NPACT- Naturally occuring Plant based Anticancerous Compound-Activity-Target DataBase

Compound: Isoliquiritigenin

TargetsGene NameGene IDCancerCell LinesIC50ED50EC50GI50RemarkReferences
AKT1v-akt murine thymoma viral oncogene homolog 1207Prostate CancerDU-145----Isoliquiritigenin inhibited both basal and EGF-induced phosphorylation of Akt. Western blot analyses revealed that treating DU145 cells with EGF led to increased phosphorylation of Akt.18824345
DDIT3DNA-damage-inducible transcript 31649Prostate CancerDU-145----Isoliquiritigenin treatment induced a marked increase in GADD153 protein level dose-dependently. GADD153 mRNA expression was enhanced more than 8-fold at 24 h after the treatment with isoliquiritigenin at a concentration of 20 mM compared with the control.12706007
ICAM1intercellular adhesion molecule 13383Prostate CancerDU-145----Isoliquiritigenin inhibits cell adhesion, which was related to decreases ICAM. The present results indicate that decreases in this adhesion-regulating molecules contribute to ISL-induced decreases in DU145 cell adhesio.18824345
ITGA2integrin, alpha 23673Prostate CancerDU-145----Isoliquiritigenin inhibits cell adhesion, which was related to decreases in integrin-alpha2. The present results indicate that decreases in this adhesion-regulating molecules contribute to ISL-induced decreases in DU145 cell adhesion.Integrins mediate adhesion between cells and their neighboring matrices and transmit important signals regulating cell survival, differentiation and migration.18824345
JUNjun proto-oncogene3725Prostate CancerDU-145----Isoliquiritigenin inhibited both basal and EGF-induced AP-1 DNA binding activity.18824345
JUNjun proto-oncogene3725Prostate CancerDU-145----Western blot analyses revealed that treating DU145 cells with EGF led to increased phosphorylation of c-Jun. ISL inhibited phosphorylation ofc-Jun. Treating cells with 10 µmol/L SP600125 led to a significant decrease in phosphorylation of c-Jun.18824345
MAPK8mitogen-activated protein kinase 85599Prostate CancerDU-145----Western blot analyses revealed that treating DU145 cells with EGF led to increased phosphorylation of JNK. ISL inhibited phosphorylation of JNK, they examined next whether the JNK inhibitor SP600125 inhibits DU145 cell migration. Treating cells with 10 µmol/L SP600125 led to a significant decrease in phosphorylation of 54-kDa JNK2. The JNK inhibitor significantly inhibited both basal and EGF-induced migration of DU145 cells.18824345
MMP9matrix metallopeptidase 9 (gelatinase B, 92kDa gelatinase, 92kDa type IV collagenase)4318Prostate CancerDU-145----Isoliquiritigenin inhibited secretion of MMP-9 protein regardless of whether the cells were treated with EGF. Results of RT-PCR revealed that EGF increased the mRNA levels of MMP-9, and Isoliquiritigenin decreased them irrespective of EGF treatment. And decreased secretion of this protease contributes to the decrease in invasion and migration of ISL-treated DU145 cells.18824345
PLAUplasminogen activator, urokinase5328Prostate CancerDU-145----Isoliquiritigenin inhibited secretion of uPA protein regardless of whether the cells were treated with EGF. Results of RT-PCR revealed that EGF increased the mRNA levels of uPA, and Isoliquiritigenin decreased them irrespective of EGF treatment. And decreased secretion of this protease contributes to the decrease in invasion and migration of ISL-treated DU145 cells.18824345
TIMP1TIMP metallopeptidase inhibitor 17076Prostate CancerDU-145----Results of Western blot analysis showed that EGF-stimulated secretion of TIMP-1 and ISL inhibited secretion of these proteins regardless of whether the cells were treated with EGF. TIMP-1 preferentially inhibits MMP-9. Increasing evidence indicates a more complex role for TIMP-1 during tumor progression, besides its regulation of MMP-mediated ECM degradation. It has been reported that TIMP-1 mediates cell survival signal transduction pathways via its interaction with CD63/integrin-Beta1 comple.18824345
TIMP2TIMP metallopeptidase inhibitor 27077Prostate CancerDU-145----Secretion of TIMP-2 was not affected by EGF but increased by ISL treatment regardless of EGF treatment. TIMP-2 preferntially inhibits MMP-2. Both activation and activity of MMP-2 depend on TIMP-2, which plays a dual role in MMP-2 activation. ISL increased TIMP-2 secretion, which probably contributed to the decreased invasion and migration of DU145 cell.18824345
VCAM1vascular cell adhesion molecule 17412Prostate CancerDU-145----Isoliquiritigenin inhibits cell adhesion, which was related to decreases in VCAM. The present results indicate that decreases in this adhesion-regulating molecules contribute to ISL-induced decreases in DU145 cell adhesio.18824345
VEGFAvascular endothelial growth factor A7422Prostate CancerDU-145----Results of VEGF ELISA and Western blot analysis showed that ISL inhibited basal and EGF-induced secretion of VEGF by DU145 cells. VEGF plays a major role in tumor angiogenesis, so inhibiting VEGF production is a promising strategy for the treatment of cancer. Here they demonstrate that ISL inhibits VEGF production in DU145 cells.18824345

 






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