Evidence map›Paper›PMID 22876838›Full record

ArticleBMC medical genomics2012

Genetic and bioinformatic analyses of the expression and function of PI3K regulatory subunit PIK3R3 in an Asian patient gastric cancer library.

Jin Zhou, Geng Bo Chen, Yew Chung Tang, Rohit Anthony Sinha, Yonghui Wu, Chui Sun Yap, Guihua Wang, Junbo Hu, Xianmin Xia, Patrick Tan and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

23 citing papers in PubMed, 46 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

12 authors at 4 institutions in 2 countries.

Jin ZhouLaboratory of Hormonal Regulation, Cardiovascular and Metabolic Disorders Program, Duke-National University of Singapore Graduate Medical School, Singapore.
Geng Bo Chen
Yew Chung Tang
Rohit Anthony Sinha
Yonghui Wu
Chui Sun Yap
Guihua Wang
Junbo Hu
Xianmin Xia
Patrick Tan
Liang Kee Goh
Paul Michael Yen
National University of Singapore · SGNational Cancer Centre Singapore · SGTongji Hospital · CNHuazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundWhile there is strong evidence for phosphatidylinositol 3-kinase (PI3K) involvement in cancer development, there is limited information about the role of PI3K regulatory subunits. PIK3R3, the gene that encodes the PI3K regulatory subunit p55γ, is over-expressed in glioblastoma and ovarian cancers, but its expression in gastric cancer (GC) is not known. We thus used genetic and bioinformatic approaches to examine PIK3R3 expression and function in GC, the second leading cause of cancer mortality world-wide and highly prevalent among Asians.

methodsPrimary GC and matched non-neoplastic mucosa tissue specimens from a unique Asian patient gastric cancer library were comprehensively profiled with platforms that measured genome-wide mRNA expression, DNA copy number variation, and DNA methylation status. Function of PIK3R3 was predicted by IPA pathway analysis of co-regulated genes with PIK3R3, and further investigated by siRNA knockdown studies. Cell proliferation was estimated by crystal violet dye elution and BrdU incorporation assay. Cell cycle distribution was analysed by FACS.

resultsPIK3R3 was significantly up-regulated in GC specimens (n = 126, p < 0.05), and 9.5 to 15% tumors showed more than 2 fold increase compare to the paired mucosa tissues. IPA pathway analysis showed that PIK3R3 promoted cellular growth and proliferation. Knockdown of PIK3R3 decreased the growth of GC cells, induced G0/G1 cell cycle arrest, decreased retinoblastoma protein (Rb) phosphorylation, cyclin D1, and PCNA expression.

conclusionUsing a combination of genetic, bioinformatic, and molecular biological approaches, we showed that PIK3R3 was up-regulated in GC and promoted cell cycle progression and proliferation; and thus may be a potential new therapeutic target for GC.

Indexed as

Gene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticAsian PeopleCell ProliferationComputational BiologyCyclin D1G1 Phase Cell Cycle CheckpointsGastric MucosaGene Knockdown TechniquesHumansPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein SubunitsProto-Oncogene Proteins c-aktResting Phase, Cell CycleCCND1 protein, humanCyclin D1Phosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPIK3R3 protein, humanProtein SubunitsProto-Oncogene Proteins c-aktRetinoblastoma ProteinRNA, MessengerRNA, Small Interfering

Identifiers

PMID22876838
PMCPMC3479415
OpenAlexW2018847550

What OpenQuestion holds

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LicenceCC BY
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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.