Evidence map›Paper›PMID 23660946›Full record

ArticleBritish journal of cancer2013

ARID1B, a member of the human SWI/SNF chromatin remodeling complex, exhibits tumour-suppressor activities in pancreatic cancer cell lines.

M Khursheed, J N Kolla, V Kotapalli, N Gupta, S Gowrishankar, S G Uppin, R A Sastry, S Koganti, C Sundaram, J R Pollack and 1 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Insights into Mechanisms of Tumorigenesis in Neuroendocrine Neoplasms.International journal of molecular sciences · 2021
    Review
  11. Cellular senescence or stemness: hypoxia flips the coin.Journal of experimental & clinical cancer research : CR · 2021
    Review
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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

11 authors at 4 institutions in 2 countries.

M KhursheedLaboratory of Molecular Oncology, Centre for DNA Fingerprinting and Diagnostics, Hyderabad, India.
J N Kolla
V Kotapalli
N Gupta
S Gowrishankar
S G Uppin
R A Sastry
S Koganti
C Sundaram
J R Pollack
M D Bashyam
Centre for DNA Fingerprinting and Diagnostics · INNizam's Institute of Medical Sciences · INApollo Hospitals · INStanford University · US

Funding

Gene Amplification and Deletion in Pancreatic CancerR01CA112016 · NCI · STANFORD UNIVERSITY · PI POLLACK, JONATHAN R · 2006 to 2010
$1.4M
NCI NIH HHS CA112016NCI NIH HHS R01 CA112016
6 · The paper itself

Abstract

backgroundThe human ATP-dependent SWItch/sucrose nonfermentable (SWI/SNF) complex functions as a primary chromatin remodeler during ontogeny, as well as in adult life. Several components of the complex have been suggested to function as important regulators of tumorigenesis in various cancers. In the current study, we have characterised a possible tumour suppressor role for the largest subunit of the complex, namely the AT-rich interaction domain 1B (ARID1B).

methodsWe performed Azacytidine and Trichostatin A treatments, followed by bisulphite sequencing to determine the possible DNA methylation-induced transcription repression of the gene in pancreatic cancer (PaCa) cell lines. Functional characterisation of effect of ARID1B ectopic expression in MiaPaCa2 PaCa cell line, which harboured ARID1B homozygous deletion, was carried out. Finally, we evaluated ARID1B protein expression in pancreatic tumour samples using immunohistochemistry on a tissue microarray.

resultsARID1B was transcriptionally repressed due to promoter hypermethylation, and ectopic expression severely compromised the ability of MiaPaCa2 cells to form colonies in liquid culture and soft agar. In addition, ARID1B exhibited significantly reduced/loss of expression in PaCa tissue, especially in samples from advanced-stage tumours, when compared with normal pancreas.

conclusionThe results therefore suggest a possible tumour-suppressor function for ARID1B in PaCa, thus adding to the growing list of SWI/SNF components with a similar function. Given the urgent need to design efficient targeted therapies for PaCa, our study assumes significance.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalCell Line, TumorChromosomal Proteins, Non-HistoneCpG IslandsDNA-Binding ProteinsDNA MethylationGene Expression Regulation, NeoplasticHumansPancreatic NeoplasmsTranscription FactorsTransfectionTumor Suppressor ProteinsARID1B protein, humanChromosomal Proteins, Non-HistoneDNA-Binding ProteinsSWI-SNF-B chromatin-remodeling complexTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID23660946
PMCPMC3670478
OpenAlexW2013974230

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.