Evidence map›Paper›PMID 20661223›Full record

ArticleOncogene2010

Sprouty-2 controls c-Met expression and metastatic potential of colon cancer cells: sprouty/c-Met upregulation in human colonic adenocarcinomas.

C Holgren, U Dougherty, F Edwin, D Cerasi, I Taylor, A Fichera, L Joseph, M Bissonnette, S Khare

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 67 citations in OpenAlex.

  1. Intact lymph node homing and CD8Frontiers in immunology · 2026
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  13. Review
  14. Loss of Spry1 reduces growth of BRAFCell death & disease · 2020
    Article
  15. Aging · 2020
    Article
  16. Review
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  18. Review
  19. Subcellular Localization of Sprouty2 in Human Glioma Cells.Frontiers in molecular neuroscience · 2019
    Article
  20. Review
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

9 authors at 3 institutions in 1 country.

C HolgrenHines Veterans Affairs Medical Center, Hines, IL, USA.
U Dougherty
F Edwin
D Cerasi
I Taylor
A Fichera
L Joseph
M Bissonnette
S Khare
University of Chicago · USLoyola University Chicago · USEdward Hines, Jr. VA Hospital · US

Funding

Roles of ErbB Signaling in Colonic CarcinogenesisR01CA036745 · NCI · UNIVERSITY OF CHICAGO · PI BISSONNETTE, BRUCE MARC · 1985 to 2007
$2.3M
Colon Cancer Chemoprevention by Ursodeoxycholic AcidR03CA097540 · NCI · UNIVERSITY OF CHICAGO · PI KHARE, SHARAD · 2002 to 2003
$153k
COLONIC EPITHELIAL CELL PLASMA MEMBRANESR37CA036745 · NCI · UNIVERSITY OF CHICAGO · PI BRASITUS, THOMAS A · 1986 to 1999
–
NCI NIH HHS CA036745NCI NIH HHS R01 CA036745NCI NIH HHS R03 CA097540NCI NIH HHS R37 CA036745
6 · The paper itself

Abstract

Sprouty negatively regulates receptor tyrosine kinase signals by inhibiting Ras/extracellular signal-regulated kinase (ERK) pathways. Sprouty is downregulated in breast, prostate and liver cancers and appears to function as a tumor suppressor. The role of sprouty in colonic neoplasia, however, has not been investigated. Sprouty-2 protein and mRNA transcripts were significantly upregulated in human colonic adenocarcinomas. Strikingly, the c-Met receptor was also upregulated in tumors with increased sprouty-2. To delineate a potential causal relationship between sprouty-2 and c-Met, K-ras mutant HCT-116 colon cancer cells were transduced with purified TAT-sprouty-2 protein or stably transfected with full-length human sprouty-2 gene. Sprouty-2 upregulation significantly increased cell proliferation by accelerating cell cycle transition. Sprouty-2 transfectants showed strong upregulation of c-Met protein and mRNA transcripts and hepatocyte growth factor-stimulated ERK and Akt phosphorylation and enhanced cell migration and invasion. In contrast, knockdown of c-Met by small interfering RNA (siRNA) significantly decreased cell proliferation, migration and invasion in sprouty-2 transfectants. Further, knockdown of sprouty-2 by siRNA in parental HT-29 and LS-174T colon cancer cells also decreased cell invasion. Sprouty-2 transfectants formed significantly larger tumor xenografts and showed increased proliferation and angiogenesis and suppressed apoptosis. Sprouty-2 tumors metastasized to the liver from cecal orthotopic implants, suggesting that sprouty-2 might also enhance metastatic signals. Thus, in colon cancer sprouty functions as an oncogene and its effects are mediated in part by c-Met upregulation.

Indexed as

Neoplasm MetastasisUp-RegulationAdenocarcinomaCell Line, TumorCell ProliferationColonic NeoplasmsHumansIntracellular Signaling Peptides and ProteinsLiver NeoplasmsMembrane ProteinsProto-Oncogene Proteins c-metRNA, Small InterferingIntracellular Signaling Peptides and ProteinsMembrane ProteinsProto-Oncogene Proteins c-metRNA, Small InterferingSPRY2 protein, human

Identifiers

PMID20661223
PMCPMC2945447
OpenAlexW1969276724

What OpenQuestion holds

Textmetadata
LicenceTDM
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.