Evidence map›Paper›PMID 25619389›Full record

ArticleActa pharmacologica Sinica2015

Piperlongumine induces apoptotic and autophagic death of the primary myeloid leukemia cells from patients via activation of ROS-p38/JNK pathways.

Xin-xin Xiong, Ju-mei Liu, Xin-yao Qiu, Feng Pan, Shang-bin Yu, Xiao-qian Chen

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
12.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 74 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Xin-xin XiongDepartment of Pathophysiology, School of Basic Medicine; Key Laboratory of Neurological Diseases, Ministry of Education; Institute of Brain Research, Huazhong University of Science and Technology, Wuhan 430030, China.
Ju-mei LiuDepartment of Pathophysiology, School of Basic Medicine; Key Laboratory of Neurological Diseases, Ministry of Education; Institute of Brain Research, Huazhong University of Science and Technology, Wuhan 430030, China.
Xin-yao QiuDepartment of Pathophysiology, School of Basic Medicine; Key Laboratory of Neurological Diseases, Ministry of Education; Institute of Brain Research, Huazhong University of Science and Technology, Wuhan 430030, China.
Feng Pan1] Department of Pathophysiology, School of Basic Medicine; Key Laboratory of Neurological Diseases, Ministry of Education; Institute of Brain Research, Huazhong University of Science and Technology, Wuhan 430030, China [2] Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Shang-bin YuDepartment of Pathophysiology, School of Basic Medicine; Key Laboratory of Neurological Diseases, Ministry of Education; Institute of Brain Research, Huazhong University of Science and Technology, Wuhan 430030, China.
Xiao-qian ChenDepartment of Pathophysiology, School of Basic Medicine; Key Laboratory of Neurological Diseases, Ministry of Education; Institute of Brain Research, Huazhong University of Science and Technology, Wuhan 430030, China.
Huazhong University of Science and Technology · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo investigate the effects of piperlongumine (PL), an anticancer alkaloid from long pepper plants, on the primary myeloid leukemia cells from patients and the mechanisms of action.

methodsHuman BM samples were obtained from 9 patients with acute or chronic myeloid leukemias and 2 patients with myelodysplastic syndrome (MDS). Bone marrow mononuclear cells (BMMNCs) were isolated and cultured. Cell viability was determined using MTT assay, and apoptosis was examined with PI staining or flow cytometry. ROS levels in the cells were determined using DCFH-DA staining and flow cytometry. Expression of apoptotic and autophagic signaling proteins was analyzed using Western blotting.

resultsPL inhibited the viability of BMMNCs from the patients with myeloid leukemias (with IC50 less than 20 μmol/L), but not that of BMMNCs from a patient with MDS. Furthermore, PL (10 and 20 μmol/L) induced apoptosis of BMMNCs from the patients with myeloid leukemias in a dose-dependent manner. PL markedly increased ROS levels in BMMNCs from the patients with myeloid leukemias, whereas pretreatment with the antioxidant N-acetyl-L-cysteine abolished PL-induced ROS accumulation and effectively reduced PL-induced cytotoxicity. Moreover, PL markedly increased the expression of the apoptotic proteins (Bax, Bcl-2 and caspase-3) and autophagic proteins (Beclin-1 and LC3B), and phosphorylation of p38 and JNK in BMMNCs from the patients with myeloid leukemias, whereas pretreatment with the specific p38 inhibitor SB203580 or the specific JNK inhibitor SP600125 partially reversed PL-induced ROS production, apoptotic/autophagic signaling activation and cytotoxicity.

conclusionPiperlongumine induces apoptotic and autophagic death of the primary myeloid leukemia cells from patients via activation of ROS-p38/JNK pathways.

Indexed as

Antineoplastic Agents, PhytogenicAntioxidantsApoptosisApoptosis Regulatory ProteinsAutophagyCell SurvivalDioxolanesDose-Response Relationship, DrugEnzyme ActivationHumansInhibitory Concentration 50JNK Mitogen-Activated Protein KinasesLeukemia, Myelogenous, Chronic, BCR-ABL PositiveLeukemia, Myeloid, AcuteOxidative Stressp38 Mitogen-Activated Protein KinasesAntineoplastic Agents, PhytogenicAntioxidantsApoptosis Regulatory ProteinsDioxolanesJNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPiperidonespiperlongumineProtein Kinase InhibitorsReactive Oxygen Species

Identifiers

PMID25619389
PMCPMC4349924
OpenAlexW2011454186

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.