Evidence map›Paper›PMID 29649138›Full record

ArticleInternational journal of molecular sciences2018

Response of Myeloid Leukemia Cells to Luteolin is Modulated by Differentially Expressed Pituitary Tumor-Transforming Gene 1 (PTTG1) Oncoprotein.

Pei-Yi Chen, Hsin-Jung Tien, Shih-Fen Chen, Chi-Ting Horng, Huei-Lin Tang, Hui-Ling Jung, Ming-Jiuan Wu, Jui-Hung Yen

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Pei-Yi ChenCenter of Medical Genetics, Buddhist Tzu Chi General Hospital, Hualien 970, Taiwan. pyc571@gmail.com.
Hsin-Jung TienDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan. tiencelia@gmail.com.
Shih-Fen ChenDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan. damaruco.csf@gmail.com.
Chi-Ting HorngDepartment of Ophthalmology, Kaohsiung Armed Force General Hospital, Kaohsiung 804, Taiwan. h56041@gmail.com.
Huei-Lin TangDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan. sophiatang0205@gms.tcu.edu.tw.
Hui-Ling JungDepartment of Pharmacy, Kaohsiung Armed Force General Hospital, Kaohsiung 804, Taiwan. tracy530917@gmail.com.
Ming-Jiuan WuDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 717, Taiwan. mingjiuanwu@gmail.com.ORCID 0000-0003-3327-828X
Jui-Hung YenDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan. imyenjh@mail.tcu.edu.tw.ORCID 0000-0003-2551-350X
Tzu Chi University · TWKaohsiung Armed Forces General Hospital · TWBuddhist Tzu Chi General Hospital · TWChia Nan University of Pharmacy and Science · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Luteolin, a flavonoid nutraceutical abundant in vegetables and fruits, exhibits a wide range of bioactive properties, including antioxidant, anti-inflammatory and anti-cancer activities. Pituitary tumor-transforming gene 1 (PTTG1), an oncoprotein that regulates cell proliferation, is highly expressed in several types of cancer cells including leukemia. In this study, we aim to investigate the anti-cancer effects of luteolin on cells with differential PTTG1 expression and their underlying mechanisms in human myeloid leukemia cells. Methyl thiazolyl tetrazolium (MTT) assay data showed that luteolin (25-100 μM) significantly reduced cell viability in THP-1, HL-60 and K562 cells but did not affect normal peripheral blood mononuclear cells (PBMCs). Flow cytometric analysis and Western blot data demonstrated that luteolin induced a stronger apoptosis on undifferentiated myeloid leukemia cells with higher PTTG1 protein levels than on 12-myristate 13-acetate (PMA)- or all-trans-retinoic acid (ATRA)-differentiated cells with lower PTTG1 expression. Furthermore, PTTG1 knockdown by shRNA in leukemia cells suppressed cell proliferation, arrested cell-cycle progression and impaired the effectiveness of luteolin on cell-cycle regulation. Moreover, PTTG1-knockdown cells with luteolin exposure presented a reduction of the apoptotic proteins and maintained higher levels of the anti-apoptotic proteins such as Mcl-1, Bcl-2 and p21, which exhibited greater resistance to apoptosis. Finally, microarray analysis showed that 20 genes associated with cell proliferation, such as

Indexed as

Antineoplastic Agents, PhytogenicCell ProliferationCell SurvivalDown-RegulationGene Expression Regulation, NeoplasticGene Regulatory NetworksHL-60 CellsHumansK562 CellsLeukemia, MyeloidLuteolinSecurinTHP-1 CellsAntineoplastic Agents, PhytogenicLuteolinpituitary tumor-transforming protein 1, humanSecurinapoptosiscell proliferationluteolinmyeloid leukemia cellsPTTG1

Identifiers

PMID29649138
PMCPMC5979486
OpenAlexW2797101525

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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.