u-50488 and Multiple-Myeloma

u-50488 has been researched along with Multiple-Myeloma* in 1 studies

Other Studies

1 other study(ies) available for u-50488 and Multiple-Myeloma

Article	Year
Reduction of cell proliferation and potentiation of Fas-induced apoptosis by the selective kappa-opioid receptor agonist U50 488 in the multiple myeloma LP-1 cells. Journal of neuroimmunology, 2010, Mar-30, Volume: 220, Issue:1-2 As opioid receptors modulate proliferation and apoptosis of immune cells, we hypothesized that they could reduce malignant haematopoietic cells. After screening, we selected the human multiple myeloma LP-1 cells which express mu- (MOP-) and kappa-opioid receptors (KOP-R). U50 488 produces a modest but significant decrease in viability associated with an arrest in the G0/G1 phase, but not antagonized by NorBNI and not associated with modulation of p21(Cip1), p27(Kip1) or p53 expression. In contrast, no effect was observed with dynorphin, U69 593 and morphine. In conclusion, the anti-proliferative effects of U50 488 are not mediated by KOP-R in the LP-1 cells. Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Analgesics, Non-Narcotic; Apoptosis; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cell Survival; Down-Regulation; Drug Evaluation, Preclinical; fas Receptor; Hematopoietic Stem Cells; Humans; Multiple Myeloma; Receptors, Opioid, kappa; Resting Phase, Cell Cycle	2010

Article

Year

Reduction of cell proliferation and potentiation of Fas-induced apoptosis by the selective kappa-opioid receptor agonist U50 488 in the multiple myeloma LP-1 cells.

Journal of neuroimmunology, 2010, Mar-30, Volume: 220, Issue:1-2

As opioid receptors modulate proliferation and apoptosis of immune cells, we hypothesized that they could reduce malignant haematopoietic cells. After screening, we selected the human multiple myeloma LP-1 cells which express mu- (MOP-) and kappa-opioid receptors (KOP-R). U50 488 produces a modest but significant decrease in viability associated with an arrest in the G0/G1 phase, but not antagonized by NorBNI and not associated with modulation of p21(Cip1), p27(Kip1) or p53 expression. In contrast, no effect was observed with dynorphin, U69 593 and morphine. In conclusion, the anti-proliferative effects of U50 488 are not mediated by KOP-R in the LP-1 cells.

Topics: 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; Analgesics, Non-Narcotic; Apoptosis; Cell Cycle Proteins; Cell Line, Tumor; Cell Proliferation; Cell Survival; Down-Regulation; Drug Evaluation, Preclinical; fas Receptor; Hematopoietic Stem Cells; Humans; Multiple Myeloma; Receptors, Opioid, kappa; Resting Phase, Cell Cycle

2010