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Plumbagin inhibits cell proliferation and promotes apoptosis in multiple myeloma cells through inhibition of the PI3K/Akt-mTOR pathway
Author(s) -
Hongwei Wu,
Xiaozhen Dai,
Enren Wang
Publication year - 2016
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2016.5048
Subject(s) - pi3k/akt/mtor pathway , apoptosis , plumbagin , cell cycle , protein kinase b , rptor , oncogene , cancer research , microbiology and biotechnology , cell growth , chemistry , multiple myeloma , biology , immunology , biochemistry , genetics
Plumbagin is the primary component of the traditional Chinese medicine Baihua Dan, and possesses anti-infection and anticancer effects with the ability to enhance the sensitivity of tumor cells to radiation therapy. The present study aimed to investigate the potential anticancer effect and mechanism of plumbagin on multiple myeloma (MM) cells. Human MM OPM1 cells were treated with plumbagin, and its impact on cell viability, cytotoxicity, apoptosis and caspase-3 activity was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, lactate dehydrogenase leakage, flow cytometry and colorimetric assays. In addition, the protein expression levels of phosphoinositide 3-kinase, phosphorylated (p)-Akt and p-mammalian target of rapamycin (mTOR) in OPM1 cells were analyzed by western blotting. The results demonstrated that plumbagin treatment inhibited cell viability, increased cell cytotoxicity, activated cell apoptosis and promoted caspase-3 activity in the OPM1 cells. Furthermore, pretreatment of plumbagin significantly suppressed PI3K, p-Akt and p-mTOR protein expression levels in the OPM1 cells. In conclusion, the present study indicates that plumbagin inhibits cell proliferation and promotes apoptosis in MM cells through inhibition of PI3K/Akt-mTOR expression.

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