Evidence map›Paper›PMID 33982869›Full record

ArticleJournal of cellular and molecular medicine2021

Targeting LIMK1 with luteolin inhibits the growth of lung cancer in vitro and in vivo.

Man Zhang, Rui Wang, Jie Tian, Mengqiu Song, Ran Zhao, Kangdong Liu, Feng Zhu, Jung-Hyun Shim, Zigang Dong, Mee-Hyun Lee

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.7field-weighted citation impact, top 5% 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

37 citing papers in PubMed, 64 citations in OpenAlex.

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  10. Potential anticancer effects and toxicity of flavones luteolin and apigeninJournal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
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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

10 authors at 5 institutions in 2 countries.

Man ZhangChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Rui WangChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Jie TianChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Mengqiu SongChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Ran ZhaoChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Kangdong LiuChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Feng ZhuCancer Research Institute, The Affiliated Hospital of Guilin Medical University, Guilin, China.
Jung-Hyun ShimDepartment of Pharmacy, College of Pharmacy, Mokpo National University, Muan, Republic of Korea.
Zigang DongChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.
Mee-Hyun LeeChina-US (Henan) Hormel Cancer Institute, Zhengzhou, China.ORCID 0000-0002-1216-0218
Zhengzhou University · CNChina-US (Henan) Hormel Cancer Institute · CNDongshin University · KRGuilin Medical University · CNMokpo National University · KR

Funding

National Natural Science Foundation of China NSFC81972839
6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related deaths. LIM domain kinase (LIMK) 1 is a member of serine/threonine kinase family and highly expressed in various cancers. Luteolin, a polyphenolic plant flavonoid, has been reported to suppress tumour proliferation through inducing apoptosis and autophagy via MAPK activation in glioma. However, the mechanism of luteolin on suppressing lung cancer growth is still unclear. We found that luteolin targeted LIMK1 from the in silico screening and significantly inhibited the LIMK1 kinase activity, which was confirmed with pull-down binding assay and computational docking models. Treatment with luteolin inhibited lung cancer cells anchorage-independent colony growth and induced apoptosis and cell cycle arrest at G1 phase. Luteolin also decreased the expression of cyclin D1 and increased the levels of cleaved caspase-3 by down-regulating LIMK1 signalling related targets, including p-LIMK and p-cofilin. Furthermore, luteolin suppressed the lung cancer patient-derived xenograft tumour growth by decreasing Ki-67, p-LIMK and p-cofilin expression in vivo. Taken together, these results provide insight into the mechanism that underlies the anticancer effects of luteolin on lung cancer, which involved in down-regulation of LIMK1 and its interaction with cofilin. It also provides valuable evidence for translation towards lung cancer clinical trials with luteolin.

Indexed as

AnimalsApoptosisCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansIn Vitro TechniquesLim KinasesLung NeoplasmsLuteolinMiceMice, SCIDTumor Cells, CulturedXenograft Model Antitumor AssaysLIMK1 protein, humanLim KinasesLuteolinLIMK1luteolinnon-small cell lung cancer

Identifiers

PMID33982869
PMCPMC8184676
OpenAlexW3161674393

What OpenQuestion holds

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LicenceCC BY
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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.