Evidence map›Paper›PMID 16156898›Full record

ArticleMolecular cancer2005

Global gene expression profiling of cells overexpressing SMC3.

Giancarlo Ghiselli, Chang-Gong Liu

Open access · goldAbstract read
In one paragraph

Article in Molecular cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 14 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

2 authors at 1 institution in 1 country.

Giancarlo GhiselliDepartment of Pathology and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA. giancarlo.ghiselli@jefferson.edu
Chang-Gong Liu
Thomas Jefferson University · US

Funding

BIOLOGY OF BAMACAN IN TUMORIGENESISR01CA082290 · NCI · THOMAS JEFFERSON UNIVERSITY · PI GHISELLI, GIANCARLO · 2001 to 2006
$1.1M
NCI NIH HHS R01 CA082290NCI NIH HHS R01-CA82290
6 · The paper itself

Abstract

backgroundThe Structural Maintenance of Chromosome 3 protein (SMC3) plays an essential role during the sister chromatid separation, is involved in DNA repair and recombination and participates in microtubule-mediated intracellular transport. SMC3 is frequently elevated in human colon carcinoma and overexpression of the protein transforms murine NIH3T3 fibroblasts. In order to gain insight into the mechanism of SMC3-mediated tumorigenesis a gene expression profiling was performed on human 293 cells line stably overexpressing SMC3.

resultsBiotinylated complementary RNA (cRNA) was used for hybridization of a cDNAmicroarray chip harboring 18,861 65-mer oligos derived from the published dEST sequences. After filtering, the hybridization data were normalized and statistically analyzed. Sixty-five genes for which a putative function could be assigned displayed at least two-fold change in their expression level. Eighteen of the affected genes is either a transcriptional factor or is involved in DNA and chromatin related mechanisms whereas most of those involved in signal transduction are members or modulators of the ras-rho/GTPase and cAMP signaling pathways. In particular the expression of RhoB and CRE-BPa, two mediators of cellular transformation, was significantly enhanced. This association was confirmed by analyzing the RhoB and CRE-BPa transcript levels in cells transiently transfected with an SMC3 expression vector. Consistent with the idea that the activation of ras-rho/GTPase and cAMP pathways is relevant in the context of the cellular changes following SMC3 overexpression, gene transactivation through the related serum (SRE) and cAMP (CRE) cis-acting response elements was significantly increased.

conclusionWe have documented a selective effect of the ectopic expression of SMC3 on a set of genes and transcriptional signaling pathways that are relevant for tumorigenesis. The results lead to postulate that RhoB and CRE-BPa two known oncogenic mediators whose expression is significantly increased following SMC3 overexpression play a significant role in mediating SMC3 tumorigenesis.

Indexed as

Gene Expression ProfilingOligonucleotide Array Sequence AnalysisAnimalsCell Cycle ProteinsCell LineCell ProliferationCell Transformation, NeoplasticChondroitin Sulfate ProteoglycansChromosomal Proteins, Non-HistoneCyclic AMPGene Expression Regulation, NeoplasticGenome, HumanHumansMiceResponse ElementsTime FactorsCell Cycle ProteinsChondroitin Sulfate ProteoglycansChromosomal Proteins, Non-HistoneCyclic AMPSMC3 protein, human

Identifiers

PMID16156898
PMCPMC1242249
OpenAlexW2144046167

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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.