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Last Updated: 2 months ago

Possible Interaction: Emodin and Hyaluronoglucosaminidase

Research Papers that Mention the Interaction

In conclusion, our results suggested that EMO inhibited EOC cell invasion by regulation of GSK-3β/β-catenin/ZEB1 signaling pathway to suppress EMT in vitro.
Inhibitory efficacy of EMO on EOC invasion and migration was previously observed, however, the underlying mechanisms have not been completely elucidated.
Transwell assay demonstrated that EMO significantly inhibited A2780 and SK-OV-3 cell invasion.
Oncology reports  •  2016  |  View Paper
The CCK-8 assay and transwell assay showed that emodin effectively repressed the abilities of proliferation, invasion , and migration in A2780 and SK-OV-3 cells.
BioMed research international  •  2016  |  View Paper
We observed that curcumin and emodin effectively down regulate TGF-β signaling pathway by decreasing the expression of TGF-β Receptor II, P-Smad3 and Smad4, and also counterbalance the tumorigenic effects of TGF-β by inhibiting the TGF-β-induced migration and invasion.
PloS one  •  2015  |  View Paper
Emodin strongly inhibited phosphatase activity of PRL-3 with IC(50) values of 3.5μM and blocked PRL-3-induced tumor cell migration and invasion in a dose-dependent manner.
Bioorganic & medicinal chemistry letters  •  2012  |  View Paper
Collectively, our results indicate that AE inhibits invasion of NPC cells by suppressing the expression of MMP-2 via the p38 MAPK-NF-kappaB signaling pathway.
The inhibition of NPC cell invasion by AE was evidenced through the suppression of matrix metalloproteinases-2 (MMP-2) expression.
Molecular carcinogenesis  •  2010  |  View Paper
We found that AE significantly inhibited invasion , migration, and adhesion capacities of HO-8910PM cells, and, furthermore, reduced the protein and mRNA expression of FAK.
Journal of Asian natural products research  •  2008  |  View Paper
So, emodin suppressed proliferation, migration and invasion in ovarian cancer cells by downregulating ILK in vitro.
OncoTargets and therapy  •  2017  |  View Paper
Then, it was observed that emodin can significantly suppress cell migration and invasion with a treatment dose <50 µmol/l compared with the control (P<0.05), which was not attributed to a decrease in cell number.
Therefore, the present study, for the first time, used MHCC-97H cells, which have the high potential of malignant invasion, to demonstrate that emodin may inhibit cell migration and invasion.
Experimental and therapeutic medicine  •  2016  |  View Paper
In our study, we found that emodin inhibited the invasion and migration abilities of RKO cells and decreased the expression of matrix metalloproteinase-7 (MMP-7), MMP-9, and vascular endothelial growth factor (VEGF) in a dose-dependent manner.
Taken together, we suggest that emodin inhibits the invasion and migration of CC cells in vitro and in vivo by blocking EMT, which is related with the inhibition of the Wnt/β-catenin signaling pathway.
Oncology research  •  2019  |  View Paper
The results showed that emodin inhibited TNBC proliferation and invasion more efficiently than epirubicin when co‑cultured with adipocytes by downregulating the level of CCL5 in adipocyte supernatants; inhibiting the expression level of protein kinase B (AKT); and activating glycogen synthase kinase‑3i (GSK3) and β‑catenin.
International journal of molecular medicine  •  2018  |  View Paper
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