Extracellular NAMPT/Visfatin induces proliferation through ERK1/2 and AKT and inhibits apoptosis in breast cancer cells

•Visfatin shows anti-apoptotic properties in breast cancer cells.•AKT and ERK1/2 phosphorylation and cell proliferation are induced by visfatin.•Visfatin exerts a positive effect on survivin which is an inhibitor of apoptosis. Visfatin is a novel adipokine and proinflammatory cytokine which is impli...

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Published in:Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2017-06, Vol.92, p.9-15
Main Authors: Gholinejad, Zafar, kheiripour, Nejat, Nourbakhsh, Mitra, Ilbeigi, Davod, Behroozfar, Kiarash, Hesari, Zahra, Golestani, Abolfazl, Shabani, Mohammad, Einollahi, Nahid
Format: Article
Language:English
Subjects:
AKT
Apoptosis
Apoptosis - drug effects
Breast cancer
Breast Neoplasms - pathology
Cell Proliferation - drug effects
Cell Survival - drug effects
Cytokines - pharmacology
Cytokines - physiology
ERK1/2
Female
Humans
Inhibitor of Apoptosis Proteins - metabolism
MCF-7 Cells
Mitogen-Activated Protein Kinase 3 - metabolism
Nicotinamide Phosphoribosyltransferase - pharmacology
Nicotinamide Phosphoribosyltransferase - physiology
Obesity - metabolism
Phosphatidylinositol 3-Kinases - metabolism
Phosphorylation - drug effects
Poly(ADP-ribose) Polymerases - metabolism
Recombinant Proteins - pharmacology
Survivin
Tumor Necrosis Factor-alpha - metabolism
Visfatin
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Summary:•Visfatin shows anti-apoptotic properties in breast cancer cells.•AKT and ERK1/2 phosphorylation and cell proliferation are induced by visfatin.•Visfatin exerts a positive effect on survivin which is an inhibitor of apoptosis. Visfatin is a novel adipokine and proinflammatory cytokine which is implicated in breast cancer progression. The exact proliferative and anti-apoptotic mechanisms of visfatin are still under debate. In this study, the effect of extracellular visfatin on proliferation and apoptosis of breast cancer cells were investigated considering key regulatory molecules in these procedures. BrdU (Bromodeoxyuridine) experiment was used to assess cell proliferation in response to visfatin treatment. Cell viability and apoptosis were assessed using MTT assay and flowcytometry, respectively. Phosphorylation levels of AKT and ERK1/2 as well as survivin levels and Poly ADP ribose polymerase (PARP) cleavage were investigated by western blot analysis. Visfatin induced proliferation of MCF-7 and MDA-MB-231 cells, an effect that was repressed by using AKT and ERK1/2 inhibitors, indicating involvement of these two signaling pathways in the proliferative effect of visfatin. Similarly, phosphorylation of AKT and ERK1/2 were elevated by visfatin treatment. On the other hand, visfatin improved cell viability and prevented TNF-α-induced apoptosis as well as PARP cleavage. Visfatin also exerted a protective effect on survivin. The results of this study suggest that visfatin induces breast cancer cell proliferation through AKT/PI3K and ERK/MAPK activation and protects against apoptosis in these cells. Thus increased visfatin levels may augment breast cancer development and attenuate treatment efficiency in breast cancer patients.
ISSN:0196-9781
1873-5169
DOI:10.1016/j.peptides.2017.04.007