Increased Expression of FosB through Reactive Oxygen Species Accumulation Functions as Pro-Apoptotic Protein in Piperlongumine Treated MCF7 Breast Cancer Cells
Jin-Ah Park1, Han-Heom Na1, Hyeon-Ok Jin2, and Keun-Cheol Kim1,*
1Department of Biological Sciences, College of Natural Sciences, Kangwon National University, Chuncheon 24341, Korea, 2KIRAMS Radiation Biobank, Korea Cancer Center Hospital, Korea Institute of Radiological and Medical Sciences, Seoul 01812, Korea
Received May 6, 2019; Revised August 22, 2019; Accepted October 24, 2019.; Published online November 15, 2019.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

ABSTRACT
Piperlongumine (PL), a natural alkaloid compound isolated from long pepper (Piper longum), can selectively kill cancer cells, but not normal cells, by accumulation of reactive oxygen species (ROS). The objective of this study was to investigate functional roles of expression of SETDB1 and FosB during PL treatment in MCF7 breast cancer cells. PL downregulates SETDB1 expression, and decreased SETDB1 expression enhanced caspase 9 dependent-PARP cleavage during PL-induced cell death. PL treatment generated ROS. ROS inhibitor NAC (N-acetyl cysteine) recovered SETDB1 expression decreased by PL. Decreased SETDB1 expression induced transcriptional activity of FosB during PL treatment. PARP cleavage and positive annexin V level were increased during PL treatment with FosB overexpression whereas PARP cleavage and positive annexin V level were decreased during PL treatment with siFosB transfection, implying that FosB might be a pro-apoptotic protein for induction of cell death in PL-treated MCF7 breast cancer cells. PL induced cell death in A549 lung cancer cells, but molecular changes involved in the induction of these cell deaths might be different. These results suggest that SETDB1 mediated FosB expression may induce cell death in PL-treated MCF7 breast cancer cells.
Keywords: breast cancer, cell death, FosB, piperlongumine, reactive oxygen species, SETDB1
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30 November 2019 Volume 42,
Number 11, pp. 739~819

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