Evidence map›Paper›PMID 25422081›Full record

ArticleJournal of experimental & clinical cancer research : CR2014

CK2α, over-expressed in human malignant pleural mesothelioma, regulates the Hedgehog signaling pathway in mesothelioma cells.

Shulin Zhang, Yi-Lin Yang, Yucheng Wang, Bin You, Yuyuan Dai, Geraldine Chan, David Hsieh, Il-Jin Kim, Li Tai Fang, Alfred Au and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 24 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

14 authors at 3 institutions in 2 countries.

Shulin ZhangDepartment of Thoracic Surgery, The Fifth Hospital of Dalian, Dalian, 116021, P.R. China. zhangshulin830814@yahoo.com.
Yi-Lin YangThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Yi-Lin.Yang@ucsfmedctr.org.
Yucheng WangDepartment of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Yucheng.Wang@ucsfmedctr.org.
Bin YouThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Yb2759@gmail.com.
Yuyuan DaiThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Yuyuan.Dai@ucsfmedctr.org.
Geraldine ChanThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Geraldine.c.chan@gmail.com.
David HsiehThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. david.hsieh4@gmail.com.
Il-Jin KimThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. kimij@cc.ucsf.edu.
Li Tai FangThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. ltfang@gmail.com.
Alfred AuDivision of Diagnostic Pathology, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Alfred.Au@ucsfmedctr.org.
Hubert J StopplerTissue Core, Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. hubert.stoppler@ucsf.edu.
Zhidong XuThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Zhidong.Xu@ucsfmedctr.org.
David M JablonsThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. David.Jablons@ucsfmedctr.org.
Liang YouThoracic Oncology Laboratory, Department of Surgery, Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA, 94143, USA. Liang.You@ucsfmedctr.org.
University of California, San Francisco · USUCSF Helen Diller Family Comprehensive Cancer Center · USThe Third People's Hospital of Dalian City · CN

Funding

The Role of Cul4A in Genome Stability and Cancer DevelopmentR01CA140654 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI YOU, LIANG · 2010 to 2014
$1.5M
NCI NIH HHS R01 CA140654NCI NIH HHS R01 CA140654-01A1
6 · The paper itself

Abstract

backgroundThe Hedgehog (Hh) signaling pathway has been implicated in stem cell maintenance and its activation is aberrant in several types of cancer including mesothelioma. Protein kinase CK2 affects several cell signaling pathways through the mechanism of phosphorylation.

methodsProtein and mRNA levels of CK2α and Gli1 were tested by quantitative RT-PCR and immunohistochemistry staining in mesothelioma samples and cell lines. Down-regulated Gli1 expression and transcriptional activity were demonstrated by RT-PCR, Western blot and luciferase reporter assay.

resultsIn this study, we show that CK2α is over-expressed and a positive regulator of Hegdehog/Gli1 signaling in human malignant pleural mesothelioma. First of all, we found that the mRNA levels of CK2α and Gli1 were broadly elevated and correlated (n = 52, r = 0.401, P < 0.05), compared with LP9 (a normal mesothelial cell line). We then investigated their expression at the protein level, and found that all the 7 mesothelioma cell lines tested showed positive staining in CK2α and Gli1 immunohistochemistry. Correlation analysis by Pearson test for CK2α and Gli1 expression in the 75 mesothelioma tumors and the 7 mesothelioma cell lines showed that the two protein expression was significantly correlated (n = 82, r = 0.554, P < 0.01). Furthermore, we demonstrated that Gli1 expression and transcriptional activity were down-regulated after CK2α was silenced in two mesothelioma cell lines (H28 and H2052). CK2α siRNA also down-regulated the expression of Hh target genes in these cell lines. Moreover, treatment with a small-molecule CK2α inhibitor CX-4945 led to dose-dependent inhibition of Gli1 expression and transcriptional activity. Conversely, forced over-expression of CK2α resulted in an increase in Gli1 transcriptional activity in H28 cells.

conclusionsThus, we report for the first time that over-expressed CK2α positively regulate Hh/Gli1 signaling in human mesothelioma.

Indexed as

Signal TransductionCasein Kinase IICell Line, TumorDose-Response Relationship, DrugGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHedgehog ProteinsHumansLung NeoplasmsMesotheliomaMesothelioma, MalignantPleural NeoplasmsProtein Kinase InhibitorsRNA InterferenceTranscription FactorsTranscription, GeneticCasein Kinase IICSNK2A1 protein, humanGLI1 protein, humanHedgehog ProteinsProtein Kinase InhibitorsTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID25422081
PMCPMC4254219
OpenAlexW2111278368

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.