of epidermal growth factor receptor (EGFR) and that inhibition of either EGFR or P-gp activity could significantly interrupt the downstream effects, and so inhibit in vitro invasion abilities motivated by P-gp substrates. These results imply that treatment of MDR tumors with P-gp substrates could adversely affect therapeutic outcomes through modulating the production of CD147, MMP-2, -9, and EGFR, and suggest that this effect may be initiated by the transporter function of P-gp. (Cancer Sci 2007; 98: 1767,1774) [source] Reversible introduction of transgenes in natural populations of insectsINSECT MOLECULAR BIOLOGY, Issue 2 2006A. Le Rouzic Abstract The most serious challenge concerning genetically modified insects remains their invasion ability. Indeed, transgenic insects often show lower fitness than wild individuals, and the transgene does not seem able to spread through a natural population without a driving system. The use of remobilizable vectors, based on the invading properties of transposable elements, has been frequently suggested. Simulations show that this strategy can be efficient. Moreover, if the transgene is designed to use transposition machinery already present in the genome, the transgene invasion appears to be potentially reversible after a few hundred generations, leading to new experimental perspectives. [source] Over-expression of phosphatase of regenerating liver-3 correlates with tumor progression and poor prognosis in nasopharyngeal carcinomaINTERNATIONAL JOURNAL OF CANCER, Issue 8 2009Jun Zhou Abstract This study aimed at clarifying the expression of phosphatase of regenerating liver-3 (PRL-3), one member of protein tyrosine phosphatase (PTP) superfamily, in nasopharyngeal carcinoma (NPC) and its correlation with clinicopathologic features, including the survival of patients with NPC. Real-time PCR and Western blot showed that the expression level of PRL-3 was markedly higher in NPC cell lines than that in the normal nasopharyngeal epithelial cell at both mRNA and protein levels. Immunohistochemical analysis revealed overexpression of PRL-3 in 97 of 174 (55.7%) paraffin-embedded archival NPC biopsies. Statistical analysis showed that PRL-3 expression was positively correlated with N classification (p = 0.033), distant metastasis (M classification, p = 0.048) and clinical stage (p = 0.005) of patients. Patients with higher PRL-3 expression had shorter overall survival time, whereas patients with lower level of PRL-3 had better survival. Multivariate analysis suggested that PRL-3 expression might be an independent prognostic indicator for the survival of patients with NPC. Disruption of endogenous PRL-3 protein through a siRNA knockdown technique was shown to suppress the invasion ability and migration potency of 5-8F and HONE1 cells, substantially. Interestingly, we also found that no significant effect on the proliferation of 5-8F and HONE1 cells was observed after PRL-3 was down-regulated. Our results suggest that PRL-3 protein is a valuable marker for progression of NPC patients. High PRL-3 expression is associated with poor overall survival in patients with NPC. © 2008 Wiley-Liss, Inc. [source] Rapamycin together with herceptin significantly increased anti-tumor efficacy compared to either alone in ErbB2 over expressing breast cancer cellsINTERNATIONAL JOURNAL OF CANCER, Issue 1 2007Lu-Hai Wang Abstract The objective of this study was to assess the anti-tumor efficacy of rapamycin alone or in combination with herceptin in breast cancer. A total of 20 human breast cancer lines were examined for expression of various receptor tyrosine kinases and activation of their down stream signaling molecules, as well as for their invasion and colony forming ability. The ErbB2 and PI3 kinase pathway inhibitors were tested for the inhibition on breast cancer cell growth and tumor development. Seven of the 20 lines displayed an elevated level of ErbB2, others had varying level of EGF, IGF-1 or insulin receptor. Over 30% of the lines also had constitutive activation of Akt and MAP kinase. The lines displayed a wide range of colony forming and invasion ability. The PI3 kinase pathway inhibitors LY294002 and rapamycin inhibited the colony forming ability of all of the lines with the ErbB2 overexpressing lines having a higher sensitivity. A similar trend was observed for inhibition of invasion by LY294002. Rapamycin alone and additively together with herceptin inhibited the breast cancer cell growth especially in ErbB2 overexpressing cells. Rapamycin and herceptin synergistically inhibited tumor growth and endpoint tumor load in a xenograft model using a MCF-7 subline and in a MMTV-ErbB2 transgenic model. Rapamycin and herceptin significantly reduced the level of cyclin D1 and D3 and increased the cleavage of caspase 3 suggesting an increased apoptosis. Our results suggest that rapamycin together with herceptin has an enhanced anti-cancer effect and could be developed as an improved therapeutic regimen for breast cancer. © 2007 