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. 2019 Jun 25;24(12):2338. doi: 10.3390/molecules24122338

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Piperlongumine and doxorubicin synergistically induce apoptosis and inhibit p-STAT3 in TNBC cells. (A) Both MDA-MB-231 and MDA-MB-453 cells were treated with DMSO, 5 µM PL, 0.5 µM DOX, or with a combination for 48 h. Cells were then harvested and stained with Annexin V/PI. The apoptotic rate was detected by flow cytometry. (B) Cells in the Annexin V-positive area were considered apoptotic. (C) Both TNBC cell lines were treated with DMSO, 5 µM PL, 0.5 µM DOX, or with a combination for 24 h. Cell lysates were then subjected to Western blot analysis. Cleaved PARP, p-STAT3, and STAT3 levels were measured. β-actin was used as an internal control. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to the compared group.

Piperlongumine and doxorubicin synergistically induce apoptosis and inhibit p-STAT3 in TNBC cells. (A) Both MDA-MB-231 and MDA-MB-453 cells were treated with DMSO, 5 µM PL, 0.5 µM DOX, or with a combination for 48 h. Cells were then harvested and stained with Annexin V/PI. The apoptotic rate was detected by flow cytometry. (B) Cells in the Annexin V-positive area were considered apoptotic. (C) Both TNBC cell lines were treated with DMSO, 5 µM PL, 0.5 µM DOX, or with a combination for 24 h. Cell lysates were then subjected to Western blot analysis. Cleaved PARP, p-STAT3, and STAT3 levels were measured. β-actin was used as an internal control. * p < 0.05, ** p < 0.01, *** p < 0.001 compared to the compared group.