Format

Send to

Choose Destination
See comment in PubMed Commons below
Exp Cell Res. 2014 Oct 1;327(2):307-17. doi: 10.1016/j.yexcr.2014.06.016. Epub 2014 Jun 30.

A soluble form of GAS1 inhibits tumor growth and angiogenesis in a triple negative breast cancer model.

Author information

1
Departamento de Farmacología, Centro de Investigación y de Estudios Avanzados del IPN, México D.F., Mexico.
2
Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, Av. IPN # 2508, México D.F. 07300, Mexico.
3
Departamento de Matemáticas, Universidad Autónoma Metropolitana-Iztapalapa, México D.F., Mexico.
4
Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del IPN, Av. IPN # 2508, México D.F. 07300, Mexico. Electronic address: jsegovia@fisio.cinvestav.mx.

Abstract

We previously demonstrated the capacity of GAS1 (Growth Arrest Specific 1) to inhibit the growth of gliomas by blocking the GDNF-RET signaling pathway. Here, we show that a soluble form of GAS1 (tGAS1), decreases the number of viable MDA MB 231 human breast cancer cells, acting in both autocrine and paracrine manners when secreted from producing cells. Moreover, tGAS1 inhibits the growth of tumors implanted in female nu/nu mice through a RET-independent mechanism which involves interfering with the Artemin (ARTN)-GFRα3-(GDNF Family Receptor alpha 3) mediated intracellular signaling and the activation of ERK. In addition, we observed that the presence of tGAS1 reduces the vascularization of implanted tumors, by preventing the migration of endothelial cells. The present results support a potential adjuvant role for tGAS1 in the treatment of breast cancer, by detaining tumor growth and inhibiting angiogenesis.

KEYWORDS:

Angiogenesis; Artemin; Breast cancer; ERK1/2; Growth Arrest Specific 1; tGAS1

PMID:
24992044
DOI:
10.1016/j.yexcr.2014.06.016
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center