Evidence map›Paper›PMID 25310002›Full record

ArticlePloS one2014

Luteolin suppresses cancer cell proliferation by targeting vaccinia-related kinase 1.

Ye Seul Kim, Seong-Hoon Kim, Joon Shin, Amaravadhi Harikishore, Jong-Kwan Lim, Youngseob Jung, Ha-Na Lyu, Nam-In Baek, Kwan Yong Choi, Ho Sup Yoon and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  7. HNRNP A1 Promotes Lung Cancer Cell Proliferation by ModulatingInternational journal of molecular sciences · 2021
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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

11 authors at 3 institutions in 2 countries.

Ye Seul KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Seong-Hoon KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Joon ShinSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Amaravadhi HarikishoreSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Jong-Kwan LimDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea.
Youngseob JungDivision of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea.
Ha-Na LyuDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Nam-In BaekThe Graduate School of Biotechnology and Plant Metabolism Research Center, Kyung-Hee University, Suwon, Republic of Korea.
Kwan Yong ChoiDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea; Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea.
Ho Sup YoonSchool of Biological Sciences, Nanyang Technological University, Singapore, Singapore.
Kyong-Tai KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea; Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang, Republic of Korea.
Pohang University of Science and Technology · KRNanyang Technological University · SGKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncontrolled proliferation, a major feature of cancer cells, is often triggered by the malfunction of cell cycle regulators such as protein kinases. Recently, cell cycle-related protein kinases have become attractive targets for anti-cancer therapy, because they play fundamental roles in cellular proliferation. However, the protein kinase-targeted drugs that have been developed so far do not show impressive clinical results and also display severe side effects; therefore, there is undoubtedly a need to investigate new drugs targeting other protein kinases that are critical in cell cycle progression. Vaccinia-related kinase 1 (VRK1) is a mitotic kinase that functions in cell cycle regulation by phosphorylating cell cycle-related substrates such as barrier-to-autointegration factor (BAF), histone H3, and the cAMP response element (CRE)-binding protein (CREB). In our study, we identified luteolin as the inhibitor of VRK1 by screening a small-molecule natural compound library. Here, we evaluated the efficacy of luteolin as a VRK1-targeted inhibitor for developing an effective anti-cancer strategy. We confirmed that luteolin significantly reduces VRK1-mediated phosphorylation of the cell cycle-related substrates BAF and histone H3, and directly interacts with the catalytic domain of VRK1. In addition, luteolin regulates cell cycle progression by modulating VRK1 activity, leading to the suppression of cancer cell proliferation and the induction of apoptosis. Therefore, our study suggests that luteolin-induced VRK1 inhibition may contribute to establish a novel cell cycle-targeted strategy for anti-cancer therapy.

Indexed as

Antineoplastic AgentsCatalytic DomainCell Line, TumorCell ProliferationDNA-Binding ProteinsHistonesHumansIntracellular Signaling Peptides and ProteinsLuteolinNuclear ProteinsPhosphorylationProtein Serine-Threonine KinasesAntineoplastic AgentsBANF1 protein, humanDNA-Binding ProteinsHistonesIntracellular Signaling Peptides and ProteinsLuteolinNuclear ProteinsProtein Serine-Threonine KinasesVRK1 protein, human

Identifiers

PMID25310002
PMCPMC4195671
OpenAlexW2019688585

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.