Evidence map›Paper›PMID 17455258›Full record

ArticleInternational journal of cancer2007

Induction of Smad1 by MT1-MMP contributes to tumor growth.

Jaclyn A Freudenberg, Wen-Tien Chen

Open access · greenAbstract read
In one paragraph

Article in International journal of cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-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

11 citing papers in PubMed, 19 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.

Jaclyn A FreudenbergDepartment of Medicine, Stony Brook University, Stony Brook, NY 11794-8151, USA.
Wen-Tien Chen
Stony Brook University · US

Funding

World Trade Center Worker and Volunteer Medical Screening ProgramM01RR010710 · NCRR · STATE UNIVERSITY NEW YORK STONY BROOK · PI GOLDSTEIN, RITA Z · 1998 to 2009
$17.6M
REGULATION OF TISSUE REPAIRR01EB002065 · NIBIB · STATE UNIVERSITY NEW YORK STONY BROOK · PI CHEN, WEN-TIEN · 2003 to 2008
$1.6M
MOLECULAR ULTRASTRUCTURE UNDERLYING CELL ADHESIONR01CA039077 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI CHEN, WEN-TIEN · 1985 to 2007
$1.6M
Gene Expression of Viable Ovarian Cancer CellsR41CA103467 · NCI · VITATEX, INC. · PI CHEN, WEN-TIEN · 2003 to 2003
$177k
NCI NIH HHS R01 CA039077NCI NIH HHS R01 CA039077-20NCI NIH HHS R01 CA039077-21NCI NIH HHS R01 CA039077-22NCI NIH HHS R41 CA103467-01NCRR NIH HHS M01 RR010710-070061NIBIB NIH HHS R01 EB002065NIBIB NIH HHS R01 EB002065-17NIBIB NIH HHS R01 EB002065-18NIBIB NIH HHS R01 EB002065-19NIBIB NIH HHS R01 EB002065-20
6 · The paper itself

Abstract

MT1-MMP is a key integral membrane protease, which regulates tumor growth by cleaving extracellular matrix components, activating growth factors and receptors, and consequently, triggering downstream signals. To study what genes or pathways are mediated by endogenous MT1-MMP during tumor growth in vivo, we stably suppressed endogenous MT1-MMP in human tumor cells using RNA interference (RNAi). Tumor growth was significantly reduced in tumors derived from MT1-MMP-suppressed cells relative to control cells; the effect was rescued in cells engineered to re-express MT1-MMP expression. Gene expression profiling of cultured and tumor-derived cells by DNA microarray and real-time RT-PCR revealed that Smad1 expression was upregulated in MT1-MMP-expressing cells and rapidly growing tumors; this was confirmed in 4 additional tumor cell lines. Furthermore, tumor growth of MT1-MMP-expressing cells was reduced when Smad1 was suppressed by RNAi. We also found that the active form, but not the latent form, of TGF-beta was capable in promoting Smad1 expression and 3D cell proliferation in MT1-MMP-suppressed cells. In addition, a dominant-negative form of the TGF-beta Type II receptor reduced Smad1 expression in MT1-MMP-expressing cells. Thus, we propose that MT1-MMP functions, in part, to promote tumor growth by inducing the expression of Smad1 via TGF-beta signaling.

Indexed as

AnimalsBase SequenceCell Line, TumorCell ProliferationDNA PrimersGene Expression ProfilingHumansMatrix Metalloproteinase 14MiceMice, NudeNeoplasmsOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionRNA InterferenceRNA, MessengerSmad1 ProteinDNA PrimersMatrix Metalloproteinase 14RNA, MessengerSmad1 ProteinTransforming Growth Factor beta

Identifiers

PMID17455258
PMCPMC2084471
OpenAlexW1988019564

What OpenQuestion holds

Textmetadata
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.