Mutual cytokine crosstalk between colon cancer cells and microenvironment initiates development of distant metastases
| Authors | |
|---|---|
| Year of publication | 2013 |
| Type | Article in Periodical |
| Magazine / Source | JAK-STAT |
| MU Faculty or unit | |
| 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. |
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