fig3

Synergistic inhibition of SCR1- and ERBB2-driven brain metastatic breast cancer cells

Figure 3. Disruption of ERBB2 and PI3K-AKT/mTOR signaling suppresses BBM cell survival. A: Schematic depicting the ERBB2/MYC/AKT and PI3K-AKT/mTOR signaling pathways that affect BBM cell proliferation; B: cells were treated with ERBB2 (Lapatinib) and PI3K (Idelalisib) inhibitors at a final concentration of 100 nmol/L for 48 h. Total protein lysates from were analyzed using antibodies specific to ERBB2, pERBB2, PIK3CA, pPIK3CA, AKT, pAKT, MYC, mTOR, and pmTOR. Tubulin was used as a loading control; C: BBM1 cells were treated with pharmaceutical inhibitors of ERBB2 (Lapatinib), PI3K (Idelalisib), AKT (AZD5363), and mTOR (Rapamycin) at final concentrations 0, 31.2, 62.5, 125, 250, 500, 1000 nmol/L. Control cells were treated with DMSO only. The viability of the cells at 72 h post-treatment is shown. The IC50 values of the compounds are in the bottom right of each plot

Journal of Cancer Metastasis and Treatment
ISSN 2454-2857 (Online) 2394-4722 (Print)

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