The Therapeutical Potential of A Novel Pterocarpanquinone LQB-118 to Target Inhibitor Of Apoptosis Proteins In Acute Myeloid Leukemia Cells

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)

Volume 14, 10 Issues, 2014

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Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

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  • 85th of 202 in Oncology

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Michelle Prudhomme
Universite Blaise Pascal - C.N.R.S
Aubiere Cedex

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The Therapeutical Potential of A Novel Pterocarpanquinone LQB-118 to Target Inhibitor Of Apoptosis Proteins In Acute Myeloid Leukemia Cells

Author(s): Flaviana Ruade de Souza Reis, Fernanda Costas Casal de Faria, Carolina Pereira Castro, , Paloma Silva de Souza, Flavia da Cunha Vasconcelos,, Reinaldo Dal Bello, Alcides Jose da Silva, Paulo Roberto Ribeiro Costa and Raquel Ciuvalschi Maia


Acute myeloid leukemia (AML) is a challenging neoplasm that despite therapeutic advances requires efforts to overcome the multidrug resistance (MDR) phenotype, the major cause of relapse. The pterocarpanquinone LQB-118 is a new compound that induces apoptosis in leukemia cells. The objective of this work was to analyze the role of LQB-118 in inhibiting the inhibitor of apoptosis proteins (IAPs), XIAP and survivin, as well as in modulating the subcellular localization of NF?B, in comparison with idarubicin. LQB-118 was more effective in inducing apoptosis than idarubicin in both AML Kasumi-1 cell line and cells from patients despite their MDR phenotype. LQB-118-induced apoptosis was accompanied by a marked inhibition of IAPs, and cytoplasmatic NF?B subcellular localization. On the other hand, idarubicin increased the IAPs expression and translocated NF?B to the nucleus. The inhibition profile of survivin induced by LQB-118 was comparable to the survivin inhibition profile when we investigated the efficiency of survivin-small interfering RNA (siRNA) treatment. LQB-118 as well as survivin-siRNA contributed similarly to the increase in apoptosis rate of Kasumi-1 cells. The data indicated that there is a functional interaction between the survivin, XIAP and NF?B, which appears to be involved in idarubicin resistance of Kasumi-1 cells. The efficacy of LQB-118 to induce cell death though inhibiting survivin suggests that this IAP may be involved in the chemoresistance phenotype in AML cells. Our findings suggest that LQB-118 might be a promising therapeutic approach for AML patients through survivin downregulation.

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Article Details

Volume: 13
First Page: 1
Page Count: 1
DOI: 10.2174/1871520613666131125125258

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