Evidence map›Paper›PMID 31671408›Full record

ArticleEndocrine connections2019

Leptin induces cell migration and invasion in a FAK-Src-dependent manner in breast cancer cells.

Juan Carlos Juárez-Cruz, Miriam Daniela Zuñiga-Eulogio, Monserrat Olea-Flores, Eduardo Castañeda-Saucedo, Miguel Ángel Mendoza-Catalán, Carlos Ortuño-Pineda, Ma Elena Moreno-Godínez, Sócrates Villegas-Comonfort, Teresita Padilla-Benavides, Napoleón Navarro-Tito

Open access · goldAbstract read
In one paragraph

Article in Endocrine connections, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.1field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 58 citations in OpenAlex.

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  16. Exploring the multifaceted role of obesity in breast cancer progression.Frontiers in cell and developmental biology · 2024
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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

10 authors at 3 institutions in 2 countries.

Juan Carlos Juárez-CruzFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Miriam Daniela Zuñiga-EulogioFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Monserrat Olea-FloresFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Eduardo Castañeda-SaucedoFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Miguel Ángel Mendoza-CatalánFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Carlos Ortuño-PinedaFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Ma Elena Moreno-GodínezFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Sócrates Villegas-ComonfortInstituto de Fisiología Celular, Universidad Nacional Autónoma de Mexico, Mexico City, México.
Teresita Padilla-BenavidesDepartment of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
Napoleón Navarro-TitoFacultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Guerrero, México.
Universidad Autónoma de Guerrero · MXUniversidad Nacional Autónoma de México · MXUniversity of Massachusetts Chan Medical School · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is the most common invasive neoplasia, and the second leading cause of the cancer deaths in women worldwide. Mammary tumorigenesis is severely linked to obesity, one potential connection is leptin. Leptin is a hormone secreted by adipocytes, which contributes to the progression of breast cancer. Cell migration, metalloproteases secretion, and invasion are cellular processes associated with various stages of metastasis. These processes are regulated by the kinases FAK and Src. In this study, we utilized the breast cancer cell lines MCF7 and MDA-MB-231 to determine the effect of leptin on FAK and Src kinases activation, cell migration, metalloprotease secretion, and invasion. We found that leptin activates FAK and Src and induces the localization of FAK to the focal adhesions. Interestingly, leptin promotes the activation of FAK through a Src- and STAT3-dependent canonical pathway. Specific inhibitors of FAK, Src and STAT3 showed that the effect exerted by leptin in cell migration in breast cancer cells is dependent on these proteins. Moreover, we established that leptin promotes the secretion of the extracellular matrix remodelers, MMP-2 and MMP-9 and invasion in a FAK and Src-dependent manner. Our findings strongly suggest that leptin promotes the development of a more aggressive invasive phenotype in mammary cancer cells.

Indexed as

breast cancercell migrationFAKinvasionleptinmetalloproteasesSrc

Identifiers

PMID31671408
PMCPMC6893313
OpenAlexW2989515740

What OpenQuestion holds

Textmetadata
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.