Evidence map›Paper›PMID 30971268›Full record

ArticleCell communication and signaling : CCS2019

Targeting p21-activated kinase 1 inhibits growth and metastasis via Raf1/MEK1/ERK signaling in esophageal squamous cell carcinoma cells.

Liang Chen, Shuning Bi, Jiuzhou Hou, Zhijun Zhao, Chaojie Wang, Songqiang Xie

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-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

24 citing papers in PubMed, 36 citations in OpenAlex.

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  9. Metastasis prevention: targeting causes and roots.Clinical & experimental metastasis · 2022
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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

6 authors at 2 institutions in 1 country.

Liang ChenInstitute of Chemical Biology, College of Pharmacy, Henan University, Kaifeng, 475004, China.
Shuning BiInstitute of Chemical Biology, College of Pharmacy, Henan University, Kaifeng, 475004, China.
Jiuzhou HouInstitute of Chemical Biology, College of Pharmacy, Henan University, Kaifeng, 475004, China.
Zhijun ZhaoDepartment of Medicine and Therapeutics, Luohe Medical College, Luohe, 462000, China. lhyzzzj@163.com.
Chaojie WangThe Key Laboratory of Natural Medicine and Immuno-Engineering, Henan University, Kaifeng, 475004, China. wcjsxq@henu.edu.cn.
Songqiang XieInstitute of Chemical Biology, College of Pharmacy, Henan University, Kaifeng, 475004, China. xiesq@vip.henu.edu.cn.ORCID 0000-0002-1663-3078
Henan University · CNLuohe Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundp21-activated kinase 1 (PAK1) plays a fundamental role in promoting the development and progression of several cancers and is a potential therapeutic target. However, the biological function and underlying mechanism of PAK1 in esophageal squamous cell carcinoma (ESCC) remain unclear.

methodsThe expression of PAK1 was detected in both ESCC cell lines and clinical samples. Cell growth was measured by MTT, focus formation and soft agar assays. Cell migration and invasion were detected by wound healing and transwell assays. Animal models of subcutaneous tumourigenicity and tail vein metastasis were performed to determine the inhibitory effect of pharmacological inhibitor IPA-3 on tumor growth and metastasis of ESCC cells.

resultsWe found that PAK1 was frequently overexpressed in ESCC. Ectopic expression of PAK1 promoted cellular growth, colony formation and anchorage-independent growth. Overexpressing PAK1 also enhanced migration, invasion and the expression of MMP-2 and MMP-9 in ESCC cells. In contrast, silencing PAK1 by lentiviral knockdown or a specific inhibitor IPA-3 resulted in a contrary effect. Subsequent investigations revealed that Raf1/MEK1/ERK signaling pathway was involved in PAK1-mediated effect. Enhanced expression of Raf1 attenuated the inhibitory functions of PAK1 shRNA. Whereas blocking of Raf1 by shRNA or specific inhibition of MEK1 by U0126 antagonized the oncogenetic effect of PAK1 on ESCC cells. More importantly, Pharmacological inhibition of PAK1 by IPA-3 significantly suppressed tumor growth and lung metastasis of ESCC cells in vivo.

conclusionsThese data support that PAK1 is an ideal target for the development of potential therapeutic drugs for ESCC patients even with metastasis.

Indexed as

AgedAged, 80 and overAnimalsCarcinogenesisCell Line, TumorCell MovementCell ProliferationDisease ProgressionDisulfidesEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaHumansMaleMAP Kinase Kinase 1MAP Kinase Signaling SystemMatrix Metalloproteinase 2DisulfidesIPA-3 compoundMAP2K1 protein, humanMAP Kinase Kinase 1Matrix Metalloproteinase 2Matrix Metalloproteinase 9Naphtholsp21-Activated KinasesPAK1 protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-rafRaf1 protein, humanRNA, Small InterferingERKESCCIPA-3MEK1MetastasisPAK1Raf1

Identifiers

PMID30971268
PMCPMC6458688
OpenAlexW2945756501

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.