Research Paper Volume 16, Issue 3 pp 2848—2865

Mechanism of Erianin anti-triple negative breast cancer based on transcriptomics methods and network pharmacology

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Figure 8. Erianin inhibits the PI3K-AKT signaling pathway in TNBC. (A) Western blot detection of PI3K and AKT expression as well as AKT phosphorylation after Erianin treatment of MDA-MB-231 and 4T1 cells. (B) Quantitative graphs of PI3K expression after Erianin treatment of MDA-MB-231 and 4T1 cells. (C) Quantitative graphs of p-AKT expression after Erianin treatment of MDA-MB-231 and 4T1 cells. (D) Immunohistochemistry detection of PI3K and AKT expression as well as AKT phosphorylation in two transplantation tumor models. (E) Quantitative graphs of PI3K expression after Erianin treatment of two transplantation tumor models. (F) Immunohistochemical detection of PI3K and AKT expression as well as AKT phosphorylation in two transplantation tumor models. (G) MDA-MB-21 cells were treated with 40 nM of Erianin and 2 ug/ml of SC79 for 24 hours, and then the viability was determined using the CCK-8 assay. (H) 4T1 cells were treated with 80 nM of Erianin and 2 ug/ml of SC79 for 24 hours, and then the viability was determined using the CCK-8 assay. (I) Western blot detection of AKT expression and AKT phosphorylation after Erianin and SC79 treatment of MDA-MB-231 and 4T1 cells. (J) Quantitative graphs of PI3K expression in MDA-MB-231 and 4T1 cells. (K) Quantitative graphs of AKT phosphorylation expression in MDA-MB-231 and 4T1 cells.