Mutual cytokine crosstalk between colon cancer cells and microenvironment initiates development of distant metastases

Warning

This publication doesn't include Faculty of Arts. It includes Faculty of Medicine. Official publication website can be found on muni.cz.
Authors

VAŇHARA Petr SOUČEK Karel

Year of publication 2013
Type Article in Periodical
Magazine / Source JAK-STAT
MU Faculty or unit

Faculty of Medicine

Citation
Web https://www.landesbioscience.com/journals/jak-stat/2012JAKS0099.pdf
Doi http://dx.doi.org/10.4161/jkst.23810
Field Genetics and molecular biology
Keywords metastasis; transforming growth factor-b; interleukin 11; metastatic niche; tumor stroma; dissemination; microenvironment
Description Tumor growth and cancer development are considered clear examples of Darwinian selection, whereby random mutational events in heterogeneous cancer cell populations that best fit the selective microenvironment are preferred.1 As a result, cancer cells evolve resistance to apoptosis, hide from immune surveillance and acquire the ability to invade other organs. Cancer cells, however, are not necessarily passive subjects of selection; they can actively subvert the host tissue to provide a favorable habitat for their growth. Recent findings by Calon et al. convincingly demonstrate that transforming growth factor-b-induced secretion of interleukin 11 by tumor stromal fibroblasts is a necessary prerequisite for the development of distant metastases in colorectal carcinoma. Thus, understanding the complex molecular feedback loops between cancer cells and the surrounding microenvironment (i.e., the tumor-associated stroma or invaded host tissue) should aid the identification of useful molecular targets for improving clinical management of advanced metastatic cancers.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.