Evidence map›Paper›PMID 23976985›Full record

ArticlePloS one2013

Inhibition of the growth factor MDK/midkine by a novel small molecule compound to treat non-small cell lung cancer.

Huifang Hao, Yutaka Maeda, Takuya Fukazawa, Tomoki Yamatsuji, Munenori Takaoka, Xiao-Hong Bao, Junji Matsuoka, Tatsuo Okui, Tsuyoshi Shimo, Nagio Takigawa and 8 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 15% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 6 institutions in 3 countries.

Huifang HaoKawasaki Hospital Research Center, Kawasaki Medical School, Okayama, Japan.
Yutaka Maeda
Takuya Fukazawa
Tomoki Yamatsuji
Munenori Takaoka
Xiao-Hong Bao
Junji Matsuoka
Tatsuo Okui
Tsuyoshi Shimo
Nagio Takigawa
Yasuko Tomono
Motowo Nakajima
Iris M Fink-Baldauf
Sandra Nelson
William Seibel
Ruben Papoian
Jeffrey A Whitsett
Yoshio Naomoto
Kawasaki Medical School · JPCincinnati Children's Hospital Medical Center · USOkayama University · JPUniversity of Cincinnati · USSBI Pharmaceuticals (Japan) · JPShigei Medical Research Institute · JP

Funding

Transcriptional Programming of Asthma Related Pathology in Respiratory EpitheliaR01HL095580 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WHITSETT, JEFFREY A · 2009 to 2017
$4.7M
Airway Progenitor Cell Profileration and Differentiation During Lung RepairU01HL110964 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI STREETER, PHILIP R, WHITSETT, JEFFREY A · 2012 to 2016
$3.3M
Transcriptional Control of Submucosal Gland Formation and FunctionR01HL108907 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WHITSETT, JEFFREY A · 2011 to 2014
$1.6M
NHLBI NIH HHS HL095580NHLBI NIH HHS HL108907NHLBI NIH HHS HL110964NHLBI NIH HHS R01 HL095580NHLBI NIH HHS R01 HL108907NHLBI NIH HHS U01 HL110964
6 · The paper itself

Abstract

Midkine (MDK) is a heparin-binding growth factor that is highly expressed in many malignant tumors, including lung cancers. MDK activates the PI3K pathway and induces anti-apoptotic activity, in turn enhancing the survival of tumors. Therefore, the inhibition of MDK is considered a potential strategy for cancer therapy. In the present study, we demonstrate a novel small molecule compound (iMDK) that targets MDK. iMDK inhibited the cell growth of MDK-positive H441 lung adenocarcinoma cells that harbor an oncogenic KRAS mutation and H520 squamous cell lung cancer cells, both of which are types of untreatable lung cancer. However, iMDK did not reduce the cell viability of MDK-negative A549 lung adenocarcinoma cells or normal human lung fibroblast (NHLF) cells indicating its specificity. iMDK suppressed the endogenous expression of MDK but not that of other growth factors such as PTN or VEGF. iMDK suppressed the growth of H441 cells by inhibiting the PI3K pathway and inducing apoptosis. Systemic administration of iMDK significantly inhibited tumor growth in a xenograft mouse model in vivo. Inhibition of MDK with iMDK provides a potential therapeutic approach for the treatment of lung cancers that are driven by MDK.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinoma, Non-Small-Cell LungCarrier ProteinsCell Line, TumorCoumarinsCytokinesFemaleFibroblastsGene Expression Regulation, NeoplasticHumansLung NeoplasmsMiceMice, Inbred BALB CMidkine3-(2-(4-fluorobenzyl)imidazo(2,1-beta)(1),(3)thiazol-6-yl)-2H-chromen-2-oneAntineoplastic AgentsCarrier ProteinsCoumarinsCytokinesMDK protein, humanMidkineNerve Growth FactorsPhosphatidylinositol 3-KinasespleiotrophinRNA, Small InterferingThiazolesVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID23976985
PMCPMC3745462
OpenAlexW2001984393

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.