Piperlongumine selectively kills glioblastoma multiforme cells via reactive oxygen species accumulation dependent JNK and p38 activation

Liu, Ju Mei; Pan, Feng; Li, L i; Liu, Qian Rong; Chen, Yong; Xiong, Xin; Cheng, Kejun; Shang, Yu; Shi, Zhi; Yu, Albert Cheung-Hoi; Chen, Xiao Qian

doi:10.1016/j.bbrc.2013.06.042

Cited by 87 publications

(79 citation statements)

References 22 publications

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“…Various types of natural agents extracted from plants, including alkaloid compounds with anticancer activity, have recently been identified (20,21). One promising therapeutic candidate is Halofuginone, an orally available synthetic derivative of a quinazolinone alkaloid that has shown preclinical antitumor activity in various models, including human melanoma bone metastases (18,22).…”

Section: Discussionmentioning

confidence: 99%

Halofuginone induces the apoptosis of breast cancer cells and inhibits migration via downregulation of matrix metalloproteinase-9

Jin

Park

Kim

et al. 2013

International Journal of Oncology

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Abstract. Halofuginone (HF) is extracted from Dichroa febrifuga, a plant used in traditional medicine. We report that the HF extract inhibits the growth of breast cancer cells and induces the generation of reactive oxygen species (ROS) and apoptosis, an important feature of potential anticancer agents. In addition, HF significantly reduces the migration and invasion of MCF-7 and MDA-MB-231 human breast cancer cells after 12-O-tetraecanoylphorbol-13-acetate (TPA) stimulation. As matrix metalloproteinase-9 plays a critical role in tumor metastasis, we analyzed its expression with the HF extract treatment. Western blot analysis and gelatin zymography showed that HF suppresses MMP-9 expression and activity concentrationdependently. HF also decreases the nuclear protein levels of nuclear factor kappa B (NF-κB) and c-fos (AP-1), critical transcription factors regulating MMP-9 expression through binding the MMP-9 promoter region. Luciferase assays showed that HF decreases TPA-induced MMP-9 promoter binding activities of NF-κB and AP-1. Taken together, these are the first results indicating that halofuginone may represent a promising new agent for breast cancer chemotherapy.

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Section: Discussionmentioning

confidence: 99%

Halofuginone induces the apoptosis of breast cancer cells and inhibits migration via downregulation of matrix metalloproteinase-9

Jin

Park

Kim

et al. 2013

International Journal of Oncology

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“…For example, curcumin induced phosphorylation of ERK1/2 and p38 MAPK, yet the curcumin-induced phosphorylation of ERK1/2 and p38 MAPK was attenuated in the presence of NAC, a scavenger of ROS (51). Furthermore, piperlongumine selectively killed glioblastoma cells via JNK and p38 activation, and these activations were blocked by NAC pre-treatment (52). Thus, FTY720 may also activate MAPK signaling pathway through ROS generation, but, to date, how FTY720 mediates MAPK has not been studied.…”

Section: Mitogen-activated Protein Kinase (Mapk) Signaling Pathwaymentioning

confidence: 97%

FTY720 for cancer therapy (Review)

Zhang

Wang

et al. 2013

Oncology Reports

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Abstract. 2-Amino-2-[2-(4-octylphenyl)]-1,3-propanediol hydrochloride (FTY720) is a potent immunosuppressant which has been approved by the Food and Drug Administration (FDA) as a new treatment for multiple sclerosis. As an immunosuppressant, it displays its anti-multiple sclerosis, immunosuppressive effects by activating sphingosine-1-phosphate receptors (S1PRs). In addition to the immunosuppressive effects, FTY720 also shows preclinical antitumor efficacy in several cancer models. In most cases, phosphorylation of FTY720 is not required for its cytotoxic effect, indicating the involvement of S1PR-independent mechanisms which are starkly different from the immunosuppressive property of FTY720. In the present study, we reviewed the rapidly advancing field of FTY720 in cancer therapy as well as some molecular targets of the unphosphorylated form of FTY720.

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“…Traditionally, PPLGM has been used for treating gastrointestinal and respiratory diseases (5). Notably, PPLGM has been shown to selectively target a wide spectrum of cancer cells (6)(7)(8)(9). PPLGM induces cancer cell death by triggering different pathways, including apoptosis, necrosis and autophagy (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%

JNK signaling pathway is involved in piperlongumine-mediated apoptosis in human colorectal cancer HCT116 cells

Wen

Bai

et al. 2015

Oncology Letters

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Abstract. Piperlongumine (PPLGM), an alkaloid isolated from the long pepper (Piper longum L.), can selectively trigger cancer cell death in colorectal cancer cells. The present study investigated whether the c-Jun NH 2 -terminal kinase (JNK) signaling pathway is involved in PPLGM-induced apoptosis in the human colorectal cancer HCT116 cell line. The results demonstrated that PPLGM reduced the cell viability and induced cell apoptosis in a time-and concentration-dependent manner, without a significant effect on cell cycle distribution. Meanwhile, treatment with 10 µM PPLGM resulted in JNK activation within 1 h, and a marked and sustained increase in c-Jun phosphorylation in the HCT116 cells. In addition, SP600125, a general inhibitor of JNK, inhibited PPLGM-induced apoptosis in the HCT116 cells by inhibiting PPLGM-induced c-Jun phosphorylation. Altogether, it can be concluded that the JNK signaling pathway, at least in part, is involved in PPLGM-mediated apoptosis in HCT116 cells.

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Piperlongumine selectively kills glioblastoma multiforme cells via reactive oxygen species accumulation dependent JNK and p38 activation

Cited by 87 publications

References 22 publications

Halofuginone induces the apoptosis of breast cancer cells and inhibits migration via downregulation of matrix metalloproteinase-9

Halofuginone induces the apoptosis of breast cancer cells and inhibits migration via downregulation of matrix metalloproteinase-9

FTY720 for cancer therapy (Review)

JNK signaling pathway is involved in piperlongumine-mediated apoptosis in human colorectal cancer HCT116 cells

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