Relationship of IL-19 to the metastatic potential of a lung tumor

Joshua Rothenberg, Russell Zhuravsky, Marlow B. Hernandez, Natasha Bray, Tony Weaver

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Interleukin 19 (IL-19), an anti-inflammatory and immunosuppressant cytokine, has been shown to affect the function and viability of lung fibroblasts, and has been implicated in lung cancer metastasis. 1-4 The purpose of this research was to compare gene expression profiles of IL-19 genes (through the collection of RNA isolates) between two lines of mice, an original tumor line (DA-3/TM), and a surgically resected metastatic tumor line (DA-3/TM-Mets). A battery of laboratory procedures were used to study metastasis of cancer from a primary tumor cell line, DA-3/TM, and from a metastatic site, DA-3/TM-Mets. Metastatic lesions in animal models were isolated, cultured, and analyzed in order to observe the changes between the primary and metastatic line. Both PCR and then Western Blots were performed to verify the initial findings from the metastatic lesions of mice. It was found that DA-3/TM-Mets, had more nodule metastasis throughout the lungs of BALB/c mice compared to that of DA-3/TM. A gene array performed showed that the key difference was IL-19, which was 30X higher in DA-3/TM-Mets than in DA-3/TM. This suggests a significant difference at the gene level. However, it is important to develop a new model to look at these tumor cell lines at the protein level in order to observe if this difference holds true. The data acquired shows promising results. Higher concentrations of IL-19 in the DA-3/ TM- Mets line may lead to the conclusion that IL-19 is exhibiting immunosuppressive activity, which does not allow the BALB/c mice's immune system to fight off a tumor, resulting in their death. Therefore, there appears to be a direct correlation between the metastasis of cancer and the protein IL-19's immunosuppressive effects.

Original languageEnglish
JournalInternet Journal of Oncology
Issue number1
StatePublished - 2010


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