Evidence map›Paper›PMID 19112600›Full record

ArticleClinical & experimental metastasis2009

Leptin utilizes Jun N-terminal kinases to stimulate the invasion of MCF-7 breast cancer cells.

Vanity McMurtry, Ann-Marie Simeone, René Nieves-Alicea, Ana M Tari

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & experimental metastasis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 36 citations in OpenAlex.

  1. Leptin-induced signaling pathways in cancer cell migration and invasion.Cellular oncology (Dordrecht, Netherlands) · 2019
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  5. Association of serum soluble leptin receptor and leptin levels with breast cancer.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2014
    Article
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  15. Leptin in human physiology and therapeutics.Frontiers in neuroendocrinology · 2010
    Review
  16. 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

4 authors at 1 institution in 1 country.

Vanity McMurtryDepartment of Experimental Therapeutics, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX, USA.
Ann-Marie Simeone
René Nieves-Alicea
Ana M Tari
The University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In breast tumors, high levels of leptin have been associated with increased incidence of breast cancer metastasis. Breast cancer metastasis is directly associated with breast cancer cell invasion. However, whether leptin could augment breast cancer cell invasion is not known. Here we showed that leptin increased the invasiveness and the matrix metallo-proteinase-2 (MMP-2) activity of the MCF-7 breast cancer cell line. Leptin stimulated the phosphorylation of extracellular signals regulated kinases, signal transducers and activators of transcription 3 and Jun N-terminal kinases (JNK); however, only inhibition of JNK decreased leptin-mediated activation of MMP-2. Furthermore, inhibition of JNK suppressed leptin-mediated breast cancer cell invasion. Here we report the novel findings that leptin increased invasion of breast cancer cells by activating JNK, resulting in increased MMP-2 activity.

Indexed as

Breast NeoplasmsCell Line, TumorExtracellular Signal-Regulated MAP KinasesFemaleHumansJNK Mitogen-Activated Protein KinasesLeptinMAP Kinase Signaling SystemMatrix Metalloproteinase 2Neoplasm InvasivenessPhosphorylationSignal TransductionExtracellular Signal-Regulated MAP KinasesJNK Mitogen-Activated Protein KinasesLeptinMatrix Metalloproteinase 2

Identifiers

PMID19112600
OpenAlexW2059407727

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.