N,N'-Dicyclohexyl-N-[4-(1H-indol-3-yl)butanoyl]urea.

The title compound, C(25)H(35)N(3)O(2), is a novel urea derivative. Pairs of intermolecular N-H..

Krit1 modulates beta 1-integrin-mediated endothelial cell proliferation.

Objective: Using ribonucleic acid interference on cultured cell lines, we examined the role of Krev interaction trapped 1 (krit1) and integrin cytoplasmic domain-associated protein-1 alpha (icap1alpha) in beta1-integrin-mediated cell proliferation.

Methods: Upon depletion of either krit1 or icap1alpha in the HeLa cells, umbilical vein endothelial cells, and microvascular endothelial cells, we examined the cell number and proliferation changes in the cells, followed by the evaluation of beta1-integrin-mediated mitogen-activated protein kinase signal pathway and microscopic study.

Results: Depletion of krit1 reduces cell number and decreases endothelial cell proliferation.

2,2'-Diazinodimethylidyne)di-o-phenyl-ene) dibenzoate.

The title compound, C(28)H(20)N(2)O(4), was synthesized by the reaction of 2-(hydrazonometh-yl)phenyl benzoate with iodine. The mol-ecule possesses a crystallographically imposed center of symmetry at the mid-point of the hydrazine N-N bond. The substituents at the ends of the C=N bonds adopt an E,E configuration.

Glucocorticoids inhibit lung cancer cell growth through both the extracellular signal-related kinase pathway and cell cycle regulators.

Glucocorticoids inhibit the proliferation of various cell types, but the mechanism of this inhibition remains unclear. We investigated the effect of dexamethasone on non-small cell lung cancer cell growth and cell cycle progression. We showed that dexamethasone suppresses the proliferation of A549 and Calu-1 cells, with accumulation of cells in G1/G0 stage of the cell cycle, as determined by fluorescence-activated cell sorter analysis.

Selective p38 activation in human non-small cell lung cancer.

The mitogen-activated protein kinase (MAPK) pathways transmit signals from the cell membrane to the nucleus. Activation of MAPK cascades may play a role in malignant transformation. We hypothesized that enhanced expression of one or more of these pathways would occur in human lung cancers.