Sentence examples for more invasive cell from inspiring English sources

Exact(9)

Transcripts of the extracellular matrix protein TGFBI were elevated in our more invasive cell lines.

Both ARTN and TWIST1 mRNA were ubiquitously expressed across different mammary carcinoma cell lines and increased ARTN and TWIST1 mRNA expression correlated with a more invasive cell phenotype.

Consequently, it is possible that PN-1 plays an important role in down-regulating the enzymatic activity of prostasin in cancer tissue resulting in more invasive cell behaviour.

In cells undergoing transition from an epithelial to a more invasive cell type decreased e-cadherin levels are often observed [ 40].

In addition, we observe that Nck1 is downregulated only with the combination treatment in MDA-MB-231 (a more invasive cell line) cells even though eIF2-α phosphorylation is upregulated in samples treated with single drugs.

In keeping with our previous report we have now demonstrated that MT1-MMP was expressed in all the UCC cell lines tested and high levels were detected in the more invasive cell lines.

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Similar(51)

Immunoblotting confirmed increased expression of two potent collagen-targeting proteases, MT1-MMP and cathepsin K, in the more invasive cells.

We also show that more invasive cells express lower levels of α5β1 integrin and lack the capacity for FNMA.

These observations suggest that the aberrant accumulation of Id2 in some specific non-aggressive epithelial tumor cells may be sufficient to convert them into more invasive cells.

We observed that more invasive cells (T4-2, MDA-MB-231 and Hs578T) displayed significantly higher (p < 0.05, p < 0.01 and p < 0.001, respectively) RECK protein levels than non-invasive breast cancer lineages (MCF-7 and T47D).

In vitro, we have previously demonstrated MT1-MMP expression in MCF-7 cells by IS-RT-PCR [ 21], however Northern analysis of MCF-7 cells failed to find MT1-MMP in MCF-7 cells, whereas more invasive HBC cell lines showed MT1-MMP expression in concordance with their ability to be induced by Con A to activate MMP-2 [ 12, 34, 35].

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