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| Naji, M. |
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| Motta, Antonella |
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| Aletan, Dirar |
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| Mohamed, Tarek |
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| Ertürk, Emre |
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| Taccardi, Nicola |
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| Petrov, R. H. | Madrid |
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| Alshaaer, Mazen | Brussels |
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| Casati, R. |
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| Kočí, Jan | Prague |
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| Šuljagić, Marija |
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| Kalteremidou, Kalliopi-Artemi | Brussels |
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| Azam, Siraj |
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| Ospanova, Alyiya |
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| Blanpain, Bart |
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| Ali, M. A. |
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| Popa, V. |
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| Rančić, M. |
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| Ollier, Nadège |
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| Azevedo, Nuno Monteiro |
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| Landes, Michael |
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Nemoto, K.
in Cooperation with on an Cooperation-Score of 37%
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article
Picrasidine G decreases viability of MDA-MB 468 EGFR-overexpressing triple-negative breast cancer cells through inhibition of EGFR/STAT3 signaling pathway.
Abstract
Targeted therapy is unavailable for treating patients with triple-negative breast cancer (TNBC), which accounts for approximately 15% of all breast cancers. Overexpression of epidermal growth factor receptor (EGFR) is observed in approximately 30-60% of TNBCs. Therefore, developing novel strategies for inhibiting EGFR signaling is required. In the present study, a natural compound library was screened to identify molecules that target TNBCs that overexpress EGFR. Picrasidine G (PG), a naturally occurring dimeric alkaloid produced by Picrasma quassioides, decreased the viability of the MDA-MB 468 cell line (TNBC<sup>EGFR+</sup>) compared with other breast cancer cell lines. PG treatment increased markers of apoptosis, including chromatin condensation, sub-G1 population, cleavage of caspase 3 and cleavage of poly (ADP-ribose) polymerase (PARP). PG inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and inhibited transcription of the STAT3-target gene encoding survivin. Further, PG inhibited EGF-induced STAT3 phosphorylation but not interleukin-6 (IL-6)-induced STAT3 phosphorylation. These results suggest that PG may contribute to the development of targeted therapy of patients with EGFR-overexpressing TNBC.