Evidence map›Paper›PMID 22912777›Full record

ArticlePloS one2012

MUC1c regulates cell survival in pancreatic cancer by preventing lysosomal permeabilization.

Sulagna Banerjee, Nameeta Mujumdar, Vikas Dudeja, Tiffany Mackenzie, Tara K Krosch, Veena Sangwan, Selwyn M Vickers, Ashok K Saluja

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 26 citations in OpenAlex.

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  19. Therapeutic cancer vaccines.Advances in cancer research · 2014
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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

8 authors at 1 institution in 1 country.

Sulagna BanerjeeDivision of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, Minnesota, United States of America.
Nameeta Mujumdar
Vikas Dudeja
Tiffany Mackenzie
Tara K Krosch
Veena Sangwan
Selwyn M Vickers
Ashok K Saluja
University of Minnesota · US

Funding

UAB / UMN SPORE in Pancreatic CancerP50CA101955 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BUCHSBAUM, DONALD J · 2010 to 2014
$11.1M
The Inhibition of HSP70 Induces Apoptosis in Pancreatic Cancer CellsR01CA124723 · NCI · UNIVERSITY OF MINNESOTA · PI GILBOA, ELI, RAMAKRISHNAN, SUNDARAM · 2007 to 2022
$4.5M
The Role of MUC1 in the Pathogenesis of Pancreatic CancerR21CA131663 · NCI · UNIVERSITY OF MINNESOTA · PI SALUJA, ASHOK K · 2008 to 2009
$374k
NCI NIH HHS R01 5R01CA124723-05NCI NIH HHS R01 CA124723NCI NIH HHS R21 5R21CA131663-02NCI NIH HHS R21 CA131663
6 · The paper itself

Abstract

backgroundMUC1 is a type I transmembrane glycoprotein aberrantly overexpressed in various cancer cells including pancreatic cancer. The cytosolic end of MUC1 (MUC1-c) is extensively involved in a number of signaling pathways. MUC1-c is reported to inhibit apoptosis in a number of cancer cells, but the mechanism of inhibition is unclear.

methodExpression of MUC1-c was studied in the pancreatic cancer cell line MIAPaCa-2 at the RNA level by using qRTPCR and at the protein level by Western blotting. MUC1-c expression was inhibited either by siRNA or by a specific peptide inhibitor, GO-201. Effect of MUC1-c inhibition on viability and proliferation and lysosomal permeabilization were studied. Association of MUC1-c with HSP70 was detected by co-immunoprecipitation of MUC1-c and HSP70. Localization of MUC1-c in cellular organelles was monitored by immunofluorescence and with immuno- blotting by MUC1-c antibody after subcellular fractionation.

resultsInhibition of MUC1-c by an inhibitor (GO-201) or siRNA resulted in reduced viability and reduced proliferation of pancreatic cancer cells. Furthermore, GO-201, the peptide inhibitor of MUC1-c, was effective in reducing tumor burden in pancreatic cancer mouse model. MUC1-c was also found to be associated with HSP70 in the cytosol, although a significant amount of MUC1 was also seen to be present in the lysosomes. Inhibition of MUC1 expression or activity showed an enhanced Cathepsin B activity in the cytosol, indicating lysosomal permeabilization. Therefore this study indicates that MUC1-c interacted with HSP70 in the cytosol of pancreatic cancer cells and localized to the lysosomes in these cells. Further, our results showed that MUC1-c protects pancreatic cancer cells from cell death by stabilizing lysosomes and preventing release of Cathepsin B in the cytosol.

Indexed as

AnimalsBlotting, WesternCell Line, TumorCell SurvivalHSP70 Heat-Shock ProteinsImmunoprecipitationLysosomesMiceMucin-1Pancreatic NeoplasmsPeptidesPermeabilityProtein SubunitsReal-Time Polymerase Chain ReactionSignal TransductionGO 201HSP70 Heat-Shock Proteinsmuc1 protein, mouseMucin-1PeptidesProtein Subunits

Identifiers

PMID22912777
PMCPMC3418232
OpenAlexW2042031862

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.