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Fig. 5 | BMC Cancer

Fig. 5

From: Everolimus restrains the paracrine pro-osteoclast activity of breast cancer cells

Fig. 5

mTOR inhibition down-regulates the NFkB pathway in BC cells. Intracellular content of mTOR, NFkB-related molecules and pro-OC effectors in BC cells before and after Everolimus treatment (measured by Western-blot). Protein lysates revealed a high native content, although at higher OD values in MCF-7 cells, as in, Additioinal file 1: Table S2, of phosphorylated mTOR and p70S6K components of the mTOR pathway, and concurrently, p-IKKα and p-p65 factors belonging to the NFkB signaling pathway. In both cell lines, Everolimus strongly suppressed the constitutive hyperphosphorylation of IKKα and p65, as well as of p-mTOR and p-P70S6K. This supports the potential of Everolimus to inhibit the NFkB pathway, since the intracellular expression of M-CSF, TNF-α, IL-6, IL-1β and MIP-1α, as major NFkB-dependent pro-OC factors, was suppressed as well as p-IKKα and p-p65. β-actin was the loading control

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