Wiley-Liss, Inc. [source] Decrease in stromal androgen receptor associates with androgen-independent disease and promotes prostate cancer cell proliferation and invasionJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6b 2008Yirong Li Abstract Androgen receptor (AR) is expressed in both stromal and epithelial cells of the prostate. The majority of studies on AR expression and function in prostate cancer is focused on malignant epithelial cells rather than stromal cells. In this study, we examined the levels of stromal AR in androgen-dependent and -independent prostate cancer and the function of stromal AR in prostate cancer growth and invasion. We showed that stromal AR levels were decreased in the areas surrounding cancerous tissue, especially in androgen-independent cancer. Using two telomerase-immortalized human stromal cell lines, one AR-positive and the other AR-negative, we demonstrated that stromal cells lacking AR stimulated cell proliferation of co-cultured prostate cancer cells in vitro and enhanced tumour growth in vivo when co-injected with PC3 epithelial cells in nude mice. In contrast, stromal cells expressing AR suppressed prostate cancer growth in vitro and in vivo. In parallel with cancer growth, in vitro invasion assays revealed that stromal cells lacking AR increased the invasion ability of PC3 cell by one order of magnitude, while stromal cells expressing AR reduced this effect. These results indicate a negative regulation of prostate cancer growth and invasion by stromal AR. This provides potentially new mechanistic insights into the failure of androgen ablation therapy, and the reactivation of stromal AR could be a novel therapeutic approach for treating hormone refractory prostate cancer. [source] Infiltration anesthetic lidocaine inhibits cancer cell invasion by modulating ectodomain shedding of heparin-binding epidermal growth factor-like growth factor (HB-EGF)JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2002Tadanori Mammoto Although the mechanism is unknown, infiltration anesthetics are believed to have membrane-stabilizing action. We report here that such a most commonly used anesthetic, lidocaine, effectively inhibited the invasive ability of human cancer (HT1080, HOS, and RPMI-7951) cells at concentrations used in surgical operations (5,20 mM). Ectodomain shedding of heparin-binding epidermal growth factor-like growth factor (HB-EGF) from the cell surface plays an important role in invasion by HT1080 cells. Lidocaine reduced the invasion ability of these cells by partly inhibiting the shedding of HB-EGF from the cell surface and modulation of intracellular Ca2+ concentration contributed to this action. The anesthetic action of lidocaine (sodium channel blocking ability) did not contribute to this anti-invasive action. In addition, lidocaine (5,30 mM), infiltrated around the inoculation site, inhibited pulmonary metastases of murine osteosarcoma (LM 8) cells in vivo. These data point to previously unrecognized beneficial actions of lidocaine and suggest that lidocaine might be an ideal infiltration anesthetic for surgical cancer operations. © 2002 Wiley-Liss, Inc. [source] Involvement of E-cadherin, ,-catenin, Cdc42 and CXCR4 in the progression and prognosis of cutaneous melanomaBRITISH JOURNAL OF DERMATOLOGY, Issue 6 2007M.G. Tucci Summary Background, A key event in cancer metastasis is the migration of tumour cells from their original location to a secondary site. The development of melanoma may be viewed as a consequence of the disruption of homeostatic mechanisms in the skin of the original site. Objectives, To investigate whether dysregulation of cell motility (Cdc42 expression), escaping the control of cell,cell and cell,matrix interactions (E-cadherin, ,-catenin expression), enhances melanoma progression, and whether chemokine receptors (CXCR4) mediate cell migration and activation during invasion and metastasis development. Methods, The immunohistochemical expression of Cdc42, E-cadherin, ,-catenin and CXCR4 was investigated in 30 patients with surgically treated nodular melanoma, 18 alive and disease free and 12 with a fatal outcome due to metastatic disease. Results, E-cadherin expression was significantly reduced (P < 0·05) and cytoplasmic ,-catenin was increased in the patients who had died compared with disease-free individuals, while membrane expression of ,-catenin was similar in the two groups. Patients with fatal outcome had increased Cdc42 (P < 0·01) and CXCR4 (P < 0·05). In this group a positive correlation was found between melanocytic Cdc42 expression and Breslow thickness (r = 0·598, P < 0·05) and between CXCR4 expression and Breslow thickness (r = 0·583, P < 0·05). Conclusions, Findings suggest that primary cutaneous melanoma with a high Breslow thickness is characterized by tumour cells with high motility and invasion ability, in line with the hypothesis that low E-cadherin levels and overexpression of Cdc42 and CXCR4 could be prognostic markers of poor outcome. [source] | |||||||||||||