invasion

KMT2C modulates migration and invasion processes in osteosarcoma cell lines

In this study we investigated the role of KMT2C (a chromatin-modifying and remodelling protein) in osteosarcoma progression through cell migration and invasion assays in osteosarcoma primary and metastatic cell lines. Wound healing and transwell assays were used to detect changes of cell migration and matrigel assay was used to evaluate changes of cell invasion in primary and metastatic osteosarcoma cell lines after KMT2C siRNA transfection.

Virulence of MRSA USA300 is enhanced by sub-inhibitory concentration of two different classes of antibiotics.

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) USA300 is responsible of many kinds of infections of skin and soft-tissue. Antibiotic resistance, biofilm formation and the ability to adhere and invade are virulence factors that contribute to MRSA pathogenesis. In some cases, decreased bioavailability of antibiotics in systemic circulation could result; in these conditions sub-therapeutic levels of the antibiotics may be established, exposing bacteria to sub-inhibitory concentrations.

Expression of the FGFR2c mesenchymal splicing variant in human keratinocytes inhibits differentiation and promotes invasion

The altered isoform switching of the fibroblast growth factor receptor 2 (FGFR2) and aberrant expression of the mesenchymal FGFR2c isoform in epithelial cells is involved in cancer progression. We have recently described that the ectopic expression of FGFR2c in normal human keratinocytes induces epithelial-mesenchymal transition and leads to invasiveness and anchorage-independent growth. Here, we extended our analysis to the effects of this FGFR2c forced expression on human keratinocyte differentiation and stratification.

Functional roles of the Ca2+-activated K+ channel, KCa3.1, in brain tumors

Glioblastoma is the most aggressive and deadly brain tumor, with low disease-free period even after surgery and combined radio and chemotherapies. Among the factors contributing to rapid tumor growth in the brain are the elevated proliferation and invasion rate, and the ability to induce a local immunosuppressive environment. The intermediate-conductance Ca2+-activated K+ channel KCa3.1 is expressed on glioblastoma cells and in tumor-infiltrating cells. In tumor cells, the functional expression of KCa3.1 is important to modulate cell invasion and proliferation.

The glycoside oleandrin reduces glioma growth with direct and indirect effects on tumor cells

Oleandrin is a glycoside that inhibits the ubiquitous enzyme Na(+)/K(+)-ATPase. In addition to its known effects on cardiac muscle, recent in vitro and in vivo evidence highlighted its potential for anticancer properties. Here, we evaluated for the first time the effect of oleandrin on brain tumors. To this aim, mice were transplanted with human or murine glioma and analyzed for tumor progression upon oleandrin treatment. In both systems, oleandrin impaired glioma development, reduced tumor size, and inhibited cell proliferation.

Radiation increases functional KCa3.1 expression and invasiveness in glioblastoma

Glioblastoma (GBM) is a deadly brain tumor, with fast recurrence even after surgical intervention, radio- and chemotherapies. One of the reasons for relapse is the early invasion of surrounding brain parenchyma by GBM, rendering tumor eradication difficult. Recent studies demonstrate that, in addition to eliminate possible residual tumoral cells after surgery, radiation stimulates the infiltrative behavior of GBM cells. The intermediate conductance of Ca2+-activated potassium channels (KCa3.1) play an important role in regulating the migration of GBM.

Nicotine increases colon cancer cell migration and invasion through epithelial to mesenchymal transition (EMT): COX-2 involvement

Cigarette smoking is a recognized risk factor for colon cancer and nicotine, the
principal active component of tobacco, plays a pivotal role in increasing colon cancer
cell growth and survival. The aim of this study was to determine the effect of
nicotine on cellular Caco-2 and HCT-8 migration and invasion, focusing on epithelial
to mesenchymal transition (EMT) induction, and COX-2 pathway involvement. In
both these cell lines, treatment with nicotine increased COX-2 expression and the

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