Evidence map›Paper›PMID 19997600›Full record

ArticlePloS one2009

JC virus mediates invasion and migration in colorectal metastasis.

Alexander Link, Sung Kwan Shin, Takeshi Nagasaka, Francesc Balaguer, Minoru Koi, Barbara Jung, C Richard Boland, Ajay Goel

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

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  14. Review
  15. Study on JV Virus in Patients with Colon Cancer Type AdenocarcinomaAsian Pacific journal of cancer prevention : APJCP · 2019
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Could JC virus provoke metastasis in colon cancer?World journal of gastroenterology · 2014
    Article
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 4 institutions in 5 countries.

Alexander LinkDivision of Gastroenterology, Department of Internal Medicine, Charles A. Sammons Cancer Center and Baylor Research Institute, Baylor University Medical Center, Dallas, Texas, United States of America.
Sung Kwan Shin
Takeshi Nagasaka
Francesc Balaguer
Minoru Koi
Barbara Jung
C Richard Boland
Ajay Goel
Baylor University Medical Center · USOkayama University · JPUniversity of California, San Diego · USYonsei University · KR

Funding

The Biology and Diagnosis of HNPCCR01CA072851 · NCI · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI GOEL, AJAY · 1996 to 2019
$6.6M
JC Virus and Tumor Formation in the Human ColonR01CA098572 · NCI · BAYLOR RESEARCH INSTITUTE · PI BOLAND, CLEMENT RICHARD · 2004 to 2014
$2.7M
Measuring Methylation Kinetics in Cancer Cells: Computations and ExperimentsR01CA129286 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI KOMAROVA, NATALIA L · 2008 to 2012
$1.5M
NCI NIH HHS CA129286NCI NIH HHS R01 CA072851NCI NIH HHS R01 CA098572NCI NIH HHS R01 CA129286NCI NIH HHS R01 CA72851
6 · The paper itself

Abstract

introductionJC Virus (JCV), a human polyomavirus, is frequently present in colorectal cancers (CRCs). JCV large T-Ag (T-Ag) expressed in approximately half of all CRC's, however, its functional role in CRC is poorly understood. We hypothesized that JCV T-Ag may mediate metastasis in CRC cells through increased migration and invasion. MATERIAL AND

methodsCRC cell lines (HCT116 and SW837) were stably transfected with JCV early transcript sequences cloned into pCR3 or empty vectors. Migration and invasion assays were performed using Boyden chambers. Global gene expression analysis was performed to identify genetic targets and pathways altered by T-Ag expression. Microarray results were validated by qRT-PCR, protein expression analyses and immunohistochemistry. Matching primary CRCs and liver metastases from 33 patients were analyzed for T-Ag expression by immunohistochemistry.

resultsT-Ag expressing cell lines showed 2 to 3-fold increase in migration and invasion compared to controls. JCV T-Ag expression resulted in differential expression of several genetic targets, including genes that mediate cell migration and invasion. Pathway analysis suggested a significant involvement of these genes with AKT and MAPK signaling. Treatment with selective PI3K/AKT and MAPK pathway inhibitors resulted in reduced migration and invasion. In support of our in-vitro results, immunohistochemical staining of the advanced stage tumors revealed frequent JCV T-Ag expression in metastatic primary tumors (92%) as well as in their matching liver metastasis (73%).

conclusionThese data suggest that JCV T-Ag expression in CRC associates with a metastatic phenotype, which may partly be mediated through the AKT/MAPK signaling pathway. Frequent expression of JCV T-Ag in CRC liver metastasis provides further clues supporting a mechanistic role for JCV as a possible mediator of cellular motility and invasion in CRC.

Indexed as

Cell MovementAgedAntigens, Viral, TumorCell Line, TumorColorectal NeoplasmsEnzyme ActivationFemaleGene Expression Regulation, NeoplasticHumansJC VirusLiver NeoplasmsMaleMiddle AgedMitogen-Activated Protein KinasesNeoplasm InvasivenessNeoplasm MetastasisAntigens, Viral, TumorMitogen-Activated Protein KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID19997600
PMCPMC2781631
OpenAlexW2070853933

What OpenQuestion holds

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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.