Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1384489 (Scratch)
 395 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Astrocytic tumours are associated with dismal prognoses due to their pronounced ability to diffusely invade the brain parenchyma. Various neuropeptides, including gastrin, are able to modulate tumour astrocyte migration. While neurotensin has been shown to influence the proliferation of glioma cells and the migratory ability of a large set of other cell types, its role in glioma cell migration has never been investigated. Neurotensin-induced modifications to the motility features of human U373 glioblastoma cells therefore constitute the topic of the present study. We evidenced that three subtypes of neurotensin receptors (NTR1, NTR2 and NTR3) are expressed in U373 glioblastoma cells, at least as far as their mRNAs are concerned. Treating U373 tumour cells with 10 nM neurotensin markedly modified the morphological patterns of these cells and also profoundly altered the organization of their actin cytoskeletons. Pull-down assays revealed that neurotensin induced the activation in U373 cells of both Rac1 and Cdc42 but not RhoA. Scratch wound assays evidenced that neurotensin (0.1 and 10 nM) very significantly inhibited wound colonization by U373 cells cultured in the absence of serum. In addition, quantitative phase-contrast videomicroscopy analyses showed that neurotensin decreases the motility levels of U373 glioblastoma cells when these cells are cultured on plastic. In sharp contrast, neurotensin stimulates the motility of U373 cells when they are cultured on laminin, which is a pro-adhesive extracellular matrix component ubiquitously secreted by glioma cells. Our data thus strongly suggest that, in addition to gastrin, neurotensin is a neuropeptide capable of modulating tumour astrocyte migration into the brain parenchyma.
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PMID:The in vitro influences of neurotensin on the motility characteristics of human U373 glioblastoma cells. 1708 72

In this study, the expression of silencing RhoA gene in gastric MGC-803 Cells was investigated, in order to discuss the effect of RhoA gene on cell proliferation, cell cycles and tumor migration. SiRNA sequence of RhoA gene was designed and synthesized; MGC-803 cells were transfected by Lipofectamine(TM2000). The expression of RhoA gene in mRNA and protein after interference was detected by RT-PCR and Western blot; flow cytometry was used to detect the cell cycle; cell proliferation was detected by CCK-8 assay and cell migration was detected by scratch healing assay. RhoA expression in mRNA and protein of the experimental group was significantly lower than that of the control group and blank group, and the difference was statistically significant (P < 0.05). The growth rate significantly slowed down in experimental group; the cell cycle was arrested in the G0/G1 phase and the number of cells in S-phase reduced; there was a statistically significant difference (P < 0.05). Scratch healing assay showed that cell migration of the experimental group was significantly decreased, with a statistically significant difference (P < 0.05). Specific interference on RhoA gene expression could inhibit the proliferation and migration of MGC-803 cells; therefore, siRNA sequences of RhoA gene may be an effective target for the treatment of gastric cancer.
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PMID:Effect of RhoA gene silencing on proliferation and migration of gastric MGC-803 cells. 2655 Apr 28