The Experts below are selected from a list of 3 Experts worldwide ranked by ideXlab platform

Yinsheng Wang - One of the best experts on this subject based on the ideXlab platform.

  • Quantitative proteomic analysis revealed lovastatin-induced perturbation of cellular pathways in HL-60 cells.
    Journal of proteome research, 2011
    Co-Authors: Xiaoli Dong, Yongsheng Xiao, Xinning Jiang, Yinsheng Wang
    Abstract:

    Lovastatin, a member of the statin family of drugs, is widely prescribed for treating hypercholesterolemia. Statin family of drugs, however, also show promise for cancer treatment and prevention. Although lovastatin is known to be an inhibitor for HMG-CoA reductase, the precise mechanisms underlying the drug’s antiproliferative activity remain unclearly defined. Here we utilized mass spectrometry, in conjunction with stable isotope labeling by amino acids in cell culture (SILAC), to analyze the perturbation of protein expression in HL-60 cells treated with lovastatin. We were able to quantify ~3200 proteins with both forward and reverse SILAC labeling experiments, among which ~120 exhibited significant alterations in expression levels upon lovastatin treatment. Apart from confirming the expected inhibition of cholesterol biosynthesis pathway, our quantitative proteomic results revealed that lovastatin perturbed estrogen receptor signaling pathway, which was manifested by the diminished expression of estrogen receptor α, steroid receptor RNA activator 1 and other related proteins. Lovastatin also altered glutamate metabolism through down-regulation of glutamine synthetase and γ-glutamylcysteine synthetase. Moreover, lovastatin treatment led to a marked down-regulation of Carbonate Dehydratase II (a.k.a. carbonic anhydrase II) and perturbed the protein ubiquitination pathway. Together, the results from the present study underscored several new cellular pathways perturbed by lovastatin.

Xiaoli Dong - One of the best experts on this subject based on the ideXlab platform.

  • Quantitative proteomic analysis revealed lovastatin-induced perturbation of cellular pathways in HL-60 cells.
    Journal of proteome research, 2011
    Co-Authors: Xiaoli Dong, Yongsheng Xiao, Xinning Jiang, Yinsheng Wang
    Abstract:

    Lovastatin, a member of the statin family of drugs, is widely prescribed for treating hypercholesterolemia. Statin family of drugs, however, also show promise for cancer treatment and prevention. Although lovastatin is known to be an inhibitor for HMG-CoA reductase, the precise mechanisms underlying the drug’s antiproliferative activity remain unclearly defined. Here we utilized mass spectrometry, in conjunction with stable isotope labeling by amino acids in cell culture (SILAC), to analyze the perturbation of protein expression in HL-60 cells treated with lovastatin. We were able to quantify ~3200 proteins with both forward and reverse SILAC labeling experiments, among which ~120 exhibited significant alterations in expression levels upon lovastatin treatment. Apart from confirming the expected inhibition of cholesterol biosynthesis pathway, our quantitative proteomic results revealed that lovastatin perturbed estrogen receptor signaling pathway, which was manifested by the diminished expression of estrogen receptor α, steroid receptor RNA activator 1 and other related proteins. Lovastatin also altered glutamate metabolism through down-regulation of glutamine synthetase and γ-glutamylcysteine synthetase. Moreover, lovastatin treatment led to a marked down-regulation of Carbonate Dehydratase II (a.k.a. carbonic anhydrase II) and perturbed the protein ubiquitination pathway. Together, the results from the present study underscored several new cellular pathways perturbed by lovastatin.

Yongsheng Xiao - One of the best experts on this subject based on the ideXlab platform.

  • Quantitative proteomic analysis revealed lovastatin-induced perturbation of cellular pathways in HL-60 cells.
    Journal of proteome research, 2011
    Co-Authors: Xiaoli Dong, Yongsheng Xiao, Xinning Jiang, Yinsheng Wang
    Abstract:

    Lovastatin, a member of the statin family of drugs, is widely prescribed for treating hypercholesterolemia. Statin family of drugs, however, also show promise for cancer treatment and prevention. Although lovastatin is known to be an inhibitor for HMG-CoA reductase, the precise mechanisms underlying the drug’s antiproliferative activity remain unclearly defined. Here we utilized mass spectrometry, in conjunction with stable isotope labeling by amino acids in cell culture (SILAC), to analyze the perturbation of protein expression in HL-60 cells treated with lovastatin. We were able to quantify ~3200 proteins with both forward and reverse SILAC labeling experiments, among which ~120 exhibited significant alterations in expression levels upon lovastatin treatment. Apart from confirming the expected inhibition of cholesterol biosynthesis pathway, our quantitative proteomic results revealed that lovastatin perturbed estrogen receptor signaling pathway, which was manifested by the diminished expression of estrogen receptor α, steroid receptor RNA activator 1 and other related proteins. Lovastatin also altered glutamate metabolism through down-regulation of glutamine synthetase and γ-glutamylcysteine synthetase. Moreover, lovastatin treatment led to a marked down-regulation of Carbonate Dehydratase II (a.k.a. carbonic anhydrase II) and perturbed the protein ubiquitination pathway. Together, the results from the present study underscored several new cellular pathways perturbed by lovastatin.

Xinning Jiang - One of the best experts on this subject based on the ideXlab platform.

  • Quantitative proteomic analysis revealed lovastatin-induced perturbation of cellular pathways in HL-60 cells.
    Journal of proteome research, 2011
    Co-Authors: Xiaoli Dong, Yongsheng Xiao, Xinning Jiang, Yinsheng Wang
    Abstract:

    Lovastatin, a member of the statin family of drugs, is widely prescribed for treating hypercholesterolemia. Statin family of drugs, however, also show promise for cancer treatment and prevention. Although lovastatin is known to be an inhibitor for HMG-CoA reductase, the precise mechanisms underlying the drug’s antiproliferative activity remain unclearly defined. Here we utilized mass spectrometry, in conjunction with stable isotope labeling by amino acids in cell culture (SILAC), to analyze the perturbation of protein expression in HL-60 cells treated with lovastatin. We were able to quantify ~3200 proteins with both forward and reverse SILAC labeling experiments, among which ~120 exhibited significant alterations in expression levels upon lovastatin treatment. Apart from confirming the expected inhibition of cholesterol biosynthesis pathway, our quantitative proteomic results revealed that lovastatin perturbed estrogen receptor signaling pathway, which was manifested by the diminished expression of estrogen receptor α, steroid receptor RNA activator 1 and other related proteins. Lovastatin also altered glutamate metabolism through down-regulation of glutamine synthetase and γ-glutamylcysteine synthetase. Moreover, lovastatin treatment led to a marked down-regulation of Carbonate Dehydratase II (a.k.a. carbonic anhydrase II) and perturbed the protein ubiquitination pathway. Together, the results from the present study underscored several new cellular pathways perturbed by lovastatin.