Evidence map›Paper›PMID 25398317›Full record

ArticleCell communication and signaling : CCS2014

An increase in integrin-linked kinase non-canonically confers NF-κB-mediated growth advantages to gastric cancer cells by activating ERK1/2.

Po-Chun Tseng, Chia-Ling Chen, Yan-Shen Shan, Wen-Teng Chang, Hsiao-Sheng Liu, Tse-Ming Hong, Chia-Yuan Hsieh, Sheng-Hsiang Lin, Chiou-Feng Lin

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 18 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

9 authors at 3 institutions in 1 country.

Po-Chun TsengInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. iluc0720@hotmail.com.
Chia-Ling ChenCenter for Translational Medicine, Taipei Medical University, Taipei, 110, Taiwan. chialing811@gmail.com.
Yan-Shen ShanInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. ysshan@mail.ncku.edu.tw.
Wen-Teng ChangDepartment of Biological Science and Technology, Chung Hwa University of Medical Technology, Tainan, 717, Taiwan. bicowtc@gmail.com.
Hsiao-Sheng LiuDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. a713@mail.ncku.edu.tw.
Tse-Ming HongInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. tmhong@mail.ncku.edu.tw.
Chia-Yuan HsiehInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. dyoushus@yahoo.com.tw.
Sheng-Hsiang LinInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. shlin922@mail.ncku.edu.tw.
Chiou-Feng LinInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, 701, Taiwan. cflin2014@tmu.edu.tw.
National Cheng Kung University · TWChung Hwa University of Medical Technology · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreased activity or expression of integrin-linked kinase (ILK), which regulates cell adhesion, migration, and proliferation, leads to oncogenesis. We identified the molecular basis for the regulation of ILK and its alternative role in conferring ERK1/2/NF-κB-mediated growth advantages to gastric cancer cells.

resultsInhibiting ILK with short hairpin RNA or T315, a putative ILK inhibitor, abolished NF-κB-mediated the growth in the human gastric cancer cells AGS, SNU-1, MKN45, and GES-1. ILK stimulated Ras activity to activate the c-Raf/MEK1/2/ERK1/2/ribosomal S6 kinase/inhibitor of κBα/NF-κB signaling by facilitating the formation of the IQ motif-containing GTPase-activating protein 1 (IQGAP1)-Ras complex. Forced enzymatic ILK expression promoted cell growth by facilitating ERK1/2/NF-κB signaling. PI3K activation or decreased PTEN expression prolonged ERK1/2 activation by protecting ILK from proteasome-mediated degradation. C-terminus of heat shock cognate 70 interacting protein, an HSP90-associated E3 ubiquitin ligase, mediated ILK ubiquitination to control PI3K- and HSP90-regulated ILK stabilization and signaling. In addition to cell growth, the identified pathway promoted cell migration and reduced the sensitivity of gastric cancer cells to the anticancer agents 5-fluorouracil and cisplatin. Additionally, exogenous administration of EGF as well as overexpression of EGFR triggered ILK- and IQGAP1-regulated ERK1/2/NF-κB activation, cell growth, and migration.

conclusionAn increase in ILK non-canonically promotes ERK1/2/NF-κB activation and leads to the growth of gastric cancer cells.

Indexed as

AnimalsApoptosisCell Line, TumorCell MovementCell ProliferationCell SurvivalHumansMaleMice, Inbred BALB CMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesPTEN Phosphohydrolaseras GTPase-Activating ProteinsIQ motif containing GTPase activating protein 1Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BPhosphatidylinositol 3-KinasesProtein Serine-Threonine KinasesPTEN Phosphohydrolaseras GTPase-Activating Proteinsras ProteinsScaffold Protein ILK

Identifiers

PMID25398317
PMCPMC4255431
OpenAlexW2104600810

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.